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Gene Information
Gene symbol: APOB
Gene name: apolipoprotein B (including Ag(x) antigen)
HGNC ID: 603
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 214369 | Although total VLDL-protein rose, the proportion of VLDL-protein that was ApoB and arginine-rich protein (ARP) fell, while ApoC rose. |
| 2 | 214369 | Although VLDL-protein rose, the proportion that was ApoB fell; both ApoC and ARP rose, ARP subunits were unchanged, while ApoC-III0 rose from 29 to 37 per cent and ApoC-III3 fell from 48 to 42 per cent. |
| 3 | 214369 | Although total VLDL-protein rose, the proportion of VLDL-protein that was ApoB and arginine-rich protein (ARP) fell, while ApoC rose. |
| 4 | 214369 | Although VLDL-protein rose, the proportion that was ApoB fell; both ApoC and ARP rose, ARP subunits were unchanged, while ApoC-III0 rose from 29 to 37 per cent and ApoC-III3 fell from 48 to 42 per cent. |
| 5 | 1289018 | In Type 1 diabetes those with CHD had significantly higher levels of systolic blood pressure, albumin excretion, serum creatinine, triglycerides, VLDL cholesterol and C-peptide, and reductions in serum concentrations of HDL and HDL2 cholesterol, in comparison to those without. |
| 6 | 1289018 | Logistic regression analysis revealed the strongest independent predictors of CHD in Type 1 diabetes were serum triglycerides, systolic blood pressure, age, serum LDL cholesterol, and the daily insulin dosage, whereas in the non-diabetic control group HDL2 cholesterol, Lp(a), ApoA1 and ApoB, total serum cholesterol and body mass index were additional predictors. |
| 7 | 1358344 | Apolipoprotein levels in normolipidemic non-insulin-dependent diabetes mellitus. |
| 8 | 1358344 | The purpose of this study was to examine the change in apolipoprotein and lipoprotein levels in patients with normolipidemic untreated non-insulin-dependent diabetes mellitus (NIDDM). |
| 9 | 1358344 | The apolipoprotein A-I (apo A-I) and apolipoprotein A-II (apo A-II) levels were decreased in NIDDM patients, while the apolipoprotein B (apo B) level remained similar to that of the control subjects. |
| 10 | 1364493 | The level of lipoprotein Lp(a), one of the risk factors of atherosclerosis, was determined in 91 children and adolescents of age ranging from 3.3 to 22 years suffering from insulin-dependent diabetes. |
| 11 | 1364493 | The relation between the level of Lp(a) and other parameters of lipid metabolism (total cholesterol, triglycerides, phospholipids, HDL-cholesterol and apolipoprotein B) as well as a degree of metabolic normalization of diabetes (as assessed by the determination of glycosylated hemoglobin and fructosamine) was studied in addition. |
| 12 | 1464889 | In men (mean age 35.6 +/- 8.7 years, n = 769), both systolic and diastolic BP were positively associated with age, body mass index, waist/hip ratio, fasting and 2h glucose and insulin, triglycerides and apolipoprotein B, and were negatively associated with glucose/insulin ration, and high density lipoprotein and cholesterol and its subfractions. |
| 13 | 1474769 | The patients also had reduced levels of ApoA-I and ApoA-II, increased levels of ApoC-II and ApoC-III, while increases in levels of ApoB and ApoE were statistically significant in patients with GFR < 20 ml/min. |
| 14 | 1512014 | Conjugated dienes in lipids of apolipoprotein B containing lipoproteins of normal and type 2 (non-insulin-dependent) diabetic patients. |
| 15 | 1512014 | Conjugated dienes present in the fatty acyl chains of cholesterol esters and triglycerides associated with plasma apolipoprotein B containing lipoproteins of normal and Type 2 (non-insulin-dependent) diabetic patients (n = 17) have been analysed using second derivative electronic absorption spectroscopy. |
| 16 | 1512014 | Conjugated dienes in lipids of apolipoprotein B containing lipoproteins of normal and type 2 (non-insulin-dependent) diabetic patients. |
| 17 | 1512014 | Conjugated dienes present in the fatty acyl chains of cholesterol esters and triglycerides associated with plasma apolipoprotein B containing lipoproteins of normal and Type 2 (non-insulin-dependent) diabetic patients (n = 17) have been analysed using second derivative electronic absorption spectroscopy. |
| 18 | 1521727 | HDL-cholesterol, and apolipoprotein A-I remained unchanged. |
| 19 | 1521727 | Total cholesterol, LDL-cholesterol, HDL-cholesterol, apolipoprotein A-I, apolipoprotein B remained unchanged during placebo treatment. |
| 20 | 1531990 | Lipoprotein cholesterol, apolipoprotein A-I and B and lipoprotein (a) abnormalities in men with premature coronary artery disease. |
| 21 | 1531990 | They also had significantly lower high density lipoprotein (HDL) cholesterol (36 +/- 11 vs. 45 +/- 12 mg/dl) and apolipoprotein A-I levels (114 +/- 26 vs. 136 +/- 32 mg/dl) (all p less than 0.005). |
| 22 | 1531990 | Stepwise discriminant analysis indicates that smoking, hypertension, decreased apolipoprotein A-I, increased apolipoprotein B, increased Lp(a) and diabetes are all significant (p less than 0.05) factors in descending order of importance in distinguishing patients with coronary artery disease from normal control subjects. |
| 23 | 1532112 | Total cholesterol, triglycerides, high- and low-density lipoprotein cholesterol, apolipoprotein A-I, apolipoprotein B and Lp(a) were compared. |
| 24 | 1561971 | Age, cigarette smoking, hypertension, obesity, diabetes, positive family history of premature coronary artery disease (CAD), and plasma levels of total cholesterol, triglyceride, lipoproteins (i.e., very low, intermediate-, low-, and high-density [HDL] lipoproteins and their subfractions [HDL2 and HDL3], and lipoprotein [a]) and apolipoproteins (apoA-1, apoA-2 and apoB, respectively) were examined using univariate analyses and multivariate logistic regression. |
| 25 | 1561971 | It is concluded that the "nontraditional" risk factors (plasma apoA-1 and apoB levels) are better predictors of premature CAD than are plasma lipoproteins and that smoking is the strongest of the traditional nonlipid risk factors. |
| 26 | 1561971 | Age, cigarette smoking, hypertension, obesity, diabetes, positive family history of premature coronary artery disease (CAD), and plasma levels of total cholesterol, triglyceride, lipoproteins (i.e., very low, intermediate-, low-, and high-density [HDL] lipoproteins and their subfractions [HDL2 and HDL3], and lipoprotein [a]) and apolipoproteins (apoA-1, apoA-2 and apoB, respectively) were examined using univariate analyses and multivariate logistic regression. |
| 27 | 1561971 | It is concluded that the "nontraditional" risk factors (plasma apoA-1 and apoB levels) are better predictors of premature CAD than are plasma lipoproteins and that smoking is the strongest of the traditional nonlipid risk factors. |
| 28 | 1562163 | The following parameters were measured: total cholesterol (Chol), triglycerides (TG), HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C), apoprotein A1 (apoA1), apoprotein B (apoB), lipoprotein (a) or Lp(a), fibrinogen, insulinemia and plasminogen activator inhibitor activity (PAI). |
| 29 | 1562163 | The levels of chol, LDL-C and ApoB were the same in the 3 groups. |
| 30 | 1562163 | In this study, TG, HDL-chol, apoA1 and the apoB ratio were better predictors of cardiovascular risk than Chol, LDL-C or apoB. |
| 31 | 1562163 | The following parameters were measured: total cholesterol (Chol), triglycerides (TG), HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C), apoprotein A1 (apoA1), apoprotein B (apoB), lipoprotein (a) or Lp(a), fibrinogen, insulinemia and plasminogen activator inhibitor activity (PAI). |
| 32 | 1562163 | The levels of chol, LDL-C and ApoB were the same in the 3 groups. |
| 33 | 1562163 | In this study, TG, HDL-chol, apoA1 and the apoB ratio were better predictors of cardiovascular risk than Chol, LDL-C or apoB. |
| 34 | 1562754 | Glomerular hyperfiltration was associated with high blood glucose in type I, insulin-dependent diabetics, and with a high apolipoprotein B/A1 ratio in type II, non-insulin-dependent diabetics without insulin treatment. |
| 35 | 1611832 | No significant differences were found in body weight, HbA1C, insulin binding to erythrocytes, insulin and drug requirements, and other circulating lipids (cholesterol, HDL-cholesterol, phospholipids, Apolipoprotein A1, Apolipoprotein B). |
| 36 | 1832357 | Fourteen male patients with Type 2 diabetes were studied to identify relationships between insulin-mediated glucose disposal, basal and glucose-stimulated insulin secretion, fasting lipoproteins and apolipoproteins, and the activities of lipoprotein lipase and hepatic lipase. |
| 37 | 1832357 | Sensitivity of glucose disposal to exogenous insulin correlated positively with HDL-cholesterol (r = 0.65, p less than 0.05), HDL2-cholesterol (r = 0.59, p less than 0.05), and apolipoprotein A1 (r = 0.57, p less than 0.05) and negatively with apolipoprotein B (r = -0.53, p less than 0.05) and total: HDL-cholesterol ratio (r = -0.68, p less than 0.01). |
| 38 | 1832357 | Insulin insensitivity and hyperinsulinaemia were both associated with higher levels of hepatic lipase activity but did not influence lipoprotein lipase activity. |
| 39 | 1838064 | Plasma lipid and apolipoprotein levels of Type 1 and Type 2 young Kuwaiti diabetic women on insulin therapy were investigated to elucidate the relationship between coronary artery disease risk factors and lipid levels. |
| 40 | 1838064 | Levels of HDL-, HDL2- and HDL3-cholesterol and plasma apolipoprotein AI were markedly decreased in both the diabetic groups compared with their control groups (all p less than 0.001 except HDL3-cholesterol in Type 1 diabetic vs control, p less than 0.05). |
| 41 | 1838064 | In Type 2 diabetic patients, HbA1c correlated positively with triglycerides (r = 0.70, p less than 0.001), cholesterol (r = 0.60, p less than 0.001), apolipoprotein B (r = 0.77, p less than 0.001), and apolipoprotein CIII (r = 0.55, p less than 0.001) and negatively with apolipoprotein AI (r = -0.49, p less than 0.001). |
| 42 | 1892482 | Subjects with IGT or newly diagnosed NIDDM had higher levels of total triglycerides and apolipoprotein B and lower levels of HDL cholesterol and apolipoprotein A1 than subjects with normal glucose tolerance, similarly as in previously diagnosed NIDDM. |
| 43 | 1936612 | We studied the molecular characteristics of three naturally occurring variants in the human apolipoprotein B (apoB) signal peptide, their frequencies in non-insulin-dependent diabetic and random populations, and their association with several measures of lipid and carbohydrate metabolism. |
| 44 | 1947727 | ApoE phenotype group E3/E2 had significantly lower values for serum cholesterol, LDL-cholesterol, and apoB and higher levels of apoE in comparison with the phenotype groups E3/E3 and E4/E3. |
| 45 | 2007844 | Fasting glucose and apolipoprotein B concentrations were higher in the hypertriglyceridaemic patients, but lipoprotein lipase activities were similar in the two groups. |
| 46 | 2064632 | This study was designed to investigate whether the presence of non-insulin-dependent diabetes mellitus (NIDDM) or coronary heart disease (CHD) in probands have different effects on serum lipid, lipoprotein and apolipoprotein concentrations in the first-degree relatives. |
| 47 | 2064632 | Total LDL and VLDL cholesterol and apolipoprotein B were higher (P less than 0.05) and HDL/total cholesterol ratio and apolipoprotein A1/B ratio lower (P less than 0.05) in the daughters of the nondiabetic and diabetic probands were pooled, CHD in the proband was associated particularly with low apolipoprotein A1/B ratio. |
| 48 | 2064632 | In conclusion, (1) the presence of NIDDM in the proband appears to be associated in siblings with more profound lipid and lipoprotein changes (especially low HDL cholesterol and high total triglycerides) than a history of CHD in the proband, (2) a history of CHD in the proband is associated in children with apolipoprotein changes favouring atherosclerosis (low apolipoprotein A1, high apolipoprotein B, low apolipoprotein A1/B ratio). |
| 49 | 2064632 | This study was designed to investigate whether the presence of non-insulin-dependent diabetes mellitus (NIDDM) or coronary heart disease (CHD) in probands have different effects on serum lipid, lipoprotein and apolipoprotein concentrations in the first-degree relatives. |
| 50 | 2064632 | Total LDL and VLDL cholesterol and apolipoprotein B were higher (P less than 0.05) and HDL/total cholesterol ratio and apolipoprotein A1/B ratio lower (P less than 0.05) in the daughters of the nondiabetic and diabetic probands were pooled, CHD in the proband was associated particularly with low apolipoprotein A1/B ratio. |
| 51 | 2064632 | In conclusion, (1) the presence of NIDDM in the proband appears to be associated in siblings with more profound lipid and lipoprotein changes (especially low HDL cholesterol and high total triglycerides) than a history of CHD in the proband, (2) a history of CHD in the proband is associated in children with apolipoprotein changes favouring atherosclerosis (low apolipoprotein A1, high apolipoprotein B, low apolipoprotein A1/B ratio). |
| 52 | 2103782 | We studied the role played by an adequate metabolic control on lipids, lipoproteins, apolipoprotein A (apo A), apolipoprotein A-I (apo A-I) and apolipoprotein B (apo B), in 30 type I diabetic patients at different states of the diseases. |
| 53 | 2105208 | Having demonstrated that plasma low density lipoproteins (LDL) bind T4 through a specific interaction with their sole apolipoprotein, apoB-100, we tested the hypothesis that cells could internalize the LDL-T4 complex via cell surface LDL receptors. |
| 54 | 2105208 | These changes were confirmed with several different LDL preparations and were mimicked by isolated apoB-100 and apoE, the sole ligands for the LDL receptors (apoB/E receptors). |
| 55 | 2105208 | The specificity of the LDL effect was shown by the finding that T4-binding globulin, prealbumin, or serum albumin, at concentrations giving 10-90% T4 bound, failed to increase T4 uptake. |
| 56 | 2105208 | Having demonstrated that plasma low density lipoproteins (LDL) bind T4 through a specific interaction with their sole apolipoprotein, apoB-100, we tested the hypothesis that cells could internalize the LDL-T4 complex via cell surface LDL receptors. |
| 57 | 2105208 | These changes were confirmed with several different LDL preparations and were mimicked by isolated apoB-100 and apoE, the sole ligands for the LDL receptors (apoB/E receptors). |
| 58 | 2105208 | The specificity of the LDL effect was shown by the finding that T4-binding globulin, prealbumin, or serum albumin, at concentrations giving 10-90% T4 bound, failed to increase T4 uptake. |
| 59 | 2109048 | Patients with 70% or greater narrowing of at least one coronary artery or greater than or equal to 50% stenosis of the left main coronary artery (n = 179) were compared to those with lesions of less than 50% stenosis (n = 217) for total cholesterol (TC), low density lipoprotein-cholesterol (LDL-C), high density lipoprotein-cholesterol (HDL-C), LDL-C/HDL-C, triglycerides, apolipoprotein A-I, apolipoprotein B, and apolipoprotein A-I/B. |
| 60 | 2109048 | Using stepwise selection multiple logistic regression analysis, the ratio of apolipoprotein A-I/B (odds ratio = 0.38, 95% confidence limits 0.24-0.61) was the only statistically significant association of CAD in women, after adjusting for the effects of age, body mass index, and histories of smoking, hypercholesterolemia, hypertension, and diabetes. |
| 61 | 2109048 | When stratified by median of total cholesterol, the ratio of apolipoprotein A-I/B was the most strongly associated with the presence of CAD in the lower half of the total cholesterol distribution (less than 208 mg/dl), whereas in the upper half of the total cholesterol distribution the total cholesterol/HDL-C ratio was more strongly associated with CAD. |
| 62 | 2117860 | Logistic regression analysis identified five factors: apolipoprotein A-I, apolipoprotein B, diabetes, age, and family history of heart disease, which account for most of the differences between the two patient groups. |
| 63 | 2132196 | Apolipoprotein and lipid ratios in treated non-insulin dependent diabetics. |
| 64 | 2132196 | Fasting total cholesterol (TC), triglycerides (TG), HDL cholesterol (HDL C), apolipoprotein A1 (apo A1) and apolipoprotein B (apo B) were measured in 35 non-insulin dependent diabetic patients treated by diet with or without sulphonylureas and 35 control subjects matched for age, sex, and body mass index. |
| 65 | 2137219 | [Lipoprotein and apolipoprotein levels in young insulin-dependent diabetic patients. |
| 66 | 2137219 | The most significant increases of TG, TC, LDL-C and ApoB levels were observed in group 3, i.e. in patients whose diabetes was the most poorly controlled (HbA 1: 12.9 +/- 1.3 per cent; fructosamine: 4.6 +/- 0.9 mmol/l). |
| 67 | 2137219 | Thus, TG, TC, LDL-C and ApoB are increased in young diabetics whose HbA1 and fructosamine levels exceed reference values by more than 5 standard deviations. |
| 68 | 2137219 | [Lipoprotein and apolipoprotein levels in young insulin-dependent diabetic patients. |
| 69 | 2137219 | The most significant increases of TG, TC, LDL-C and ApoB levels were observed in group 3, i.e. in patients whose diabetes was the most poorly controlled (HbA 1: 12.9 +/- 1.3 per cent; fructosamine: 4.6 +/- 0.9 mmol/l). |
| 70 | 2137219 | Thus, TG, TC, LDL-C and ApoB are increased in young diabetics whose HbA1 and fructosamine levels exceed reference values by more than 5 standard deviations. |
| 71 | 2147637 | Serum apolipoprotein B and apolipoprotein (a) showed no statistically significant changes. |
| 72 | 2148134 | To investigate whether persistent microalbuminuria is related to altered levels of both lipids and apolipoproteins in Type 2 diabetes mellitus serum total-cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, apolipoprotein A-I, and apolipoprotein B were measured by standard methods in a group of Type 2 diabetic patients affected by persistent microalbuminuria (albumin excretion rate (AER) 20-200 micrograms min-1) as compared with a group of sex- and age-matched non-microalbuminuric patients (AER less than 20 micrograms min-1). |
| 73 | 2182032 | Effect of different insulin regimens on plasma lipoprotein and apolipoprotein concentrations in patients with non-insulin-dependent diabetes mellitus. |
| 74 | 2182032 | Mean plasma apolipoprotein A1 concentration increased with 9% (P less than 0.05) while there was no significant change in the plasma apolipoprotein B concentration. |
| 75 | 2200727 | Effect of insulin therapy on metabolic fate of apolipoprotein B-containing lipoproteins in NIDDM. |
| 76 | 2200727 | Postheparin plasma lipoprotein lipase (LPL) and hepatic lipase levels were unaffected by insulin, although the hormone did increase LPL in adipose tissue. |
| 77 | 2200727 | This lack of effect on lipase activities correlated well with the observation that the rates of catabolism of apoB in VLDL1, VLDL2, and IDL were not significantly affected by insulin therapy. |
| 78 | 2200727 | Effect of insulin therapy on metabolic fate of apolipoprotein B-containing lipoproteins in NIDDM. |
| 79 | 2200727 | Postheparin plasma lipoprotein lipase (LPL) and hepatic lipase levels were unaffected by insulin, although the hormone did increase LPL in adipose tissue. |
| 80 | 2200727 | This lack of effect on lipase activities correlated well with the observation that the rates of catabolism of apoB in VLDL1, VLDL2, and IDL were not significantly affected by insulin therapy. |
| 81 | 2200808 | In this study, kinetics of VLDL, intermediate density lipoprotein (IDL), and LDL apoprotein B and VLDL triglyceride were determined in seven nondiabetic (ND) and seven non-insulin-dependent diabetic (NIDDM) Pima Indian subjects on high-fat and high-carbohydrate (HICHO) diets. |
| 82 | 2200808 | Means for total LDL apoB transport rate, LDL apoB FCR, and LDLC/apoB ratios were unchanged. |
| 83 | 2200808 | There was also evidence in some subjects for increased activity of LDL apoB clearance mechanisms, and a decrease in the LDLC to apoB ratio. |
| 84 | 2200808 | In this study, kinetics of VLDL, intermediate density lipoprotein (IDL), and LDL apoprotein B and VLDL triglyceride were determined in seven nondiabetic (ND) and seven non-insulin-dependent diabetic (NIDDM) Pima Indian subjects on high-fat and high-carbohydrate (HICHO) diets. |
| 85 | 2200808 | Means for total LDL apoB transport rate, LDL apoB FCR, and LDLC/apoB ratios were unchanged. |
| 86 | 2200808 | There was also evidence in some subjects for increased activity of LDL apoB clearance mechanisms, and a decrease in the LDLC to apoB ratio. |
| 87 | 2226312 | We conclude that the three T4-binding sites of apoB-100 are outside the LDL receptor binding domain, distant from the heparin binding sites and, assuming no allosteric effects, in the vicinity of residues 474-539 (T4 site of apoB-26), 1438-1481 (T4 site of apoB-44), and in the C terminal quarter of apoB-30. |
| 88 | 2243143 | Insulin regulates apolipoprotein B turnover and phosphorylation in rat hepatocytes. |
| 89 | 2347619 | In a subset of patients in whom lipoproteins were measured, sodium-lithium countertransport activity was related to total and very low density lipoprotein triglycerides (r = 0.41, p less than 0.05 and r = 0.48, p less than 0.05) and to apolipoprotein B (r = 0.56, p less than 0.05), independently of body mass index, albumin excretion rate, glycemic control, and insulin dose. |
| 90 | 2365166 | Current glycemia, average glycemia, fructosamine, glycosylated hemoglobin, triglycerides, LDL-cholesterol and apolipoprotein B were obviously much higher than normal in the individuals admitted to the study. |
| 91 | 2404717 | Linkage studies of the insulin gene, insulin-receptor gene, erythrocyte/HepG2 glucose-transporter locus, and apolipoprotein B locus have shown no association with MODY. |
| 92 | 2501960 | In addition to the above mentioned differences, CHD in long-term type I diabetes was also accompanied by lower HDL cholesterol, lower apolipoprotein A-I, and a higher apolipoprotein B/apolipoprotein A-I ratio. |
| 93 | 2507381 | The relationships between serum lipid, apolipoprotein levels and urinary albumin excretion were investigated in 20 male Type 1 (insulin-dependent) diabetic patients with microalbuminuria (overnight urinary albumin excretion between 10 and 200 micrograms/min), in 18 male Type 1 diabetic patients without microalbuminuria and in 18 male control subjects. |
| 94 | 2507381 | In the 2 combined Type 1 diabetic groups there were significant correlations between urinary albumin excretion and the high density lipoprotein/low density lipoprotein cholesterol ratio (R -0.40, p less than 0.02), apolipoprotein B (R 0.35, p less than 0.05) and the apolipoprotein A1/B ratio (R -0.44, p les than 0.01). |
| 95 | 2562831 | Insulin-receptor and apolipoprotein genes contribute to development of NIDDM in Chinese Americans. |
| 96 | 2562831 | The frequencies of restriction-fragment-length polymorphism (RFLP) alleles as well as RFLP haplotypes at six genetic loci responsible for carbohydrate and lipid metabolism [insulin/insulin-like growth factor II complex, insulin receptor (INSR), HepG2/erythrocyte-type glucose transporter, apolipoprotein A-II, apolipoprotein B (APOB), and the apolipoprotein A-I/C-III/A-IV cluster (APOA1/C3/A4)] were compared between nondiabetic and diabetic Chinese Americans. |
| 97 | 2562831 | The disease-association data suggest that genetic variation at the INSR, APOB, and APOA1/C3/A4 loci contributes to the development of non-insulin-dependent diabetes mellitus (NIDDM). |
| 98 | 2562831 | The APOB and APOA1/C3/A4 loci appear to contribute to the development of NIDDM in individuals who are of lean/normal weight and overweight, respectively. |
| 99 | 2562831 | Insulin-receptor and apolipoprotein genes contribute to development of NIDDM in Chinese Americans. |
| 100 | 2562831 | The frequencies of restriction-fragment-length polymorphism (RFLP) alleles as well as RFLP haplotypes at six genetic loci responsible for carbohydrate and lipid metabolism [insulin/insulin-like growth factor II complex, insulin receptor (INSR), HepG2/erythrocyte-type glucose transporter, apolipoprotein A-II, apolipoprotein B (APOB), and the apolipoprotein A-I/C-III/A-IV cluster (APOA1/C3/A4)] were compared between nondiabetic and diabetic Chinese Americans. |
| 101 | 2562831 | The disease-association data suggest that genetic variation at the INSR, APOB, and APOA1/C3/A4 loci contributes to the development of non-insulin-dependent diabetes mellitus (NIDDM). |
| 102 | 2562831 | The APOB and APOA1/C3/A4 loci appear to contribute to the development of NIDDM in individuals who are of lean/normal weight and overweight, respectively. |
| 103 | 2562831 | Insulin-receptor and apolipoprotein genes contribute to development of NIDDM in Chinese Americans. |
| 104 | 2562831 | The frequencies of restriction-fragment-length polymorphism (RFLP) alleles as well as RFLP haplotypes at six genetic loci responsible for carbohydrate and lipid metabolism [insulin/insulin-like growth factor II complex, insulin receptor (INSR), HepG2/erythrocyte-type glucose transporter, apolipoprotein A-II, apolipoprotein B (APOB), and the apolipoprotein A-I/C-III/A-IV cluster (APOA1/C3/A4)] were compared between nondiabetic and diabetic Chinese Americans. |
| 105 | 2562831 | The disease-association data suggest that genetic variation at the INSR, APOB, and APOA1/C3/A4 loci contributes to the development of non-insulin-dependent diabetes mellitus (NIDDM). |
| 106 | 2562831 | The APOB and APOA1/C3/A4 loci appear to contribute to the development of NIDDM in individuals who are of lean/normal weight and overweight, respectively. |
| 107 | 2612004 | Total Apo-B in diabetics (1.02 +/- 0.53 g/l) was increased (controls: 0.75 +/- 0.18 g/l; p less than 0.05) and a positive correlation between HbA1 and Apo-B (r = 0.36, p less than 0.05) was present in this group. |
| 108 | 2629300 | A significant correlation was demonstrated between the concentrations of cholesterol and apolipoprotein A, on the one hand, and blood glucose level, on the other, and apolipoprotein A was found to be a better indicator of lipid disturbances in the aspect of diabetes control then apolipoprotein B. |
| 109 | 2653924 | However, enthusiasm for the use of omega-3 fatty acids in diabetes has been dampened by reports of potentially deleterious effects of these agents, including increased plasma glucose, glycosylated hemoglobin, plasma total cholesterol and LDL cholesterol, and serum apolipoprotein B levels. |
| 110 | 2656141 | Concentrations of total cholesterol, very-low-density lipoprotein cholesterol, low-density lipoprotein (LDL) cholesterol, triglyceride (TG), LDL TG, high-density lipoprotein triglyceride (HDL TG), phospholipid, glucose, glycosylated hemoglobin (HbAtc), apolipoprotein B (apoB), LDL-apoB, and apoB/apoAl were significantly elevated in diabetic women compared with control subjects. |
| 111 | 2656141 | Despite normal body weight and insulin therapy, abnormalities in lipids, lipoprotein lipids, and apoB persisted in NIDDM patients compared with control subjects. |
| 112 | 2656141 | Concentrations of total cholesterol, very-low-density lipoprotein cholesterol, low-density lipoprotein (LDL) cholesterol, triglyceride (TG), LDL TG, high-density lipoprotein triglyceride (HDL TG), phospholipid, glucose, glycosylated hemoglobin (HbAtc), apolipoprotein B (apoB), LDL-apoB, and apoB/apoAl were significantly elevated in diabetic women compared with control subjects. |
| 113 | 2656141 | Despite normal body weight and insulin therapy, abnormalities in lipids, lipoprotein lipids, and apoB persisted in NIDDM patients compared with control subjects. |
| 114 | 2673217 | Insulin effects on apolipoprotein B production by normal, diabetic and treated-diabetic rat liver and cultured rat hepatocytes. |
| 115 | 2673217 | The effect of insulin on apolipoprotein (apo B) secretion was studied in 24 h recirculating liver perfusions of isolated normal, diabetic and insulin-treated diabetic rats. |
| 116 | 2678583 | Increased plasminogen activator inhibitor activity in non insulin dependent diabetic patients--relationship with plasma insulin. |
| 117 | 2678583 | Type 2 diabetic patients are known to frequently have a high insulin level and were recently described as having high plasminogen activator inhibitor (PAI) activity, compared to normal controls. |
| 118 | 2678583 | As we have shown in several clinical conditions (normal subjects, obese patients, angina pectoris patients) that plasma PAI activity was linked with plasma insulin, we have studied in 38 type 2 diabetic patients the relationship between PAI activity, insulin and other parameters. |
| 119 | 2678583 | Patients showed higher level of PAI activity, as well as plasma glucose, insulin, triglyceride, cholesterol and Apolipoprotein B levels than normal controls; highest values were observed with diabetic patients also affected by coronary artery disease. |
| 120 | 2678583 | A significant correlation was found between PAI activity and insulin (r = 0.60, p less than 0.001), body mass index (r = 0.32, p less than 0.05) and Apolipoprotein B (r = 0.33, p less than 0.05). |
| 121 | 2678583 | These results are in agreement with our previous report showing an in vitro effect of insulin on the synthesis of PAI by a hepatocellular cell line. |
| 122 | 2678583 | Increased plasminogen activator inhibitor activity in non insulin dependent diabetic patients--relationship with plasma insulin. |
| 123 | 2678583 | Type 2 diabetic patients are known to frequently have a high insulin level and were recently described as having high plasminogen activator inhibitor (PAI) activity, compared to normal controls. |
| 124 | 2678583 | As we have shown in several clinical conditions (normal subjects, obese patients, angina pectoris patients) that plasma PAI activity was linked with plasma insulin, we have studied in 38 type 2 diabetic patients the relationship between PAI activity, insulin and other parameters. |
| 125 | 2678583 | Patients showed higher level of PAI activity, as well as plasma glucose, insulin, triglyceride, cholesterol and Apolipoprotein B levels than normal controls; highest values were observed with diabetic patients also affected by coronary artery disease. |
| 126 | 2678583 | A significant correlation was found between PAI activity and insulin (r = 0.60, p less than 0.001), body mass index (r = 0.32, p less than 0.05) and Apolipoprotein B (r = 0.33, p less than 0.05). |
| 127 | 2678583 | These results are in agreement with our previous report showing an in vitro effect of insulin on the synthesis of PAI by a hepatocellular cell line. |
| 128 | 2689121 | Linkage studies of the insulin gene, the insulin receptor gene, the erythrocyte/Hep G2 glucose transporter locus, and the apolipoprotein B locus have shown no association with MODY. |
| 129 | 2702919 | Failure to achieve tight control of plasma cholesterol and apolipoprotein B with intraperitoneal insulin infusion in type 1 diabetes. |
| 130 | 2707515 | The cholesterylester transfer activity was correlated positively with HbA1, urinary albumin excretion rate, serum cholesterol, very low + low density lipoprotein cholesterol and apolipoprotein B. |
| 131 | 2773912 | NIDDM patients had higher age-adjusted serum triglyceride and apolipoprotein B levels and a higher apolipoprotein B/apolipoprotein A-I ratio, lower serum high density lipoprotein (HDL) cholesterol and apolipoprotein A-1 levels, and a lower HDL cholesterol/apolipoprotein A-1 ratio than nondiabetic subjects. |
| 132 | 2776655 | We report here a new formula for estimating apolipoprotein (apo) B concentration in the low-density lipoprotein (LDL) fraction from measurements of plasma triglyceride and apoB. |
| 133 | 2871420 | Despite the increased risk of atherosclerosis in diabetes mellitus, levels of serum cholesterol, triglycerides, low-density-lipoprotein (LDL) cholesterol, and high-density-lipoprotein (HDL) cholesterol were similar in 57 men with insulin-dependent diabetes mellitus (IDDM) and 81 non-diabetic controls. |
| 134 | 2871420 | However, substantially lower serum levels of apolipoprotein B, the principal apolipoprotein of LDL, and a concomitant increase in the cholesterol-loading of apolipoprotein B were found in IDDM. |
| 135 | 2953658 | Serum levels of apolipoprotein B were measured, and investigations of the platelet function were carried out in 32 patients with insulin-dependent diabetes and in 34 healthy controls similar in age. |
| 136 | 2953658 | Plasma levels of beta-thromboglobulin and platelet factor 4 were raised and, in the presence of N-ethyl maleimide, platelets from diabetic patients produced significantly more malondialdehyde than those from normal controls. |
| 137 | 3044889 | To evaluate possible mechanisms by which insulin inhibits hepatic apolipoprotein B (apoB) secretion, we incubated primary cultures of rat hepatocytes with sodium orthovanadate, a phosphotyrosine phosphatase inhibitor and insulin-mimetic agent. |
| 138 | 3044889 | Vanadate (10 microM) and insulin (10 nM) inhibited the medium accumulation of apoB (secretion) by 21 and 37%, respectively, without increasing intracellular apoB. |
| 139 | 3044889 | Unlike insulin, vanadate, at a concentration that inhibited apoB secretion (10 microM), had no effect on intracellular lipogenesis, inhibited the secretion of newly synthesized hepatic proteins, and had a delayed onset and termination of action on inhibition of apoB secretion. |
| 140 | 3044889 | In conclusion, our data indicate that vanadate mimics insulin action in hepatocytes with regard to the inhibition of medium accumulation of apoB. |
| 141 | 3044889 | To evaluate possible mechanisms by which insulin inhibits hepatic apolipoprotein B (apoB) secretion, we incubated primary cultures of rat hepatocytes with sodium orthovanadate, a phosphotyrosine phosphatase inhibitor and insulin-mimetic agent. |
| 142 | 3044889 | Vanadate (10 microM) and insulin (10 nM) inhibited the medium accumulation of apoB (secretion) by 21 and 37%, respectively, without increasing intracellular apoB. |
| 143 | 3044889 | Unlike insulin, vanadate, at a concentration that inhibited apoB secretion (10 microM), had no effect on intracellular lipogenesis, inhibited the secretion of newly synthesized hepatic proteins, and had a delayed onset and termination of action on inhibition of apoB secretion. |
| 144 | 3044889 | In conclusion, our data indicate that vanadate mimics insulin action in hepatocytes with regard to the inhibition of medium accumulation of apoB. |
| 145 | 3044889 | To evaluate possible mechanisms by which insulin inhibits hepatic apolipoprotein B (apoB) secretion, we incubated primary cultures of rat hepatocytes with sodium orthovanadate, a phosphotyrosine phosphatase inhibitor and insulin-mimetic agent. |
| 146 | 3044889 | Vanadate (10 microM) and insulin (10 nM) inhibited the medium accumulation of apoB (secretion) by 21 and 37%, respectively, without increasing intracellular apoB. |
| 147 | 3044889 | Unlike insulin, vanadate, at a concentration that inhibited apoB secretion (10 microM), had no effect on intracellular lipogenesis, inhibited the secretion of newly synthesized hepatic proteins, and had a delayed onset and termination of action on inhibition of apoB secretion. |
| 148 | 3044889 | In conclusion, our data indicate that vanadate mimics insulin action in hepatocytes with regard to the inhibition of medium accumulation of apoB. |
| 149 | 3044889 | To evaluate possible mechanisms by which insulin inhibits hepatic apolipoprotein B (apoB) secretion, we incubated primary cultures of rat hepatocytes with sodium orthovanadate, a phosphotyrosine phosphatase inhibitor and insulin-mimetic agent. |
| 150 | 3044889 | Vanadate (10 microM) and insulin (10 nM) inhibited the medium accumulation of apoB (secretion) by 21 and 37%, respectively, without increasing intracellular apoB. |
| 151 | 3044889 | Unlike insulin, vanadate, at a concentration that inhibited apoB secretion (10 microM), had no effect on intracellular lipogenesis, inhibited the secretion of newly synthesized hepatic proteins, and had a delayed onset and termination of action on inhibition of apoB secretion. |
| 152 | 3044889 | In conclusion, our data indicate that vanadate mimics insulin action in hepatocytes with regard to the inhibition of medium accumulation of apoB. |
| 153 | 3053747 | Furthermore, pulsatile rather than continuous insulin administration significantly reduced plasma triglyceride, very low density lipoprotein triglyceride, and FFA levels and increased high density lipoprotein cholesterol and apolipoprotein-B levels. |
| 154 | 3094958 | Blood lipid assays repeated after 1, 3, 6, 9, and 12 months of treatment revealed consistent and statistically significant reductions of all atherogenic lipid fractions (total cholesterol, low-density lipoprotein cholesterol, and apolipoprotein B) with parallel increases of high-density lipoprotein cholesterol and apolipoprotein A. |
| 155 | 3134288 | [Effects of different types of treatment on serum HDL-C apoA I and apoB100 in non-insulin dependent diabetes mellitus]. |
| 156 | 3141685 | LDL, which are rich in cholesterol, can also be taken up by the liver or extrahepatic tissues by a receptor-mediated endocytosis that specifically recognises apoB or apoE. |
| 157 | 3141685 | The changes in binding produced by insulin and dexamethasone are paralleled by alterations in the rate of degradation of apoB. |
| 158 | 3141685 | LDL, which are rich in cholesterol, can also be taken up by the liver or extrahepatic tissues by a receptor-mediated endocytosis that specifically recognises apoB or apoE. |
| 159 | 3141685 | The changes in binding produced by insulin and dexamethasone are paralleled by alterations in the rate of degradation of apoB. |
| 160 | 3152618 | Effects of glyburide treatment on serum lipoprotein and apolipoprotein concentrations and ratios in non-insulin-dependent diabetes mellitus. |
| 161 | 3152618 | The pretrial levels of total serum cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A1 and A2, and apolipoprotein B were similar to or even lower than those of nondiabetics; however, high-density lipoprotein cholesterol (HDL-C) levels and HDL-C% (the percentage of TC bound to HDL) were significantly lower in the diabetic patients. |
| 162 | 3152618 | Among the lipid, lipoprotein, and apolipoprotein ratios in the patients, only the ratios HDL-C:LDL-C, apolipoprotein A1:apolipoprotein B, and HDL-C: apolipoprotein B increased significantly as a result of the opposing responses of the protective lipoprotein HDL-C and apolipoprotein A1 and the atherogenic lipoprotein LDL-C and apolipoprotein B. |
| 163 | 3152618 | Effects of glyburide treatment on serum lipoprotein and apolipoprotein concentrations and ratios in non-insulin-dependent diabetes mellitus. |
| 164 | 3152618 | The pretrial levels of total serum cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A1 and A2, and apolipoprotein B were similar to or even lower than those of nondiabetics; however, high-density lipoprotein cholesterol (HDL-C) levels and HDL-C% (the percentage of TC bound to HDL) were significantly lower in the diabetic patients. |
| 165 | 3152618 | Among the lipid, lipoprotein, and apolipoprotein ratios in the patients, only the ratios HDL-C:LDL-C, apolipoprotein A1:apolipoprotein B, and HDL-C: apolipoprotein B increased significantly as a result of the opposing responses of the protective lipoprotein HDL-C and apolipoprotein A1 and the atherogenic lipoprotein LDL-C and apolipoprotein B. |
| 166 | 3267003 | Poor glycaemic control (n = 16) was associated with increased levels of atherogenic lipoproteins as reflected by higher concentrations of total cholesterol, LDL cholesterol, apolipoprotein B, and triglycerides, as well as a changed HDL composition indicated by a decreased HDL cholesterol/apolipoprotein A--I ratio. |
| 167 | 3267003 | Higher ratios of total cholesterol to HDL cholesterol and apolipoprotein B to apolipoprotein A--I point to an increased risk of developing atherosclerotic diseases in poorly controlled diabetics. 86% of the well controlled long-term diabetics had non-pathological values of LDL cholesterol, triglycerides, apolipoprotein B, HDL cholesterol, and apolipoprotein A--I but only 31% of the poorly controlled patients did so. |
| 168 | 3267003 | Diabetic nephropathy in the absence of chronic renal failure (n = 10) was characterized by higher values of LDL cholesterol, triglycerides, total cholesterol/HDL cholesterol, and apolipoprotein B/apolipoprotein A--I. 80% of the subjects with a pathological lipoprotein pattern were proteinuric or in poor glycaemic control or both. |
| 169 | 3267003 | Poor glycaemic control (n = 16) was associated with increased levels of atherogenic lipoproteins as reflected by higher concentrations of total cholesterol, LDL cholesterol, apolipoprotein B, and triglycerides, as well as a changed HDL composition indicated by a decreased HDL cholesterol/apolipoprotein A--I ratio. |
| 170 | 3267003 | Higher ratios of total cholesterol to HDL cholesterol and apolipoprotein B to apolipoprotein A--I point to an increased risk of developing atherosclerotic diseases in poorly controlled diabetics. 86% of the well controlled long-term diabetics had non-pathological values of LDL cholesterol, triglycerides, apolipoprotein B, HDL cholesterol, and apolipoprotein A--I but only 31% of the poorly controlled patients did so. |
| 171 | 3267003 | Diabetic nephropathy in the absence of chronic renal failure (n = 10) was characterized by higher values of LDL cholesterol, triglycerides, total cholesterol/HDL cholesterol, and apolipoprotein B/apolipoprotein A--I. 80% of the subjects with a pathological lipoprotein pattern were proteinuric or in poor glycaemic control or both. |
| 172 | 3267003 | Poor glycaemic control (n = 16) was associated with increased levels of atherogenic lipoproteins as reflected by higher concentrations of total cholesterol, LDL cholesterol, apolipoprotein B, and triglycerides, as well as a changed HDL composition indicated by a decreased HDL cholesterol/apolipoprotein A--I ratio. |
| 173 | 3267003 | Higher ratios of total cholesterol to HDL cholesterol and apolipoprotein B to apolipoprotein A--I point to an increased risk of developing atherosclerotic diseases in poorly controlled diabetics. 86% of the well controlled long-term diabetics had non-pathological values of LDL cholesterol, triglycerides, apolipoprotein B, HDL cholesterol, and apolipoprotein A--I but only 31% of the poorly controlled patients did so. |
| 174 | 3267003 | Diabetic nephropathy in the absence of chronic renal failure (n = 10) was characterized by higher values of LDL cholesterol, triglycerides, total cholesterol/HDL cholesterol, and apolipoprotein B/apolipoprotein A--I. 80% of the subjects with a pathological lipoprotein pattern were proteinuric or in poor glycaemic control or both. |
| 175 | 3288528 | VLDL production is significantly reduced; thus, a decreased production of LDL supports the contention that intensive therapy with insulin in normolipemic type I diabetic patients reduces the production of lipoproteins containing apolipoprotein B rather than increasing the clearance, and therapy also increases HDL cholesterol. |
| 176 | 3439403 | Increased plasma apolipoprotein B levels and blood hyperviscosity in non-insulin-dependent diabetic patients: role in the occurrence of arterial hypertension. |
| 177 | 3530855 | To evaluate mechanisms of diabetes-induced changes in very-low-density lipoprotein (VLDL), VLDL triglyceride (TG) and VLDL apolipoprotein B (apoB) metabolism were studied in 12 obese Pima Indian control subjects and in 15 Pima Indian obese non-insulin-dependent diabetics. |
| 178 | 3544765 | Coordination of very low-density lipoprotein triglyceride and apolipoprotein B metabolism in humans: effects of obesity and non-insulin-dependent diabetes mellitus. |
| 179 | 3669495 | In comparison with type IV, hyperlipoproteinemic patients, CRF patients had lower concentrations of ApoA-I, ApoA-II, ApoB, ApoC-I and, particularly, ApoE; there was no difference in ApoC-III levels reflecting the hypertriglyceridemia common to both disorders. |
| 180 | 3732634 | These classes contained retinyl esters and low-molecular-weight apolipoprotein B (components of intestinal lipoprotein remnants) as well as apolipoprotein E and high-molecular-weight apolipoprotein B. |
| 181 | 3794549 | Distribution of apolipoprotein E in the plasma of insulin-dependent and noninsulin-dependent diabetics and its relation to cholesterol net transport. |
| 182 | 3794549 | Noninsulin-dependent diabetics, whose plasma contained no detectable beta-VLDL (very low density lipoprotein), had a proportion (0.23 +/- 0.04) of plasma apolipoprotein E in the form of an abnormal lipoprotein not recognized by antibodies to apoB-100 from LDL (low density lipoprotein) or apoA-I from HDL (high density lipoprotein). |
| 183 | 3794549 | A much lower proportion of apoE (0.04 +/- 0.03) was in this form in the plasma of patients with insulin-dependent diabetes who had a comparable degree of hyperglycemia. |
| 184 | 3907293 | When the LDL receptor activity is low a large fraction of VLDL apolipoprotein B (apoB), the major structural protein in VLDL, is converted to LDL, and LDL production is high. |
| 185 | 3907293 | On the other hand, only a small part of VLDL apoB is converted to LDL resulting in low LDL synthesis rate in conditions with high LDL receptor activity. |
| 186 | 3907293 | When the LDL receptor activity is low a large fraction of VLDL apolipoprotein B (apoB), the major structural protein in VLDL, is converted to LDL, and LDL production is high. |
| 187 | 3907293 | On the other hand, only a small part of VLDL apoB is converted to LDL resulting in low LDL synthesis rate in conditions with high LDL receptor activity. |
| 188 | 3928411 | In adolescents, haemoglobin AIc correlated directly with triglycerides, total cholesterol, phospholipids, apolipoprotein B and inversely with HDL-cholesterol, HDL-phospholipids and (HDL/LDL + VLDL)-cholesterol. |
| 189 | 6225845 | Diabetic animals had higher HDL-apoA-I (apolipoprotein A-I) levels than did CO- and LF- but not BT-fed rats. |
| 190 | 6225845 | In LDL, apoB levels were lower and apoE levels were higher in LF-fed rats than in animals fed high fat diets. |
| 191 | 6734981 | Retarded chylomicron apolipoprotein-B catabolism in type 2 (non-insulin-dependent) diabetic subjects with lipaemia. |
| 192 | 6734981 | These studies suggest a key role for insulin-dependent, lipoprotein lipase-mediated triglyceride hydrolysis in the removal of chylomicrons from plasma. |
| 193 | 6799600 | To determine the acute effects of insulin on lipoprotein metabolism, we have followed the plasma lipoprotein lipid and apolipoprotein levels during insulin therapy for the first 24 hr in 13 patients with diabetic ketoacidosis. |
| 194 | 6799600 | Plasma apoprotein (apo) B levels were in the upper normal range (101 mg/dl) before treatment and decreased with therapy due to significant decreases in VLDL, but not IDL or LDL apoB. |
| 195 | 6860065 | [Apolipoproteins and glycosylated hemoglobin in the young insulin-dependent diabetic]. |
| 196 | 6860065 | In boys, triglycerides levels were significantly high in group G1, apolipoprotein B, total cholesterol, triglycerides, VLDL cholesterol levels and Alc glycosylated hemoglobin were raised in group G3. |
| 197 | 6860065 | Furthermore, there was a positive correlation between the percentage of Alc glycosylated hemoglobin and LDL cholesterol level. |
| 198 | 6860065 | In girls, triglycerides levels were significantly high in group G1, as were apolipoprotein B, triglycerides and VLDL cholesterol levels in group G2 and apolipoprotein B, triglycerides, LDL cholesterol, VLDL cholesterol levels and the percentage of Alc glycosylated hemoglobin in group G3. |
| 199 | 6860065 | A positive correlation between the percentage of Alc glycosylated hemoglobin and LDL cholesterol level was also found. |
| 200 | 6860065 | [Apolipoproteins and glycosylated hemoglobin in the young insulin-dependent diabetic]. |
| 201 | 6860065 | In boys, triglycerides levels were significantly high in group G1, apolipoprotein B, total cholesterol, triglycerides, VLDL cholesterol levels and Alc glycosylated hemoglobin were raised in group G3. |
| 202 | 6860065 | Furthermore, there was a positive correlation between the percentage of Alc glycosylated hemoglobin and LDL cholesterol level. |
| 203 | 6860065 | In girls, triglycerides levels were significantly high in group G1, as were apolipoprotein B, triglycerides and VLDL cholesterol levels in group G2 and apolipoprotein B, triglycerides, LDL cholesterol, VLDL cholesterol levels and the percentage of Alc glycosylated hemoglobin in group G3. |
| 204 | 6860065 | A positive correlation between the percentage of Alc glycosylated hemoglobin and LDL cholesterol level was also found. |
| 205 | 7098378 | From these data, the LDL-cholesterol and the atherosclerosis indices (LDL-cholesterol/HDL-cholesterol and apolipoprotein B/apolipoprotein A) were determined. |
| 206 | 7152129 | Integrated regulation of very low density lipoprotein triglyceride and apolipoprotein-B kinetics in non-insulin-dependent diabetes mellitus. |
| 207 | 7484901 | After we classified patients according to the quartiles of serum insulin level, we noted in the top quartile the presence of practically all manifestations of insulin resistance syndrome in persons of both sexes (e.g., increased waist/hip ratio, body mass index, glucose, uric acid, triglycerides, apolipoprotein B and decreased high-density lipoprotein cholesterol levels as well as apolipoprotein A-I/B ratios, and so forth). |
| 208 | 7500552 | Total cholesterol, LDL cholesterol, apolipoprotein B (apo B), and the ratio of apoB/apoA1 in the elderly group were significantly lower than those in the younger group. |
| 209 | 7556961 | Levels of lipoprotein(a), apolipoprotein B, and lipoprotein cholesterol distribution in IDDM. |
| 210 | 7583559 | In addition, each of the size measures was correlated with a variety of measures of HDL and beta-lipoprotein concentrations, which included HDL-C, LDL-C, triglycerides, and apoAI, apoB, and apoE. |
| 211 | 7589821 | Loci included the insulin-responsive (GLUT4) glucose transporter, hexokinase 2, glucagon, growth hormone, insulin receptor substrate 1 (IRS1), phosphoenolpyruvate carboxykinase, hepatic and muscle forms of pyruvate kinase, hepatic phosphofructokinase, the apolipoprotein B and the apolipoprotein A2 cluster, lipoprotein lipase, hepatic triglyceride lipase, the very-low-density-lipoprotein receptor, and the Pima insulin resistance locus on chromosome 4. |
| 212 | 7589883 | We measured the hepatic secretion of very-low-density lipoprotein apolipoprotein B-100 (VLDL apoB) using a stable isotope gas-chromatography mass-spectrometry method in six patients with non-insulin-dependent diabetes mellitus (NIDDM) (four males, two females, age 57.5 +/- 2.2 years (mean +/- SEM), weight 88.2 +/- 5.5 kg, glycated haemoglobin (HbA1) 8.5 +/- 0.5%, plasma total cholesterol concentration 5.7 +/- 0.5 mmol/l, triglyceride 3.8 +/- 0.9 mmol/l, high-density lipoprotein (HDL) cholesterol 1.0 +/- 0.1 mmol/l) and six non-diabetic subjects matched for age, sex and weight (four males, two females, age 55.7 +/- 2.8 years, weight 85.8 +/- 5.6 kg, HbA1 6.5 +/- 0.1%, plasma total cholesterol concentration 5.7 +/- 0.5 mmol/l, triglyceride 1.2 +/- 0.1 mmol/l, HDL cholesterol 1.4 +/- 0.1 mmol/l). |
| 213 | 7595089 | Increased proportion of plasma apoB-48 to apoB-100 in non-insulin-dependent diabetic rats: contribution of enhanced apoB mRNA editing in the liver. |
| 214 | 7595089 | To assess the alteration of apolipoprotein (apo) B mRNA editing in non-insulin-dependent diabetes mellitus (NIDDM), we measured plasma apoB-100 and apoB-48 levels and apoB mRNA editing efficiency in the liver and intestine from GK (Goto-Kakizaki) rats, a genetically NIDDM animal. |
| 215 | 7595089 | In conclusion, an enhanced apoB mRNA editing was indicated in the non-insulin-dependent diabetic rats, which might contribute to the increase of plasma apoB-48 levels. |
| 216 | 7595089 | Increased proportion of plasma apoB-48 to apoB-100 in non-insulin-dependent diabetic rats: contribution of enhanced apoB mRNA editing in the liver. |
| 217 | 7595089 | To assess the alteration of apolipoprotein (apo) B mRNA editing in non-insulin-dependent diabetes mellitus (NIDDM), we measured plasma apoB-100 and apoB-48 levels and apoB mRNA editing efficiency in the liver and intestine from GK (Goto-Kakizaki) rats, a genetically NIDDM animal. |
| 218 | 7595089 | In conclusion, an enhanced apoB mRNA editing was indicated in the non-insulin-dependent diabetic rats, which might contribute to the increase of plasma apoB-48 levels. |
| 219 | 7595089 | Increased proportion of plasma apoB-48 to apoB-100 in non-insulin-dependent diabetic rats: contribution of enhanced apoB mRNA editing in the liver. |
| 220 | 7595089 | To assess the alteration of apolipoprotein (apo) B mRNA editing in non-insulin-dependent diabetes mellitus (NIDDM), we measured plasma apoB-100 and apoB-48 levels and apoB mRNA editing efficiency in the liver and intestine from GK (Goto-Kakizaki) rats, a genetically NIDDM animal. |
| 221 | 7595089 | In conclusion, an enhanced apoB mRNA editing was indicated in the non-insulin-dependent diabetic rats, which might contribute to the increase of plasma apoB-48 levels. |
| 222 | 7604805 | A pattern of lipoprotein abnormalities characterized by increased hepatic production of apolipoprotein B-containing lipoprotein particles, high blood pressure, visceral obesity, and peripheral insulin resistance are identified with increasing frequency in subjects with premature coronary artery disease (CAD). |
| 223 | 7604805 | Further work in the field of hemostatic factors has shown that fibrinogen, activated coagulation factor VII, spontaneous platelet aggregation, and elevated levels of plasminogen activator inhibitor-1 (PAI-1), are all associated with CAD. |
| 224 | 7604805 | There is a strong association between lipids (especially triglyceride-rich lipoproteins) and fibrinogen, PAI-1, and activation of factor VII. |
| 225 | 7646575 | Atherogenic index and apolipoprotein B/apolipoprotein A-I ratio were also significantly decreased after 4 weeks. |
| 226 | 7657029 | In a randomized crossover study, we measured the hepatic secretion rate of very-low-density lipoprotein (VLDL) apolipoprotein B-100 (apoB) in seven patients with well-controlled non-insulin-dependent diabetes mellitus (NIDDM) (HbA1 8.4 +/- 0.4% [mean +/- SE]) on two occasions: during a 13-h hyperinsulinemic (plasma insulin concentration 586 +/- 9.7 pmol/l) euglycemic (plasma glucose concentration 5.2 +/- 0.1 mmol/l) clamp; and during a 13-h saline (control) infusion. |
| 227 | 7695175 | The major apolipoproteins of LDL and high-density lipoprotein (HDL), apoB and apoA1 respectively, and levels of Lp(a) lipoprotein are often abnormal in children born in a family with premature coronary artery disease (CAD). |
| 228 | 7738020 | Identification of the major site of apolipoprotein B modification by advanced glycosylation end products blocking uptake by the low density lipoprotein receptor. |
| 229 | 7738020 | These data point to the high reactivity and specificity of this site for AGE formation and provide further evidence for important structural interactions between the LDL receptor binding domain and remote regions of the apolipoprotein B polypeptide. |
| 230 | 7738020 | Identification of the major site of apolipoprotein B modification by advanced glycosylation end products blocking uptake by the low density lipoprotein receptor. |
| 231 | 7738020 | These data point to the high reactivity and specificity of this site for AGE formation and provide further evidence for important structural interactions between the LDL receptor binding domain and remote regions of the apolipoprotein B polypeptide. |
| 232 | 7740031 | Analysis of the baseline values showed increased levels of apolipoprotein B, cholesterol, triglycerides, insulin, and reduced levels of apolipoprotein A1, high-density lipoprotein cholesterol in obese youths vs. controls. |
| 233 | 7740031 | A atherogenic pattern of changes in the lipoprotein and apolipoprotein spectra of the plasma obese youths was clearly seen under conditions of fat food loading, these changes being associated with disordered insulin reaction to intake if exogenous fat. |
| 234 | 7781495 | These favorable effects on LDL cholesterol and apolipoprotein B were not influenced by gender, the type of diabetic therapy, baseline hemoglobin A1c levels and by the presence of hypertension or gross proteinuria, although a decrease in the two variables were less in those with body mass index > or = 26.4 kg/m2 or in those with age < 60 years. |
| 235 | 7810485 | Relation of angiographically defined coronary artery disease and plasma concentrations of insulin, lipid, and apolipoprotein in normolipidemic subjects with varying degrees of glucose tolerance. |
| 236 | 7810485 | The CAD group had a significantly lower plasma level of high-density lipoprotein (HDL) cholesterol and apolipoprotein A-I (apo A-I) and a higher level of apolipoprotein B (apo B) than the normal group with normal glucose tolerance. |
| 237 | 7819429 | Thirty six individuals with angiographic evidence of coronary atherosclerosis and thirty six individuals without coronary disease, matched for a variety of cardiovascular risk factors including age, sex, smoking, hypertension, diabetes and family history, were evaluated for their serum concentrations of vitamin E, total cholesterol, triacylglycerols, high density lipoprotein-cholesterol, low density lipoprotein-cholesterol, apolipoprotein A-I, and apolipoprotein B. |
| 238 | 7856176 | The major protein constituents of lipoprotein (a) are apolipoprotein B 100 und apolipoprotein (a) (apo(a)). |
| 239 | 7856176 | After subdivision of the diabetic patients according to different stages of diabetic nephropathy (DN), determined by urinary albumin excretion, significant relationships were found between DN and triglycerides (P = 0.04), LDL (P = 0.03) and apolipoprotein B (P = 0.008, Kruskal-Wallis test) levels. |
| 240 | 7856176 | The major protein constituents of lipoprotein (a) are apolipoprotein B 100 und apolipoprotein (a) (apo(a)). |
| 241 | 7856176 | After subdivision of the diabetic patients according to different stages of diabetic nephropathy (DN), determined by urinary albumin excretion, significant relationships were found between DN and triglycerides (P = 0.04), LDL (P = 0.03) and apolipoprotein B (P = 0.008, Kruskal-Wallis test) levels. |
| 242 | 7895421 | Compared to fasting with fluid and salt replacement, fasting with no fluids was associated with higher (mean, 95% confidence interval) total serum cholesterol (8.1%, 4.3-11.9%), HDL cholesterol (7.5%, 1.8-13.1%), LDL cholesterol (10.5%, 2.2-18.8%), apolipoprotein A-1 (8.9%, 5.0-12.8%), and apolipoprotein B (10.5%, 5.2-15.8%). |
| 243 | 7923754 | Lipoprotein(a) [Lp(a)] is a plasma macromolecular complex that is assembled from low-density lipoproteins (LDL) and a large hydrophilic glycoprotein, named apolipoprotein(a) [apo(a)], linked by a disulfide bond to apolipoprotein B-100. |
| 244 | 7937426 | Positive associations were found between serum uric acid concentration and body mass index, waist hip ratio, systolic and diastolic blood pressure, urea, creatinine, protein, glucose (fasting and 2 hours after 75 g oral glucose load), 2 hour insulin, triglycerides, and apolipoprotein B in men. |
| 245 | 7946245 | Plasma lipids, chemical composition of various lipoprotein fractions, apolipoprotein B concentrations and apolipoprotein E phenotypes were studied in 12 uraemic patients on conservative treatment (CT), in 16 patients on haemodialysis (HD) and in 18 patients on continuous ambulatory peritoneal dialysis treatment (CAPD). |
| 246 | 7955992 | We therefore studied factors relating to albumin excretion rate in children with insulin-dependent diabetes. |
| 247 | 7955992 | HbA1c since diagnosis, mean blood pressure, lipoprotein(a), and apolipoprotein B did not correlate with albumin excretion rate, after controlling for other variables. |
| 248 | 7986307 | NIDDM subjects also have altered apolipoprotein concentrations, including increased apoB, apoC-III, and decreased apoA-I; in addition, apoE-2 may be over-represented in diabetic populations. |
| 249 | 8116554 | Increased meal frequency reduces post-prandial insulin and glucose responses in people with non-insulin-dependent diabetes and in nondiabetic volunteers and lowers serum concentrations of LDL cholesterol and apolipoprotein B. |
| 250 | 8139126 | Six fractions of serum apolipoproteins (apolipoprotein A-I, A-II, B, C-II, C-III and E) obtained from 100 patients with diabetes mellitus not administered any antihyperlipidemic drugs were measured to clarify the relationship between diabetes mellitus and the abnormal lipidosis. |
| 251 | 8139126 | The serum concentrations of apolipoprotein B, C-II and C-III were significantly higher in these diabetics than in the controls (p < 0.05), and that of apolipoprotein E was significantly lower (p < 0.01). |
| 252 | 8139126 | The serum concentrations of apolipoprotein C-II, C-III and E (p < 0.05) as well as HbA1C and FRA (p < 0.001) were significantly higher in the insufficient control group (FPG > or = 140 mg/dl) of diabetes mellitus. |
| 253 | 8139126 | The serum concentrations of apolipoprotein C-II, C-III and E were significantly higher in the treated groups (p < 0.05). |
| 254 | 8139126 | The serum concentrations of apolipoprotein B, C-II, C-III and E were significantly higher (p < 0.01) in the high cholesterol group (> 220mg/dl) and the high triglyceride group (> 150mg/dl) among the diabetic groups, but no significant differences were observed in the concentrations of apolipoprotein A-I and A-II. |
| 255 | 8139126 | Six fractions of serum apolipoproteins (apolipoprotein A-I, A-II, B, C-II, C-III and E) obtained from 100 patients with diabetes mellitus not administered any antihyperlipidemic drugs were measured to clarify the relationship between diabetes mellitus and the abnormal lipidosis. |
| 256 | 8139126 | The serum concentrations of apolipoprotein B, C-II and C-III were significantly higher in these diabetics than in the controls (p < 0.05), and that of apolipoprotein E was significantly lower (p < 0.01). |
| 257 | 8139126 | The serum concentrations of apolipoprotein C-II, C-III and E (p < 0.05) as well as HbA1C and FRA (p < 0.001) were significantly higher in the insufficient control group (FPG > or = 140 mg/dl) of diabetes mellitus. |
| 258 | 8139126 | The serum concentrations of apolipoprotein C-II, C-III and E were significantly higher in the treated groups (p < 0.05). |
| 259 | 8139126 | The serum concentrations of apolipoprotein B, C-II, C-III and E were significantly higher (p < 0.01) in the high cholesterol group (> 220mg/dl) and the high triglyceride group (> 150mg/dl) among the diabetic groups, but no significant differences were observed in the concentrations of apolipoprotein A-I and A-II. |
| 260 | 8171526 | ApoA1, ApoB, and ApoA1/ApoB before and after combined pancreas-kidney transplantation. |
| 261 | 8174836 | Lipid and apolipoprotein B48 transport in mesenteric lymph and the effect of hyperphagia on the clearance of chylomicron-like emulsions in insulin-deficient rats. |
| 262 | 8174836 | Insulin-deficiency had no effect on triglyceride or apoB48 transport in lymph. |
| 263 | 8174836 | Lipid and apolipoprotein B48 transport in mesenteric lymph and the effect of hyperphagia on the clearance of chylomicron-like emulsions in insulin-deficient rats. |
| 264 | 8174836 | Insulin-deficiency had no effect on triglyceride or apoB48 transport in lymph. |
| 265 | 8197611 | After correction for these 7 variables, cyclosporine blood levels remained significantly associated with high-density lipoprotein cholesterol, high-density lipoprotein3 cholesterol, apolipoprotein A-1, apolipoprotein B, low-density lipoprotein cholesterol, and the cholesterol/high-density lipoprotein cholesterol ratio. |
| 266 | 8212622 | The fasting insulin levels correlated significantly positively with triglyceride levels, apolipoprotein B, atherogenic indices and negatively with HDL-cholesterol. |
| 267 | 8261646 | Apolipoprotein B gene DNA polymorphisms are associated with macro- and microangiopathy in non-insulin-dependent diabetes mellitus. |
| 268 | 8261646 | The relationship between diabetic macroangiopathy or microangiopathy and apolipoprotein B (apoB) polymorphism was studied in 139 male and 129 female patients with non-insulin-dependent diabetes (NIDDM) mellitus, comprising consecutive patients with poor diabetic control (HBA1 13.2% +/- 2.7 (SD)) referred to our hospital. |
| 269 | 8261646 | Apolipoprotein B gene DNA polymorphisms are associated with macro- and microangiopathy in non-insulin-dependent diabetes mellitus. |
| 270 | 8261646 | The relationship between diabetic macroangiopathy or microangiopathy and apolipoprotein B (apoB) polymorphism was studied in 139 male and 129 female patients with non-insulin-dependent diabetes (NIDDM) mellitus, comprising consecutive patients with poor diabetic control (HBA1 13.2% +/- 2.7 (SD)) referred to our hospital. |
| 271 | 8265249 | Lipoprotein(a) (Lp(a)) consists of a unique apolipoprotein, apolipoprotein(a), (apo(a)) linked by a disulphide bridge to apolipoprotein B of low density lipoprotein (LDL). |
| 272 | 8316757 | Apolipoprotein-A1, Apolipoprotein-B (Apo-B), Lipoprotein(a) (Lp[a]) HDL-Cholesterol, Cholesterol (Chol) and Triglycerides (TG). were estimated in serum. |
| 273 | 8322798 | During diabetes the apolipoprotein B of LDL undergoes nonenzymatic glycation, which may alter its affinity for the LDL receptor. |
| 274 | 8334821 | Significant decreases of total and LDL cholesterol, triglycerides, apolipoprotein B, and free fatty acids were observed, while HDL-cholesterol and apoA1 increased by 10%. |
| 275 | 8354314 | Patients with insulin dependent diabetes (IDDM) have been reported to have increased incidence of E2/2 homozygosity. |
| 276 | 8354314 | Apolipoprotein A1 (apoA1) and B (apoB) were measured by turbidometry. |
| 277 | 8354314 | In the diabetic children, there was a distinct relation between apoE phenotype and plasma lipids; presence of apoE2 was associated with the lowest and that of apoE4 with the highest concentrations of total and low density lipoprotein (LDL) C, and apoB. |
| 278 | 8354314 | Ratios of HDL-C/LDL-C and apoA1/apoB showed on opposite trend. |
| 279 | 8354314 | Patients with insulin dependent diabetes (IDDM) have been reported to have increased incidence of E2/2 homozygosity. |
| 280 | 8354314 | Apolipoprotein A1 (apoA1) and B (apoB) were measured by turbidometry. |
| 281 | 8354314 | In the diabetic children, there was a distinct relation between apoE phenotype and plasma lipids; presence of apoE2 was associated with the lowest and that of apoE4 with the highest concentrations of total and low density lipoprotein (LDL) C, and apoB. |
| 282 | 8354314 | Ratios of HDL-C/LDL-C and apoA1/apoB showed on opposite trend. |
| 283 | 8354314 | Patients with insulin dependent diabetes (IDDM) have been reported to have increased incidence of E2/2 homozygosity. |
| 284 | 8354314 | Apolipoprotein A1 (apoA1) and B (apoB) were measured by turbidometry. |
| 285 | 8354314 | In the diabetic children, there was a distinct relation between apoE phenotype and plasma lipids; presence of apoE2 was associated with the lowest and that of apoE4 with the highest concentrations of total and low density lipoprotein (LDL) C, and apoB. |
| 286 | 8354314 | Ratios of HDL-C/LDL-C and apoA1/apoB showed on opposite trend. |
| 287 | 8364758 | Although it is quite true that total blood cholesterol levels in excess of 200 mg/dl (5.2 mmol/l) are not automatically dangerous, they nonetheless require complete profiling of cholesterol distribution among the different fractions and, if possible, a complementary study of ApoB, ApoA1 and Lpa fractions. |
| 288 | 8378574 | However HbA1c levels were positive and significantly (p < 0.05) correlated with the Apo-B and Apo-E and negative but significantly correlated (p < 0.05) with Apo-CII and Apo-CIII from VLDL particle in both groups of diabetic patients. |
| 289 | 8422793 | Metabolic studies indicated multiple alterations in VLDL metabolism induced by NIDDM, including overproduction of VLDL TG, impaired clearance of VLDL TG and apoB, and decreases in adipose tissue lipoprotein lipase. |
| 290 | 8444504 | The following factors were thus assessed: lipid factors: cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, apolipoprotein AI, apolipoprotein B; coagulation factors: fibrinogen, antithrombin III, fibrinopeptide A, factor VIII coagulant, factor VIII antigen, protein C; factors of physiological fibrinolysis: plasminogen, alpha 2-antiplasmin, tissue plasminogen activator and euglobulin clot lysis time before and after venous occlusion, plasminogen activator inhibitor before venous occlusion; and factors of platelet release: beta-thromboglobulin, platelet factor 4. |
| 291 | 8444504 | There were no differences in lipid factors, but significant differences were observed in hemostatic variables: fibrinogen (without restenosis: 3.18 +/- 0.83; restenosis: 3.83 +/- 0.51 milligrams, p = 0.05), tissue plasminogen activator before venous occlusion (without restenosis: 10.9 +/- 26.8; restenosis: 232.5 +/- 371.2 IU, p < 0.04), euglobulin clot lysis time after venous occlusion (without restenosis: 176.5 +/- 100.5; restenosis: 78.6 +/- 40.2 min, p < 0.05) and for marker of the platelet release: platelet factor 4 (without restenosis: 10.8 +/- 7.9; restenosis: 20.5 +/- 7.5 ng/l, p < 0.04). |
| 292 | 8485116 | For apolipoprotein B predictive significance was observed in the middle-aged populations, whereas apolipoprotein A-I had a protective effect in elderly women. |
| 293 | 8486262 | Simultaneously, the levels of apolipoprotein (apo- A-1, B, E) were determined in blood sera of the males-donors, long-living and elderly individuals depending on the phenotypes for ear wax consistency. |
| 294 | 8486262 | However, the ratio apoB/apoA-1 proved higher in the donors with humid ear wax than in those with the dry variant under P < 0.06, which can stimulate this disease. |
| 295 | 8486262 | The results of this study support the statement that low level of apoB and especially apoB/apoA-1 may be one of the longevity markers. |
| 296 | 8486262 | Simultaneously, the levels of apolipoprotein (apo- A-1, B, E) were determined in blood sera of the males-donors, long-living and elderly individuals depending on the phenotypes for ear wax consistency. |
| 297 | 8486262 | However, the ratio apoB/apoA-1 proved higher in the donors with humid ear wax than in those with the dry variant under P < 0.06, which can stimulate this disease. |
| 298 | 8486262 | The results of this study support the statement that low level of apoB and especially apoB/apoA-1 may be one of the longevity markers. |
| 299 | 8513980 | Leucine kinetics and fractional synthetic rates of albumin, fibrinogen, antithrombin III, and apoB-100 were determined in 6 normal subjects, on two different occasions during either the infusion of saline (control study) or a euglycemic-hyperinsulinemic (0.4 mU.kg-1 x min-1 for 240 min) clamp, by a primed-constant infusion of [1-14C]Leu. |
| 300 | 8513980 | The insulin infusion significantly decreased the rates of nonoxidative Leu disposal (1.70 +/- 0.10 vs. control 2.06 +/- 0.09 mol.kg-1 x min-1), increased the albumin (7.2 +/- 0.4 vs. 6.2 +/- 0.6%/day), decreased the fibrinogen (18 +/- 1 vs. 23 +/- 2%/day), and antithrombin III (28 +/- 3 vs. 40 +/- 4%/day) fractional synthetic rate, whereas it did not affect the total apoB-100 (49 +/- 5 vs. 52 +/- 6%/day) fractional synthetic rate. |
| 301 | 8513980 | The positive effect of insulin on albumin synthesis may play an important anabolic role during nutrient absorption by promoting the capture of a relevant amount of dietary essential amino acids into the protein, whereas the negative effect of insulin on fibrinogen synthesis might, at least partially, account for the increased plasma fibrinogen concentrations previously reported in poorly controlled diabetic patients. |
| 302 | 8513980 | Leucine kinetics and fractional synthetic rates of albumin, fibrinogen, antithrombin III, and apoB-100 were determined in 6 normal subjects, on two different occasions during either the infusion of saline (control study) or a euglycemic-hyperinsulinemic (0.4 mU.kg-1 x min-1 for 240 min) clamp, by a primed-constant infusion of [1-14C]Leu. |
| 303 | 8513980 | The insulin infusion significantly decreased the rates of nonoxidative Leu disposal (1.70 +/- 0.10 vs. control 2.06 +/- 0.09 mol.kg-1 x min-1), increased the albumin (7.2 +/- 0.4 vs. 6.2 +/- 0.6%/day), decreased the fibrinogen (18 +/- 1 vs. 23 +/- 2%/day), and antithrombin III (28 +/- 3 vs. 40 +/- 4%/day) fractional synthetic rate, whereas it did not affect the total apoB-100 (49 +/- 5 vs. 52 +/- 6%/day) fractional synthetic rate. |
| 304 | 8513980 | The positive effect of insulin on albumin synthesis may play an important anabolic role during nutrient absorption by promoting the capture of a relevant amount of dietary essential amino acids into the protein, whereas the negative effect of insulin on fibrinogen synthesis might, at least partially, account for the increased plasma fibrinogen concentrations previously reported in poorly controlled diabetic patients. |
| 305 | 8534686 | Fasting serum Lp(a), total cholesterol, triglycerides, LDL-cholesterol, HDL-cholesterol, apolipoprotein-A and apolipoprotein-B levels were measured on entering the CAPD program and at 3 monthly intervals. |
| 306 | 8567315 | The serum concentration of lipoprotein(a) [Lp(a)], lipids, lipoproteins, apolipoprotein A-I, and apolipoprotein B were determined in 228 patients with cerebral infarction, composed of 87 cases of asymptomatic lacunar infarction, 99 cases of lacunar infarction, and 42 cases of atherothrombotic infarction, and in a control group of 138 healthy subjects with normal MRI. |
| 307 | 8578698 | Changes of ApoB, ApoA1 and Lp(a) serum levels did not attain statistical significance but trends were revealed (e.g. a drop of the ApoB/ApoA1 index) which are consistent with the expected favourable action of EPC on the CH distribution in lipoproteins. |
| 308 | 8595706 | Nonenzymic glycation of apolipoprotein B in patients with insulin- and noninsulin-dependent diabetes mellitus. |
| 309 | 8641120 | Albuminuria correlated with mean arterial pressure (r = 0.31, p < 0.001), triglyceride (r = 0.36, p < 0.001), total cholesterol (r = 0.28, p = 0.001), apolipoprotein B (apo B) (r = 0.25, p = 0.003), and insulin resistance (r = 0.25, p < 0.002). |
| 310 | 8646198 | This review is aiming to study the values of apolipoprotein AI and B and plasma lipid levels (total cholesterol, HDL cholesterol, LDL cholesterol and triglyceride) in well-treated diabetic patients, and their possible relationship with hemoglobin A1, body mass index and insulin levels. |
| 311 | 8646198 | The study groups were 26 insulin-dependent diabetic (IDDM) patients, 30 non-insulin-dependent diabetic (NIDDM) subjects and 20 non diabetic subjects (controls). |
| 312 | 8646198 | Apolipoprotein AI concentrations were similar in the three groups, but apolipoprotein B values and apo B/apo AI ratio were significantly higher in IDDM as related to NIDDM patients (p < 0.001) and to non-diabetic subjects (p < 0.001). |
| 313 | 8646198 | We found a weak correlation between apo B and hemoglobin AI in IDDM (r = 0.45; 0.02 < p < 0.05), but not in NIDDM patients. |
| 314 | 8674884 | The overall effect of hyperinsulinemia on VLDL production is postulated to reflect both the effect of insulin on apolipoprotein B production and the hepatic synthesis of TG from either plasma FFAs or newly made fatty acids. |
| 315 | 8682012 | Fibrinogen, total cholesterol, triglycerides, high and low density lipoprotein cholesterol, apolipoprotein A-1, apolipoprotein B and lipoprotein (a) were measured. |
| 316 | 8697305 | Accessibility of human apolipoprotein B-100 epitopes in insulin-dependent diabetes: relation with the surface lipid environment of atherogenic particles. |
| 317 | 8697305 | The physicochemical modifications (composition and conformation) of lipoproteins containing apolipoprotein B-100 (apo B-100) were studied in normocholesterolaemic adequately controlled Type 1 insulin-dependent diabetic patients. |
| 318 | 8697305 | Accessibility of human apolipoprotein B-100 epitopes in insulin-dependent diabetes: relation with the surface lipid environment of atherogenic particles. |
| 319 | 8697305 | The physicochemical modifications (composition and conformation) of lipoproteins containing apolipoprotein B-100 (apo B-100) were studied in normocholesterolaemic adequately controlled Type 1 insulin-dependent diabetic patients. |
| 320 | 8729170 | We found a rapid suppression of plasma free fatty acid (FFA) levels in response to insulin and a consistent 50-60% insulin-induced suppression of both VLDL TG and VLDL apolipoprotein (apo) B in lean insulin-sensitive individuals. |
| 321 | 8729170 | In addition, we found that chronically insulin-resistant hyperinsulinemic obese individuals were resistant to this suppressive effect of insulin on VLDL apoB production, in keeping with similar findings by others performing in vitro experiments using cultured hepatocytes isolated from insulin-resistant or hyperinsulinemic rats. |
| 322 | 8732773 | In a multivariate regression analysis, very low density lipoprotein (VLDL) triglyceride level was significantly and independently related to serum apolipoprotein B concentration, the presence of the A291S mutation, serum insulin concentration, and postheparin plasma LPL activity. |
| 323 | 8750763 | We have previously demonstrated alterations in apolipoprotein B-48 metabolism in the post-prandial state in patients with non-insulin-dependent diabetes mellitus. |
| 324 | 8763631 | Recent data suggest the existence of a relationship between ischemic heart diseases and apolipoprotein A-I containing lipoproteins. |
| 325 | 8763631 | Compared to a control group, non-insulin-dependent diabetics have higher levels of plasma cholesterol (p < 0.05), triacylglycerol, apolipoprotein B (p < 0.001). |
| 326 | 8763631 | In contrast, their lipoprotein particles containing only apolipoprotein AI without apolipoprotein AII and apoAI/apoB ratio were lowered (p < 0.001). |
| 327 | 8763631 | Also, the distribution of particles containing apolipoprotein A-I without apolipoprotein A-II in non-insulin-dependent diabetics was found abnormal. |
| 328 | 8763631 | Recent data suggest the existence of a relationship between ischemic heart diseases and apolipoprotein A-I containing lipoproteins. |
| 329 | 8763631 | Compared to a control group, non-insulin-dependent diabetics have higher levels of plasma cholesterol (p < 0.05), triacylglycerol, apolipoprotein B (p < 0.001). |
| 330 | 8763631 | In contrast, their lipoprotein particles containing only apolipoprotein AI without apolipoprotein AII and apoAI/apoB ratio were lowered (p < 0.001). |
| 331 | 8763631 | Also, the distribution of particles containing apolipoprotein A-I without apolipoprotein A-II in non-insulin-dependent diabetics was found abnormal. |
| 332 | 8778000 | Patients with insulin-dependent diabetes mellitus (IDDM) have a pathological increase in cholesteryl ester transfer (CET) that enriches the apolipoprotein B-containing lipoproteins with cholesteryl ester and increases their atherogenicity. |
| 333 | 8781297 | Apolipoprotein B independently predicts progression of very-low-level albuminuria in insulin-dependent diabetes mellitus. |
| 334 | 8781297 | The purpose of the study was to examine the contribution of alterations in lipoprotein metabolism to the progression of very-low-level albuminuria in insulin-dependent diabetes mellitus (IDDM). |
| 335 | 8781297 | In multiple linear regression analysis, serum apo B (P < .05) and glycated hemoglobin ([HbA] P < .05) at baseline were significant independent predictors of the increase in albuminuria, with no significant associations found for sex, smoking, duration of diabetes, mean arterial blood pressure (BP), or family history of cardiovascular disease and hypertension; the regression model predicted 42% of the variation in UA/UC at 10 years. |
| 336 | 8826978 | The apoB-100 gene EcoRI polymorphism influences the relationship between features of the insulin resistance syndrome and the hyper-apoB and dense LDL phenotype in men. |
| 337 | 8826978 | The aim of this study was to investigate whether the EcoRI polymorphism of the apolipoprotein B (apoB) gene influences the relationships between features of the insulin resistance syndrome and the dense LDL phenotype and apoB concentrations. |
| 338 | 8826978 | The apoB-100 gene EcoRI polymorphism influences the relationship between features of the insulin resistance syndrome and the hyper-apoB and dense LDL phenotype in men. |
| 339 | 8826978 | The aim of this study was to investigate whether the EcoRI polymorphism of the apolipoprotein B (apoB) gene influences the relationships between features of the insulin resistance syndrome and the dense LDL phenotype and apoB concentrations. |
| 340 | 8865367 | The frequencies of restriction fragment length polymorphism (RFLP) of the genes for apoB, a major LDL apolipoprotein, and apoAII, a major HDL apolipoprotein, were studied in 45 Tunisian diabetics and an equal number of sex and age matched controls. |
| 341 | 8865367 | Southern blot analysis of an EcoR1 apoB polymorphism and an Msp1 apo AII polymorphism indicates that there was no statistically significant difference in the incidence of different genotypes or alleles among diabetics compared to controls. |
| 342 | 8865367 | The frequencies of restriction fragment length polymorphism (RFLP) of the genes for apoB, a major LDL apolipoprotein, and apoAII, a major HDL apolipoprotein, were studied in 45 Tunisian diabetics and an equal number of sex and age matched controls. |
| 343 | 8865367 | Southern blot analysis of an EcoR1 apoB polymorphism and an Msp1 apo AII polymorphism indicates that there was no statistically significant difference in the incidence of different genotypes or alleles among diabetics compared to controls. |
| 344 | 8883280 | We measured PAI-1 activity, tissue-type plasminogen activator (t-PA) antigen, a2-antiplasmin, fibrinogen, lipids and apolipoproteins in both groups. |
| 345 | 8883280 | PAI-1 activity levels were higher in cases compared to controls (3.13 +/- 1.9 vs 2.17 +/- 1.9 U/ml, p = 0.0014). t-PA antigen and a2-antiplasmin did not differ significantly between the two groups, while fibrinogen, total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B and lipoprotein(a) were significantly higher in group A. |
| 346 | 8883280 | PAI-1 was positively correlated with triglycerides (r = 0.22, p = 0.024), apolipoprotein B (r = 0.21, p = 0.039) and fibrinogen (r = 0.22, p = 0.029) in cases and with BMI in both cases (r = 0.37, p = 0.0003) and controls (r = 0.23, p = 0.044). |
| 347 | 8883280 | In stepwise multiple regression analysis, only apolipoprotein B (p = 0.008) and BMI (p = 0.0014) were significant determinants of PAI-1 activity in cases. |
| 348 | 8883280 | We measured PAI-1 activity, tissue-type plasminogen activator (t-PA) antigen, a2-antiplasmin, fibrinogen, lipids and apolipoproteins in both groups. |
| 349 | 8883280 | PAI-1 activity levels were higher in cases compared to controls (3.13 +/- 1.9 vs 2.17 +/- 1.9 U/ml, p = 0.0014). t-PA antigen and a2-antiplasmin did not differ significantly between the two groups, while fibrinogen, total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B and lipoprotein(a) were significantly higher in group A. |
| 350 | 8883280 | PAI-1 was positively correlated with triglycerides (r = 0.22, p = 0.024), apolipoprotein B (r = 0.21, p = 0.039) and fibrinogen (r = 0.22, p = 0.029) in cases and with BMI in both cases (r = 0.37, p = 0.0003) and controls (r = 0.23, p = 0.044). |
| 351 | 8883280 | In stepwise multiple regression analysis, only apolipoprotein B (p = 0.008) and BMI (p = 0.0014) were significant determinants of PAI-1 activity in cases. |
| 352 | 8883280 | We measured PAI-1 activity, tissue-type plasminogen activator (t-PA) antigen, a2-antiplasmin, fibrinogen, lipids and apolipoproteins in both groups. |
| 353 | 8883280 | PAI-1 activity levels were higher in cases compared to controls (3.13 +/- 1.9 vs 2.17 +/- 1.9 U/ml, p = 0.0014). t-PA antigen and a2-antiplasmin did not differ significantly between the two groups, while fibrinogen, total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B and lipoprotein(a) were significantly higher in group A. |
| 354 | 8883280 | PAI-1 was positively correlated with triglycerides (r = 0.22, p = 0.024), apolipoprotein B (r = 0.21, p = 0.039) and fibrinogen (r = 0.22, p = 0.029) in cases and with BMI in both cases (r = 0.37, p = 0.0003) and controls (r = 0.23, p = 0.044). |
| 355 | 8883280 | In stepwise multiple regression analysis, only apolipoprotein B (p = 0.008) and BMI (p = 0.0014) were significant determinants of PAI-1 activity in cases. |
| 356 | 8904350 | Transfers or exchanges of cholesterol esters and triglycerides between lipoproteins are mediated by a specialized protein referred to as cholesteryl ester transfer protein (CETP), whereas those of phospholipids (PLs) are facilitated by both CETP and a specific phospholipid transfer protein (PLTP). |
| 357 | 8904350 | VLDL + LDL-dependent PLT was found to be negatively correlated with the PL/apolipoprotein B ratio, whereas HDL-dependent PLT was positively correlated with the HDL2/HDL3 and PL/apolipoprotein A-I ratios and negatively correlated with the flow activation energy at the HDL surface. |
| 358 | 8904350 | The HDL2/HDL3 ratio was positively correlated with PLTA but not with CETP, which confirms previous reports suggesting that PLTP might act as an HDL conversion factor. |
| 359 | 8904926 | This study examines the relationship between fasting and post-prandial apolipoprotein B-48 in type 2 (non-insulin-dependent) diabetic and non-diabetic subjects. |
| 360 | 9012639 | In multivariate regression analyses, 2-hour FFA levels were strongly related to fasting triglyceride and apoB levels, respectively, after adjustment for age, fasting and 2-hour insulin concentrations, and fasting FFA concentrations. |
| 361 | 9012639 | In summary, elevated plasma apoB and triglyceride concentrations associated with male gender and with glucose intolerance are partly accounted for by differences in the ability of insulin to suppress FFA concentrations. |
| 362 | 9012639 | In multivariate regression analyses, 2-hour FFA levels were strongly related to fasting triglyceride and apoB levels, respectively, after adjustment for age, fasting and 2-hour insulin concentrations, and fasting FFA concentrations. |
| 363 | 9012639 | In summary, elevated plasma apoB and triglyceride concentrations associated with male gender and with glucose intolerance are partly accounted for by differences in the ability of insulin to suppress FFA concentrations. |
| 364 | 9044301 | Despite the large size of apoB (4536 amino acid residues) and its high content of potentially reactive lysines, the predominant site of AGE-immunoreactivity was found to lie within a single 67 amino acid domain located 1791 residues N-terminal to the LDL receptor binding site. |
| 365 | 9044301 | These data point to the high specificity and reactivity of this site toward AGE formation and to a significant structural interaction between this region of apoB and the LDL receptor binding domain. |
| 366 | 9044301 | Despite the large size of apoB (4536 amino acid residues) and its high content of potentially reactive lysines, the predominant site of AGE-immunoreactivity was found to lie within a single 67 amino acid domain located 1791 residues N-terminal to the LDL receptor binding site. |
| 367 | 9044301 | These data point to the high specificity and reactivity of this site toward AGE formation and to a significant structural interaction between this region of apoB and the LDL receptor binding domain. |
| 368 | 9069522 | There were no significant differences in serum total cholesterol, apolipoprotein A, apolipoprotein B or lipoprotein(a) levels between the study groups. |
| 369 | 9115542 | The mean ApoB and Apo-A1 values were 112 mg/dl and 167 mg/dl for males and females. |
| 370 | 9117913 | Metabolic factors clustering, lipoprotein cholesterol, apolipoprotein B, lipoprotein (a) and apolipoprotein E phenotypes in premature coronary artery disease in French Canadians. |
| 371 | 9126663 | The analysis suggests that variations in insulin levels are a common metabolic basis for sex/age trends in fasting glucose, apolipoprotein B, total cholesterol, total cholesterol/HDL cholesterol ratio, LDL density (LDL cholesterol/apolipoprotein B), triglycerides and systolic blood pressure. |
| 372 | 9229197 | In bivariate analyses, the urinary albumin excretion rate had statistically significant (P < 0.05) relationships with age, duration of diabetes, male sex, waist-to-hip ratio, systolic and diastolic pressure, coronary heart disease, cerebrovascular disease, peripheral vascular disease, hypertension, antihypertensive therapy, laser-treated retinopathy, kind of treatment, smoking habit, fasting glycaemia, HbA1c, creatinine, uric acid, triglycerides, high density lipoprotein (HDL)-cholesterol and apolipoprotein B. |
| 373 | 9229197 | Borderline statistically significant (P < 0.1) relationships were found with hypolipidaemic therapy, insulin dose, non-HDL-cholesterol, apolipoprotein A1 and lipoprotein (a). |
| 374 | 9240769 | Intra-abdominal fat area was correlated with insulin concentration at 120 min in oral glucose tolerance tests and triglyceride level in male, on the other hand, in female were HDL-cholesterol level, apolipoprotein B, glucose area under curve and insulin concentration at 60 and 120 min. |
| 375 | 9300246 | After incubations with plasma d > 1.21 g/ml or with purified cholesteryl ester transfer protein, apoB-containing lipoproteins were precipitated with a dextran sulfate/MgCl2 solution. |
| 376 | 9387640 | Lp(a) concentration was not significantly correlated with the levels of total cholesterol, low-density lipoprotein cholesterol, triglyceride, high-density lipoprotein cholesterol (HDL-C), HDL2-C, HDL3-C, apolipoprotein A-I, apolipoprotein B in both groups. |
| 377 | 9392416 | The enzyme lipoprotein lipase, with apolipoprotein (apo)C-II as a co-factor, hydrolyzes chylomicron triglyceride allowing the delivery of free fatty acids to muscle and adipose tissue. |
| 378 | 9392416 | This particle is enriched in cholesteryl ester and fat-soluble vitamins and contains apoB-48 and apoE. |
| 379 | 9392416 | Here, it may 1) be removed directly by LDL receptors; 2) acquire additional apoE that is secreted free into the space, and then be removed directly by the LDL receptor-related protein (LRP); or 3) it may be sequestered in the space. |
| 380 | 9392416 | Sequestration occurs by binding of apoE to heparan sulfate proteoglycans and/or binding of apoB to hepatic lipase. |
| 381 | 9392416 | The enzyme lipoprotein lipase, with apolipoprotein (apo)C-II as a co-factor, hydrolyzes chylomicron triglyceride allowing the delivery of free fatty acids to muscle and adipose tissue. |
| 382 | 9392416 | This particle is enriched in cholesteryl ester and fat-soluble vitamins and contains apoB-48 and apoE. |
| 383 | 9392416 | Here, it may 1) be removed directly by LDL receptors; 2) acquire additional apoE that is secreted free into the space, and then be removed directly by the LDL receptor-related protein (LRP); or 3) it may be sequestered in the space. |
| 384 | 9392416 | Sequestration occurs by binding of apoE to heparan sulfate proteoglycans and/or binding of apoB to hepatic lipase. |
| 385 | 9402091 | Apolipoprotein B, fibrinogen, HDL cholesterol, and apolipoprotein(a) phenotypes predict coronary artery disease in hemodialysis patients. |
| 386 | 9409302 | Common genetic variations of apolipoprotein E [apoE], XbaI, polymorphism of apolipoprotein B [apoB], and PvuII polymorphism of the intact LDLR allele contributed little to serum lipid variation in established carriers of the FH-NK allele, although apoE2/4 genotype and the presence of the PvuII restriction site tended to be associated with relatively low LDL-C levels. |
| 387 | 9455439 | The colorimetric dozing with thyo-barbituric acid of the malonly dialdehyde (MAD) each is a product of the lipidic peroxidation, as well as the interpreting or correlation of the registered values with an evolutive clinic stage, and with the existence of some existing diseases (diabetes, chronic hepatitis etc.) along with signification of other dismethabolical parameters (cholesterol, triglycerides, LDLc, apoB) have confirmed the necessity of a complex therapy, including an antioxidative treatment, having the role to directly inhibit or exclude the free radicals resulted after the oxidative stress of the infarct. |
| 388 | 9458276 | We have investigated hepatic de novo lipogenesis and the ratio of apoB-48/apoB-100 during chronic carbohydrate supplementation with or without administration of exogenous insulin in rats. |
| 389 | 9458276 | The ratio of apoB-48/apoB-100, i.e. apoB-48 enrichment, in VLDL was positively correlated with insulin levels (r = 0.41, P < 0.01) and with FSR (r = 0.39, P < 0.01). |
| 390 | 9458276 | We have investigated hepatic de novo lipogenesis and the ratio of apoB-48/apoB-100 during chronic carbohydrate supplementation with or without administration of exogenous insulin in rats. |
| 391 | 9458276 | The ratio of apoB-48/apoB-100, i.e. apoB-48 enrichment, in VLDL was positively correlated with insulin levels (r = 0.41, P < 0.01) and with FSR (r = 0.39, P < 0.01). |
| 392 | 9462657 | To elucidate the mechanism of hyperlipidemia observed in OLETF rats, we focused on the production of VLDL by the liver and investigated hepatic messenger RNA (mRNA) levels of microsomal triglyceride transfer protein (MTP), acyl-coenzyme A synthetase (ACS), and apolipoprotein B (apo B), which play important roles in VLDL synthesis and secretion. |
| 393 | 9462657 | Hepatic ACS activity and mRNA levels, and MTP mRNA levels were also increased in OLETF rats, whereas apo B mRNA levels were similar; these results suggest that the enhanced expression of both ACS and MTP genes associated with visceral fat accumulation before developing insulin resistance may be involved in the pathogenesis of hyperlipidemia in obese animal models with NIDDM. |
| 394 | 9463740 | Subjects in group 1 were younger, had lower blood pressure, body mass index (BMI), waist-to-hip ratio (WHR), fasting and 2 h plasma insulin levels, triglyceride, very-low density lipoprotein and apolipoprotein-B concentrations than both groups 2 and 3. |
| 395 | 9507999 | The effect on apolipoprotein B kinetics of a diet enriched in either fish oil or safflower oil was investigated in five hypertriglyceridemic (HTG), non-insulin-dependent diabetic subjects. |
| 396 | 9544725 | In the non-diabetic group apolipoprotein[a] (365 [239-554] versus 184 [17-266] U/l; P < 0.01), total cholesterol (6.3 +/- 0.2 versus 5.6 +/- 0.2 mmol/l; P < 0.05), LDL cholesterol (4.1 +/- 0.2 versus 3.6 +/- 0.2 mmol/l; P < 0.05) and apolipoprotein B (146 +/- 8 versus 117 +/- 5 mg/dl; P < 0.05) were also found to be associated with PVD although these associations were not observed in the group with diabetes. |
| 397 | 9569171 | Studies that have used imaging techniques to assess the regional distribution of body fat have shown that an excess of visceral adipose tissue, that is, a high accumulation of fat in the abdominal cavity, was associated with a cluster of metabolic disturbances such as insulin resistance, hyperinsulinemia, glucose intolerance, hypertriglyceridemia, elevated apolipoprotein B (apoB) concentrations, small, dense low-density lipoprotein (LDL) particles, as well as low HDL cholesterol levels. |
| 398 | 9588450 | Effects of insulin and acipimox on VLDL1 and VLDL2 apolipoprotein B production in normal subjects. |
| 399 | 9588450 | The objective of the study was to examine the potential differential effect of insulin and acipimox (both of which reduce free fatty acid [FFA] availability) on VLDL apolipoprotein (apo) B metabolism. |
| 400 | 9592639 | No other consistent associations were found between insulin dose and other cardiovascular risk factors: body mass index, central adiposity, arterial blood pressures, serum total cholesterol, apoA1, apoB, Lp(a), uric acid, or urinary albumin excretion. |
| 401 | 9592640 | Serum glycated apolipoprotein B (apo B-G) levels were determined in 31 non-insulin-dependent diabetic patients and 13 control subjects by an enzyme-linked immunosorbent assay. |
| 402 | 9636203 | Epitopes close to the apolipoprotein B low density lipoprotein receptor-binding site are modified by advanced glycation end products. |
| 403 | 9636203 | Advanced glycation end products (AGEs) are thought to contribute to the abnormal lipoprotein profiles and increased risk of cardiovascular disease of patients with diabetes and renal failure, in part by preventing apolipoprotein B (apoB)-mediated cellular uptake of low density lipoproteins (LDL) by LDL receptors (LDLr). |
| 404 | 9636203 | It has been proposed that AGE modification at one site in apoB, almost 1,800 residues from the putative apoB LDLr-binding domain, may be sufficient to induce an apoB conformational change that prevents binding to the LDLr. |
| 405 | 9636203 | Glycation of LDL caused a time-dependent decrease in its ability to bind to the LDLr and in the immunoreactivity of six distinct apoB epitopes, including two that flank the apoB LDLr-binding domain. |
| 406 | 9636203 | Moreover, residues directly within the putative apoB LDLr-binding site are not apparently modified in glycated LDL. |
| 407 | 9636203 | AGE modification either eliminates the direct participation of the residues in LDLr binding or indirectly alters the conformation of the apoB LDLr-binding site. |
| 408 | 9636203 | Epitopes close to the apolipoprotein B low density lipoprotein receptor-binding site are modified by advanced glycation end products. |
| 409 | 9636203 | Advanced glycation end products (AGEs) are thought to contribute to the abnormal lipoprotein profiles and increased risk of cardiovascular disease of patients with diabetes and renal failure, in part by preventing apolipoprotein B (apoB)-mediated cellular uptake of low density lipoproteins (LDL) by LDL receptors (LDLr). |
| 410 | 9636203 | It has been proposed that AGE modification at one site in apoB, almost 1,800 residues from the putative apoB LDLr-binding domain, may be sufficient to induce an apoB conformational change that prevents binding to the LDLr. |
| 411 | 9636203 | Glycation of LDL caused a time-dependent decrease in its ability to bind to the LDLr and in the immunoreactivity of six distinct apoB epitopes, including two that flank the apoB LDLr-binding domain. |
| 412 | 9636203 | Moreover, residues directly within the putative apoB LDLr-binding site are not apparently modified in glycated LDL. |
| 413 | 9636203 | AGE modification either eliminates the direct participation of the residues in LDLr binding or indirectly alters the conformation of the apoB LDLr-binding site. |
| 414 | 9636203 | Epitopes close to the apolipoprotein B low density lipoprotein receptor-binding site are modified by advanced glycation end products. |
| 415 | 9636203 | Advanced glycation end products (AGEs) are thought to contribute to the abnormal lipoprotein profiles and increased risk of cardiovascular disease of patients with diabetes and renal failure, in part by preventing apolipoprotein B (apoB)-mediated cellular uptake of low density lipoproteins (LDL) by LDL receptors (LDLr). |
| 416 | 9636203 | It has been proposed that AGE modification at one site in apoB, almost 1,800 residues from the putative apoB LDLr-binding domain, may be sufficient to induce an apoB conformational change that prevents binding to the LDLr. |
| 417 | 9636203 | Glycation of LDL caused a time-dependent decrease in its ability to bind to the LDLr and in the immunoreactivity of six distinct apoB epitopes, including two that flank the apoB LDLr-binding domain. |
| 418 | 9636203 | Moreover, residues directly within the putative apoB LDLr-binding site are not apparently modified in glycated LDL. |
| 419 | 9636203 | AGE modification either eliminates the direct participation of the residues in LDLr binding or indirectly alters the conformation of the apoB LDLr-binding site. |
| 420 | 9636203 | Epitopes close to the apolipoprotein B low density lipoprotein receptor-binding site are modified by advanced glycation end products. |
| 421 | 9636203 | Advanced glycation end products (AGEs) are thought to contribute to the abnormal lipoprotein profiles and increased risk of cardiovascular disease of patients with diabetes and renal failure, in part by preventing apolipoprotein B (apoB)-mediated cellular uptake of low density lipoproteins (LDL) by LDL receptors (LDLr). |
| 422 | 9636203 | It has been proposed that AGE modification at one site in apoB, almost 1,800 residues from the putative apoB LDLr-binding domain, may be sufficient to induce an apoB conformational change that prevents binding to the LDLr. |
| 423 | 9636203 | Glycation of LDL caused a time-dependent decrease in its ability to bind to the LDLr and in the immunoreactivity of six distinct apoB epitopes, including two that flank the apoB LDLr-binding domain. |
| 424 | 9636203 | Moreover, residues directly within the putative apoB LDLr-binding site are not apparently modified in glycated LDL. |
| 425 | 9636203 | AGE modification either eliminates the direct participation of the residues in LDLr binding or indirectly alters the conformation of the apoB LDLr-binding site. |
| 426 | 9636203 | Epitopes close to the apolipoprotein B low density lipoprotein receptor-binding site are modified by advanced glycation end products. |
| 427 | 9636203 | Advanced glycation end products (AGEs) are thought to contribute to the abnormal lipoprotein profiles and increased risk of cardiovascular disease of patients with diabetes and renal failure, in part by preventing apolipoprotein B (apoB)-mediated cellular uptake of low density lipoproteins (LDL) by LDL receptors (LDLr). |
| 428 | 9636203 | It has been proposed that AGE modification at one site in apoB, almost 1,800 residues from the putative apoB LDLr-binding domain, may be sufficient to induce an apoB conformational change that prevents binding to the LDLr. |
| 429 | 9636203 | Glycation of LDL caused a time-dependent decrease in its ability to bind to the LDLr and in the immunoreactivity of six distinct apoB epitopes, including two that flank the apoB LDLr-binding domain. |
| 430 | 9636203 | Moreover, residues directly within the putative apoB LDLr-binding site are not apparently modified in glycated LDL. |
| 431 | 9636203 | AGE modification either eliminates the direct participation of the residues in LDLr binding or indirectly alters the conformation of the apoB LDLr-binding site. |
| 432 | 9636203 | Epitopes close to the apolipoprotein B low density lipoprotein receptor-binding site are modified by advanced glycation end products. |
| 433 | 9636203 | Advanced glycation end products (AGEs) are thought to contribute to the abnormal lipoprotein profiles and increased risk of cardiovascular disease of patients with diabetes and renal failure, in part by preventing apolipoprotein B (apoB)-mediated cellular uptake of low density lipoproteins (LDL) by LDL receptors (LDLr). |
| 434 | 9636203 | It has been proposed that AGE modification at one site in apoB, almost 1,800 residues from the putative apoB LDLr-binding domain, may be sufficient to induce an apoB conformational change that prevents binding to the LDLr. |
| 435 | 9636203 | Glycation of LDL caused a time-dependent decrease in its ability to bind to the LDLr and in the immunoreactivity of six distinct apoB epitopes, including two that flank the apoB LDLr-binding domain. |
| 436 | 9636203 | Moreover, residues directly within the putative apoB LDLr-binding site are not apparently modified in glycated LDL. |
| 437 | 9636203 | AGE modification either eliminates the direct participation of the residues in LDLr binding or indirectly alters the conformation of the apoB LDLr-binding site. |
| 438 | 9699898 | Cholesterol, triglycerides, apolipoprotein A-I and apolipoprotein B concentrations were measured in serum; the lipoprotein fractions very low density, intermediate density, low density and high density lipoprotein were prepared by sequential flotation ultracentrifugation and their composition investigated. |
| 439 | 9699898 | Relatives had higher serum apolipoprotein B concentrations than control subjects [0.9 (0.3) vs 0.8 (0.3) g/l, p = 0.02) and lower serum apolipoprotein A-I concentrations (1.4 (0.3) vs 1.5 (0.3), p = 0.02). |
| 440 | 9699898 | In multivariate linear regression analysis of all subjects log insulin resistance (p = 0.0001), age (p = 0.002) and waist:hip ratio (p = 0.01) were independent predicators of apolipoprotein B concentrations while waist:hip ratio (p < 0.001) and smoking status (p = 0.002) were independent predictors of apolipoprotein A-I concentrations. |
| 441 | 9699898 | We conclude that atherogenic apolipoprotein abnormalities occur in normoglycaemic relatives of non-insulin dependent diabetic patients. |
| 442 | 9699898 | Cholesterol, triglycerides, apolipoprotein A-I and apolipoprotein B concentrations were measured in serum; the lipoprotein fractions very low density, intermediate density, low density and high density lipoprotein were prepared by sequential flotation ultracentrifugation and their composition investigated. |
| 443 | 9699898 | Relatives had higher serum apolipoprotein B concentrations than control subjects [0.9 (0.3) vs 0.8 (0.3) g/l, p = 0.02) and lower serum apolipoprotein A-I concentrations (1.4 (0.3) vs 1.5 (0.3), p = 0.02). |
| 444 | 9699898 | In multivariate linear regression analysis of all subjects log insulin resistance (p = 0.0001), age (p = 0.002) and waist:hip ratio (p = 0.01) were independent predicators of apolipoprotein B concentrations while waist:hip ratio (p < 0.001) and smoking status (p = 0.002) were independent predictors of apolipoprotein A-I concentrations. |
| 445 | 9699898 | We conclude that atherogenic apolipoprotein abnormalities occur in normoglycaemic relatives of non-insulin dependent diabetic patients. |
| 446 | 9699898 | Cholesterol, triglycerides, apolipoprotein A-I and apolipoprotein B concentrations were measured in serum; the lipoprotein fractions very low density, intermediate density, low density and high density lipoprotein were prepared by sequential flotation ultracentrifugation and their composition investigated. |
| 447 | 9699898 | Relatives had higher serum apolipoprotein B concentrations than control subjects [0.9 (0.3) vs 0.8 (0.3) g/l, p = 0.02) and lower serum apolipoprotein A-I concentrations (1.4 (0.3) vs 1.5 (0.3), p = 0.02). |
| 448 | 9699898 | In multivariate linear regression analysis of all subjects log insulin resistance (p = 0.0001), age (p = 0.002) and waist:hip ratio (p = 0.01) were independent predicators of apolipoprotein B concentrations while waist:hip ratio (p < 0.001) and smoking status (p = 0.002) were independent predictors of apolipoprotein A-I concentrations. |
| 449 | 9699898 | We conclude that atherogenic apolipoprotein abnormalities occur in normoglycaemic relatives of non-insulin dependent diabetic patients. |
| 450 | 9733217 | Elevated plasma cholesteryl ester transfer in NIDDM: relationships with apolipoprotein B-containing lipoproteins and phospholipid transfer protein. |
| 451 | 9733217 | Phospholipid transfer protein (PLTP), lipoprotein lipase (LPL) and hepatic lipase (HL) are involved in plasma phospholipid and triglyceride metabolism and also affect HDL. |
| 452 | 9733217 | In 16 NIDDM men with plasma triglycerides < or = 4.5 mmol/l and cholesterol < or = 8.0 mmol/l. plasma cholesteryl ester transfer (CET), cholesterol esterification rate, LCAT and PLTP activity levels were higher (P < 0.05 to P < 0.02) in conjunction with higher plasma triglycerides (P < 0.01) and lower HDL cholesterol and cholesteryl ester levels (P < 0.05) compared to 16 matched healthy men. |
| 453 | 9733217 | Multiple stepwise regression analysis demonstrated that CET was positively related to VLDL + LDL cholesterol (P < 0.001), triglycerides (P = 0.001), PLTP activity (P = 0.007) and CETP activity (P = 0.008, multiple r = 0.94). |
| 454 | 9733217 | Furthermore, our data suggest that in normo- and moderately dyslipidaemic subjects PLTP and CETP activity levels per se may influence the rate of cholesteryl ester transfer in plasma. |
| 455 | 9801804 | The biochemical parameters-total protein, transferrin in LP group, glucose in DM group, total cholesterol, triacylglycerols, LDL-cholesterol, apolipoprotein B and A-I did not correlate with serum Cr concentration. |
| 456 | 9807971 | After 12 weeks of treatment with lovastatin alone, improvement was observed in total cholesterol (21% reduction), triglyceride (32% reduction), low-density lipoprotein (LDL) cholesterol (5.5% reduction), HDL cholesterol (11.6% elevation), apolipoprotein A-I (4.6% elevation), and apolipoprotein B (20.5% reduction). |
| 457 | 9807971 | However, HDL cholesterol and apolipoprotein A-I levels were significantly increased by the addition of acipimox (a 14.2% and 9.0% elevation, respectively). |
| 458 | 9807971 | Combination treatment with lovastatin and acipimox appears to be a safe and effective therapy in patients with type 2 diabetes and mixed dyslipidemia, and has particular benefit in elevating serum HDL cholesterol and apolipoprotein A-I levels. |
| 459 | 9878681 | While a few genes have been identified whose mutant alleles have large effects on this trait (e.g., LDLR, familial defective apoB-100), variability in cholesterol levels among individuals in most families is influenced by allelic variation in many genes (polymorphisms) as well as environmental exposures. |
| 460 | 9878681 | High density lipoprotein cholesterol levels are genetically influenced and are related to apoA1 and hepatic lipase (LIPC) gene functions. |
| 461 | 9878681 | Mutations in the apoA1 gene are rare and there are data which suggest a role of allelic variation at or linked LIPC gene in high density lipoprotein cholesterol levels. |
| 462 | 9888643 | Insulin resistance causes increased flux of free fatty acids, and thus enhanced VLDL apolipoprotein B (apo B) synthesis in the liver. |
| 463 | 10027576 | Insulin suppresses apolipoprotein(a) synthesis by primary cultures of cynomolgus monkey hepatocytes. |
| 464 | 10027576 | To investigate the biochemical background of these changes, we studied the effect of insulin on apolipoprotein(a) (apo(a)) synthesis and mRNA levels in primary cultures of cynomolgus monkey hepatocytes. |
| 465 | 10027576 | Low concentrations of insulin (10 nmol/l) had a small but significant decreasing effect (p < 0.046) on apolipoprotein(a) secretion (-16%). |
| 466 | 10027576 | Apolipoprotein B-100 secretion was 30%-36% decreased when using 10-1000 nmol/l and no change was observed for the secretion of apolipoprotein A-1 and albumin which were measured as control proteins. |
| 467 | 10027576 | Steady state apolipoprotein(a) mRNA concentrations paralleled the decrease in apolipoprotein(a) synthesis (-29% after incubating the cells for 48 h with 100 nmol/l insulin) indicating that the decreased synthesis is regulated at the (post)-transcriptional level. |
| 468 | 10027576 | Concentrations of apolipoprotein B-100 and apolipoprotein A-1 mRNA were not changed after incubation with insulin. |
| 469 | 10027576 | We conclude that high concentrations of insulin suppress apolipoprotein(a) synthesis in monkey hepatocytes at the (post)-transcriptional level. |
| 470 | 10027576 | Insulin suppresses apolipoprotein(a) synthesis by primary cultures of cynomolgus monkey hepatocytes. |
| 471 | 10027576 | To investigate the biochemical background of these changes, we studied the effect of insulin on apolipoprotein(a) (apo(a)) synthesis and mRNA levels in primary cultures of cynomolgus monkey hepatocytes. |
| 472 | 10027576 | Low concentrations of insulin (10 nmol/l) had a small but significant decreasing effect (p < 0.046) on apolipoprotein(a) secretion (-16%). |
| 473 | 10027576 | Apolipoprotein B-100 secretion was 30%-36% decreased when using 10-1000 nmol/l and no change was observed for the secretion of apolipoprotein A-1 and albumin which were measured as control proteins. |
| 474 | 10027576 | Steady state apolipoprotein(a) mRNA concentrations paralleled the decrease in apolipoprotein(a) synthesis (-29% after incubating the cells for 48 h with 100 nmol/l insulin) indicating that the decreased synthesis is regulated at the (post)-transcriptional level. |
| 475 | 10027576 | Concentrations of apolipoprotein B-100 and apolipoprotein A-1 mRNA were not changed after incubation with insulin. |
| 476 | 10027576 | We conclude that high concentrations of insulin suppress apolipoprotein(a) synthesis in monkey hepatocytes at the (post)-transcriptional level. |
| 477 | 10094113 | In both genders, VAT accumulation was positively correlated with fasting plasma insulin, triglyceride (TG), and low-density lipoprotein (LDL)-apolipoprotein B (apo B) levels and the cholesterol (CHOL)/high-density lipoprotein (HDL)-CHOL ratio (.24 < or = r < or = .71, P < .05). |
| 478 | 10211632 | Increased plasma apolipoprotein B-containing lipoproteins associated with increased urinary albumin within the microalbuminuria range in type 2 diabetes. |
| 479 | 10337867 | Reductions in body weight (P < .001) and improvements in fasting blood glucose, insulin, fructosamine (P < .001), and free fatty acids (P < .01) by intervention were associated with reductions in serum cholesterol and apolipoprotein B (apo B) concentrations in very-low-density lipoprotein (VLDL) (P < .01), intermediate-density lipoprotein (IDL), and small, dense (>1.040 g/mL) LDL particles (P < .001). |
| 480 | 10376396 | Specific phenotypic manifestations of diabetic dyslipidaemia include hypertriacylglycerolaemia, hypercholesterolaemia, elevated plasma levels of LDL-cholesterol and apolipoprotein B and reduced levels of HDL-cholesterol and apolipoprotein B and reduced levels of HDL-cholesterol and apolipoprotein A-I. |
| 481 | 10393218 | The gene for apolipoprotein apoB lies within the region, but apoB levels were similar in strains B6 and BKS. |
| 482 | 10393218 | We conclude that susceptibilities to diabetes and atherosclerosis are not conferred by the same genes in these strains and that a major gene on Chr 12, which we name Ath6, determines the difference in atherosclerosis susceptibility. |
| 483 | 10428305 | To obtain some information on the metabolic basis of this difference, we compared anthropometric data as well as serum levels of leptin, insulin, testosterone (T), estradiol (E2), and sex hormone binding globuline (SHBG) in 289 German and 120 Turkish men as well as in 108 German and 182 Turkish women aged 20-60. |
| 484 | 10428305 | Mean values of age, waist-hip-ratio (WHR), leptin, triglycerides, LDL-C, and apoB did not differ significantly among Germans and Turks. |
| 485 | 10428305 | Upon univariate analysis HDL-C had inverse correlations with BMI, waist circumference, WHR, leptin, and insulin as well as positive correlations with SHBG in both sexes. |
| 486 | 10450539 | In comparison with initial values, a decrease in the following was noted for the whole study group: triglyceride level (226.0 +/- 27.1 vs. 288.0 +/- 51.9 mg/dl; p < 0.05), percent LDL-cholesterol (72.4 +/- 1.8 vs. 75.8 +/- 1.7; p < 0.05), apolipoprotein B (111.2 +/- 4.6 vs. 115.3 +/- 5.4 mg/dl; p < 0.05), atherogenic indices: LDL/HDL (5.06 +/- 0.58 vs. 5.95 +/- 0.50; p < 0.02) and apolipoprotein B and A (apoB/apoA) (0.92 +/- 0.04 vs. 1.02 +/- 0.06; p < 0.05). |
| 487 | 10479666 | In addition, HDL(2) from diabetics did not protect against apolipoprotein B-100 fragmentation in LDL. |
| 488 | 10479666 | Cross-linking in apolipoprotein A-I, oxidized in the presence of LDL, was extensive in HDL(2) from diabetics compared with that from controls. |
| 489 | 10484613 | Thus, in normolipidemic carriers the LPL Asn291Ser gene variant delays postprandial triglyceride, apoB-48, apoB-100, and retinyl ester metabolism in VLDL1 fraction and alters postprandial HDL composition compared to matched non-carriers. |
| 490 | 10499189 | Results from the Québec Cardiovascular Study have indicated that individuals displaying three of the numerous features of insulin resistance (elevated plasma insulin and apolipoprotein B concentrations and small, dense LDL particles) showed a remarkable increase in CHD risk. |
| 491 | 10522991 | To determine whether cholesterol esterification rate (CER) and transfer of cholesteryl esters from high density lipoproteins to apolipoprotein B-containing lipoproteins are affected by menopause and HRT, plasma newly synthesized cholesteryl ester transfer (NCET) activity, CER and plasma lipids, lipoproteins, and apolipoprotein concentrations were measured in perimenopausal women (age range: 40-55 yr), including 49 premenopausal women and 32 postmenopausal women who were subsequently randomized to receive either placebo or 17-beta estradiol/norethisterone for 6 months. |
| 492 | 10523010 | Patients were separated into groups, 231 males (78 B1B1, 108 B1B2, 45 B2B2) and 175 females (48 B1B1, 94 B1B2, 33 B2B2), and compared on the basis of their lipid parameters (total cholesterol, triglycerides, high-density lipoprotein-cholesterol (HDL-C), ApoA1 ApoB, and low-density lipoprotein-cholesterol), their micro and macrovascular complications. |
| 493 | 10588944 | The effects of diabetes and lipoprotein lipase (LpL) on plasma lipids were studied in mice expressing human apolipoprotein B (HuBTg). |
| 494 | 10591679 | Apolipoprotein B was distributed among a much broader spectrum of LDL particles, and apolipoprotein E was partially redistributed from high-density lipoprotein to apolipoprotein B-containing lipoproteins in diabetic pigs. |
| 495 | 10591679 | There was little change in apolipoprotein A-I distribution. |
| 496 | 10663213 | Significant improvement of apolipoprotein B-containing lipoprotein metabolism by insulin treatment in patients with non-insulin-dependent diabetes mellitus. |
| 497 | 10692751 | Decreases in total cholesterol (p = 0.018), apolipoprotein B (p = 0.042) and apolipoprotein A1 (p = 0.025), were significant for the comparison of 80 mg valsartan and captopril. |
| 498 | 10744773 | Two proteins that may be important in this process are apolipoprotein B (apoB, the major structural protein of secreted lipoproteins) and microsomal triglyceride transfer protein (MTP) whose normal activity is required for the secretion of apoB-containing lipoproteins. |
| 499 | 10744773 | Although no abnormalities of conception and embryonic lethality are known in humans who inherit genetic deficiencies of either of these proteins, homozygous mice bearing knockouts of either apoB or MTP show early embryonic lethality. |
| 500 | 10744773 | Two proteins that may be important in this process are apolipoprotein B (apoB, the major structural protein of secreted lipoproteins) and microsomal triglyceride transfer protein (MTP) whose normal activity is required for the secretion of apoB-containing lipoproteins. |
| 501 | 10744773 | Although no abnormalities of conception and embryonic lethality are known in humans who inherit genetic deficiencies of either of these proteins, homozygous mice bearing knockouts of either apoB or MTP show early embryonic lethality. |
| 502 | 10798086 | Apolipoprotein A-I (Apo A-1) and apolipoprotein B (Apo B) levels, Apo A-I/Apo B and HDL-C/Apo A-I ratios were similar in between groups. |
| 503 | 10852461 | We have recently demonstrated that subjects having Pro7 in the signal peptide ofneuropeptide Y (NPY) have higher serum cholesterol and apolipoprotein B levels than individuals with wild-type (Leu7Leu7) signal peptide sequence. |
| 504 | 10862796 | Delayed catabolism of apoB-48 lipoproteins due to decreased heparan sulfate proteoglycan production in diabetic mice. |
| 505 | 10862796 | Delayed clearance of postprandial apoB-48-containing lipoproteins in DM appears to be due to decreased hepatic perlecan HSPG. |
| 506 | 10862796 | Delayed catabolism of apoB-48 lipoproteins due to decreased heparan sulfate proteoglycan production in diabetic mice. |
| 507 | 10862796 | Delayed clearance of postprandial apoB-48-containing lipoproteins in DM appears to be due to decreased hepatic perlecan HSPG. |
| 508 | 10946033 | Compared with placebo, simvastatin produced significant (p <0.01) and dose-dependent changes in all lipid and lipoprotein parameters (LDL cholesterol 2.1%, -28.9%, and -35.5%; triglycerides -3.5%, -27.8%, and -33.0%; high-density lipoprotein cholesterol 3.3%, 13.1%, and 15. 7%; apolipoprotein B 3.8%, -23.1%, and -30.6%; and apolipoprotein A-I 4.0%, 8.2%, and 10.5% with placebo, and simvastatin 40 and 80 mg/day, respectively). |
| 509 | 10964160 | Metabolic abnormalities of apolipoprotein B-containing lipoproteins in non-insulin-dependent diabetes: a stable isotope kinetic study. |
| 510 | 10978257 | Human paraoxonase (PON1) is a calcium-dependent esterase closely associated with high density lipoprotein (HDL)-containing apolipoprotein AI (apoAI), which has been shown to confer antioxidant properties to HDL. |
| 511 | 10978257 | We have undertaken a study of the effect of the lipid-lowering drug simvastatin on serum PON1 activity (in relation to paraoxon and arylesterase activity), on apoAI-containing and apolipoprotein B (apoB)-containing lipoproteins, and on lipid peroxide concentrations in 64 (39 women and 25 men) unrelated FH patients. |
| 512 | 10979539 | Plasma lipids and apolipoprotein B levels were determined as well as two antioxidants: alpha-tocopherol level and superoxide dismutase activity. |
| 513 | 11122699 | In The Copenhagen City Heart Study, apolipoprotein B Arg3500Gln and Arg3531Cys increased plasma cholesterol 41% and 0%, lipoprotein lipase Gly188Glu, Asn291Ser, and Asp9Asn increased plasma triglycerides 42%, 13% (women only), and 13% (men only), and angiotensin converting enzyme DD increased plasma ACE activity 57%. |
| 514 | 11231977 | When compared with 8 weeks of placebo, estrogen reduced fasting serum glucose (7.2 +/- 0.3 vs. 8.4 +/- 0.4 mmol/L, P = 0.0003), glycated hemoglobin (8.7 +/- 0.4% vs. 9.3 +/- 0.4%, P = 0.04), total cholesterol (5.27 +/- 0.20 vs. 5.50 +/- 0.21 mmol/L, P = 0.04), low-density lipoprotein cholesterol (2.47 +/- 0.13 vs. 2.69 +/- 0.14 mmol/L, P = 0.02), serum apolipoprotein B (114 +/- 6 vs. 121 +/- 5 mg/dL, P = 0.03), and postprandial glucose area under the curve (by 12%, P = 0.015). |
| 515 | 11272161 | We found a strong positive correlation during the 6-h postprandial period between apolipoprotein (apo) B-48 plasma concentration and insulin plasma concentration (r2 = 0.70; P = 0.0001). |
| 516 | 11272161 | A biphasic response was observed with markedly reduced levels of plasma apoB-48 during insulin infusion, followed by a late accumulation of plasma apoB-48 and triglycerides. |
| 517 | 11272161 | Overall, the data obtained showed that portal and peripheral hyperinsulinism delays and exacerbates postprandial accumulation of intestinally derived chylomicrons in plasma and thus is involved in the regulation of apoB-48-triglyceride-rich lipoprotein metabolism, in the absence of insulin-resistance syndrome. |
| 518 | 11272161 | We found a strong positive correlation during the 6-h postprandial period between apolipoprotein (apo) B-48 plasma concentration and insulin plasma concentration (r2 = 0.70; P = 0.0001). |
| 519 | 11272161 | A biphasic response was observed with markedly reduced levels of plasma apoB-48 during insulin infusion, followed by a late accumulation of plasma apoB-48 and triglycerides. |
| 520 | 11272161 | Overall, the data obtained showed that portal and peripheral hyperinsulinism delays and exacerbates postprandial accumulation of intestinally derived chylomicrons in plasma and thus is involved in the regulation of apoB-48-triglyceride-rich lipoprotein metabolism, in the absence of insulin-resistance syndrome. |
| 521 | 11301562 | No statistically significant changes in mean concentrations of total cholesterol, low-density lipoprotein (LDL) cholesterol, triglycerides, very low-density lipoprotein (VLDL) triglycerides, apolipoprotein A1, or apolipoprotein B were evident. |
| 522 | 11374763 | Plasma levels of lipids (TC, TG), apolipoproteins (A-I, B, C-III, E), lipoprotein (a) (Ip(a)), and individual apoA and apoB containing lipoproteins (LP-A-I, LP-A-I:A-II, LP-B, LP-Bc) were determined. |
| 523 | 11383676 | Nevertheless, in Type 2 diabetes mellitus (T2DM) a profound reduction in the fibrinolytic activity has been demonstrated to be involved in vascular complications, probably due to plasminogen activator inhibitor type 1 (PAI-1) overproduction. |
| 524 | 11383676 | Significant differences were found for PAI-1 antigen (p=0.006), PAI-1 activity (p=0.028), apolipoprotein B (p=0.015) and antioxidant defence, evaluated as ferric reducing ability of plasma (FRAP) values (p=0.005). |
| 525 | 11423487 | Once glycated, LDL is only poorly recognized by lipoprotein receptors including the LDL receptor (LDL-R), the LDL-R-related protein (LRP), and scavenger receptors. |
| 526 | 11423487 | The addition of exogenous LPL to the culture medium of human skin fibroblasts, porcine aortic endothelial cells, and mouse peritoneal macrophages enhanced the binding, uptake, and degradation of gLDL markedly, and the relative effect of LPL on lipoprotein uptake increased with the degree of apoB glycation. |
| 527 | 11423487 | The efficient uptake of gLDL by LDL-R-deficient fibroblasts and LRP-deficient Chinese hamster ovary cells in the presence of LPL suggested a mechanism that was independent of the LDL-R and LRP. |
| 528 | 11433351 | Apolipoprotein B secretion and atherosclerosis are decreased in mice with phospholipid-transfer protein deficiency. |
| 529 | 11433351 | Increased secretion and levels of ApoB-containing lipoproteins (BLp) commonly occur in familial hyperlipidemia, obesity and diabetes. |
| 530 | 11433351 | The plasma phospholipid-transfer protein (PLTP) is known to mediate transfer of phospholipids between BLp and HDL during their intravascular metabolism. |
| 531 | 11433351 | In ApoB-transgenic and ApoE-deficient backgrounds, PLTP deficiency resulted in reduced production and levels of BLp and markedly decreased atherosclerosis. |
| 532 | 11433351 | BLp secretion was diminished in hepatocytes from ApoB-transgenic PLTP-deficient mice, a defect that was corrected when PLTP was reintroduced in adenovirus. |
| 533 | 11433351 | Apolipoprotein B secretion and atherosclerosis are decreased in mice with phospholipid-transfer protein deficiency. |
| 534 | 11433351 | Increased secretion and levels of ApoB-containing lipoproteins (BLp) commonly occur in familial hyperlipidemia, obesity and diabetes. |
| 535 | 11433351 | The plasma phospholipid-transfer protein (PLTP) is known to mediate transfer of phospholipids between BLp and HDL during their intravascular metabolism. |
| 536 | 11433351 | In ApoB-transgenic and ApoE-deficient backgrounds, PLTP deficiency resulted in reduced production and levels of BLp and markedly decreased atherosclerosis. |
| 537 | 11433351 | BLp secretion was diminished in hepatocytes from ApoB-transgenic PLTP-deficient mice, a defect that was corrected when PLTP was reintroduced in adenovirus. |
| 538 | 11433351 | Apolipoprotein B secretion and atherosclerosis are decreased in mice with phospholipid-transfer protein deficiency. |
| 539 | 11433351 | Increased secretion and levels of ApoB-containing lipoproteins (BLp) commonly occur in familial hyperlipidemia, obesity and diabetes. |
| 540 | 11433351 | The plasma phospholipid-transfer protein (PLTP) is known to mediate transfer of phospholipids between BLp and HDL during their intravascular metabolism. |
| 541 | 11433351 | In ApoB-transgenic and ApoE-deficient backgrounds, PLTP deficiency resulted in reduced production and levels of BLp and markedly decreased atherosclerosis. |
| 542 | 11433351 | BLp secretion was diminished in hepatocytes from ApoB-transgenic PLTP-deficient mice, a defect that was corrected when PLTP was reintroduced in adenovirus. |
| 543 | 11433351 | Apolipoprotein B secretion and atherosclerosis are decreased in mice with phospholipid-transfer protein deficiency. |
| 544 | 11433351 | Increased secretion and levels of ApoB-containing lipoproteins (BLp) commonly occur in familial hyperlipidemia, obesity and diabetes. |
| 545 | 11433351 | The plasma phospholipid-transfer protein (PLTP) is known to mediate transfer of phospholipids between BLp and HDL during their intravascular metabolism. |
| 546 | 11433351 | In ApoB-transgenic and ApoE-deficient backgrounds, PLTP deficiency resulted in reduced production and levels of BLp and markedly decreased atherosclerosis. |
| 547 | 11433351 | BLp secretion was diminished in hepatocytes from ApoB-transgenic PLTP-deficient mice, a defect that was corrected when PLTP was reintroduced in adenovirus. |
| 548 | 11472752 | Plasma insulin, leptin, and soluble TNF receptors levels in relation to obesity-related atherogenic and thrombogenic cardiovascular disease risk factors among men. |
| 549 | 11472752 | Plasma leptin and tumor necrosis factor-alpha (TNF-alpha), two adipocyte products, are also proposed to be associated with the development of CVD risk. |
| 550 | 11472752 | The purpose of this study is to evaluate the association of plasma leptin, soluble TNF receptors (sTNF-R), and insulin levels as possible mediators of the effect of obesity on atherogenic and thrombogenic CVD risk factors among men. |
| 551 | 11472752 | We measured plasma insulin and leptin levels by radioimmunoassay and sTNF-R levels by ELISA. |
| 552 | 11472752 | Men in the highest quintile of body mass index (BMI, mean=30.5 kg/m(2)) were less physically active and had a more adverse cardiovascular lipid and homeostatic profile, as indicated by levels of insulin, triglyceride (TG), tissue plasminogen activator (t-PA) antigen levels, and apolipoprotein A1 (Apo-A1). |
| 553 | 11472752 | In a multivariate regression model controlling for age, smoking, alcohol intake, physical activity and diet, BMI was inversely associated with HDL-cholesterol (HDL-C) and Apo-A1 and positively associated with TG, Apo-B and t-PA antigen levels. |
| 554 | 11472752 | The associations between BMI and these CVD risk factors were only slightly changed after adjusting for leptin and/or sTNF-R; but were substantially attenuated after controlling for insulin levels. |
| 555 | 11472752 | These data suggest that the association between obesity and biological predictors of CVD may be mediated through changes in plasma insulin, rather than leptin or sTNF-R levels. |
| 556 | 11552052 | The ratio of apolipoprotein b to apolipoprotein a-1 was shown to be associated with carotid atheroma. |
| 557 | 11583309 | The study population consisted of 1,045 postinfarction patients (846 non-diabetic, 125 non-insulin- and 74 insulin-requiring diabetics) with the following blood tests performed 2 months after an index myocardial infarction: lipoprotein (a), apolipoprotein-B, apolipoprotein-A, cholesterol, HDL cholesterol, triglycerides, insulin, von Willebrand factor (vWF), fibrinogen, factor VII, D-dimer, and plasminogen activator inhibitor (PAI-1). |
| 558 | 11583309 | After adjustment for relevant clinical covariates, non-insulin-requiring diabetes was significantly (p < 0.05) associated with elevated levels of (odd ratios per 1 log unit increase in parenthesis) vWF (1.74) and PAI-1 (1.42) whereas insulin requiring diabetes was associated with even more elevated levels of vWF (4.68), but not with increased levels of PAI-1. |
| 559 | 11597941 | LY 294002 (80 micromol/L), an inhibitor of phosphoinositide 3-kinase, was used to investigate the involvement of this enzyme in the insulin-mediated regulation of very low density lipoprotein (VLDL) apolipoprotein B (apoB) output from cultured rat hepatocytes. |
| 560 | 11597941 | Brefeldin A (BFA, 0.2 microgram/mL) was used to discriminate between the role of insulin in the regulation of the early, compared with the later, events of VLDL assembly, including apoB degradation. |
| 561 | 11597941 | Insulin (78 nmol/L), when present during the pulse-labeling and subsequent chase periods, inhibited the secretion of apoB-100 and apoB-48 as VLDL by 53% and 56%, respectively. |
| 562 | 11597941 | Furthermore, when insulin remained present during this period, the simultaneous presence of LY 294002 also reversed the inhibitory effect of insulin on VLDL apoB output and abolished the increase in apoB degradation. |
| 563 | 11597941 | The results suggest that insulin signaling via phosphoinositide 3-kinase inhibited the maturation phase of VLDL assembly by preventing bulk lipid transfer to a VLDL precursor, thus enhancing the degradation of apoB. |
| 564 | 11597941 | LY 294002 (80 micromol/L), an inhibitor of phosphoinositide 3-kinase, was used to investigate the involvement of this enzyme in the insulin-mediated regulation of very low density lipoprotein (VLDL) apolipoprotein B (apoB) output from cultured rat hepatocytes. |
| 565 | 11597941 | Brefeldin A (BFA, 0.2 microgram/mL) was used to discriminate between the role of insulin in the regulation of the early, compared with the later, events of VLDL assembly, including apoB degradation. |
| 566 | 11597941 | Insulin (78 nmol/L), when present during the pulse-labeling and subsequent chase periods, inhibited the secretion of apoB-100 and apoB-48 as VLDL by 53% and 56%, respectively. |
| 567 | 11597941 | Furthermore, when insulin remained present during this period, the simultaneous presence of LY 294002 also reversed the inhibitory effect of insulin on VLDL apoB output and abolished the increase in apoB degradation. |
| 568 | 11597941 | The results suggest that insulin signaling via phosphoinositide 3-kinase inhibited the maturation phase of VLDL assembly by preventing bulk lipid transfer to a VLDL precursor, thus enhancing the degradation of apoB. |
| 569 | 11597941 | LY 294002 (80 micromol/L), an inhibitor of phosphoinositide 3-kinase, was used to investigate the involvement of this enzyme in the insulin-mediated regulation of very low density lipoprotein (VLDL) apolipoprotein B (apoB) output from cultured rat hepatocytes. |
| 570 | 11597941 | Brefeldin A (BFA, 0.2 microgram/mL) was used to discriminate between the role of insulin in the regulation of the early, compared with the later, events of VLDL assembly, including apoB degradation. |
| 571 | 11597941 | Insulin (78 nmol/L), when present during the pulse-labeling and subsequent chase periods, inhibited the secretion of apoB-100 and apoB-48 as VLDL by 53% and 56%, respectively. |
| 572 | 11597941 | Furthermore, when insulin remained present during this period, the simultaneous presence of LY 294002 also reversed the inhibitory effect of insulin on VLDL apoB output and abolished the increase in apoB degradation. |
| 573 | 11597941 | The results suggest that insulin signaling via phosphoinositide 3-kinase inhibited the maturation phase of VLDL assembly by preventing bulk lipid transfer to a VLDL precursor, thus enhancing the degradation of apoB. |
| 574 | 11597941 | LY 294002 (80 micromol/L), an inhibitor of phosphoinositide 3-kinase, was used to investigate the involvement of this enzyme in the insulin-mediated regulation of very low density lipoprotein (VLDL) apolipoprotein B (apoB) output from cultured rat hepatocytes. |
| 575 | 11597941 | Brefeldin A (BFA, 0.2 microgram/mL) was used to discriminate between the role of insulin in the regulation of the early, compared with the later, events of VLDL assembly, including apoB degradation. |
| 576 | 11597941 | Insulin (78 nmol/L), when present during the pulse-labeling and subsequent chase periods, inhibited the secretion of apoB-100 and apoB-48 as VLDL by 53% and 56%, respectively. |
| 577 | 11597941 | Furthermore, when insulin remained present during this period, the simultaneous presence of LY 294002 also reversed the inhibitory effect of insulin on VLDL apoB output and abolished the increase in apoB degradation. |
| 578 | 11597941 | The results suggest that insulin signaling via phosphoinositide 3-kinase inhibited the maturation phase of VLDL assembly by preventing bulk lipid transfer to a VLDL precursor, thus enhancing the degradation of apoB. |
| 579 | 11597941 | LY 294002 (80 micromol/L), an inhibitor of phosphoinositide 3-kinase, was used to investigate the involvement of this enzyme in the insulin-mediated regulation of very low density lipoprotein (VLDL) apolipoprotein B (apoB) output from cultured rat hepatocytes. |
| 580 | 11597941 | Brefeldin A (BFA, 0.2 microgram/mL) was used to discriminate between the role of insulin in the regulation of the early, compared with the later, events of VLDL assembly, including apoB degradation. |
| 581 | 11597941 | Insulin (78 nmol/L), when present during the pulse-labeling and subsequent chase periods, inhibited the secretion of apoB-100 and apoB-48 as VLDL by 53% and 56%, respectively. |
| 582 | 11597941 | Furthermore, when insulin remained present during this period, the simultaneous presence of LY 294002 also reversed the inhibitory effect of insulin on VLDL apoB output and abolished the increase in apoB degradation. |
| 583 | 11597941 | The results suggest that insulin signaling via phosphoinositide 3-kinase inhibited the maturation phase of VLDL assembly by preventing bulk lipid transfer to a VLDL precursor, thus enhancing the degradation of apoB. |
| 584 | 11704692 | At baseline, those who died had significantly higher serum creatinine (p=0.001) and urine albumin/creatinine ratio (p=0.016), greater prevalence of retinopathy (p=0.006), lower serum apolipoprotein A1 (p=0.046), and lower daily insulin dose (p=0.024) than those who survived. |
| 585 | 11704692 | The CAD group also had higher baseline serum creatinine (p=0.02), lower HDL cholesterol (p=0.004) and apolipoprotein A1 (p=0.007) and higher LDL cholesterol (p=0.028) and apolipoprotein B concentrations (p=0.027). |
| 586 | 11704692 | Under logistic regression analysis (adjusted for age and sex), baseline urine albumin/creatinine ratio (p=0.003), presence of retinopathy (p=0.004), serum creatinine (p=0.028), and serum urea (p=0.034) were the most powerful predictors of mortality, while duration of diabetes (p<0.0001), baseline HDL cholesterol (p=0.012), serum creatinine (p=0.02), apolipoprotein B (p=0.038), LDL cholesterol (p=0.039), and systolic blood pressure (p=0.055) were the strongest predictors of CAD. |
| 587 | 11704692 | At baseline, those who died had significantly higher serum creatinine (p=0.001) and urine albumin/creatinine ratio (p=0.016), greater prevalence of retinopathy (p=0.006), lower serum apolipoprotein A1 (p=0.046), and lower daily insulin dose (p=0.024) than those who survived. |
| 588 | 11704692 | The CAD group also had higher baseline serum creatinine (p=0.02), lower HDL cholesterol (p=0.004) and apolipoprotein A1 (p=0.007) and higher LDL cholesterol (p=0.028) and apolipoprotein B concentrations (p=0.027). |
| 589 | 11704692 | Under logistic regression analysis (adjusted for age and sex), baseline urine albumin/creatinine ratio (p=0.003), presence of retinopathy (p=0.004), serum creatinine (p=0.028), and serum urea (p=0.034) were the most powerful predictors of mortality, while duration of diabetes (p<0.0001), baseline HDL cholesterol (p=0.012), serum creatinine (p=0.02), apolipoprotein B (p=0.038), LDL cholesterol (p=0.039), and systolic blood pressure (p=0.055) were the strongest predictors of CAD. |
| 590 | 11714842 | Our understanding of apolipoprotein A-II (apoA-II) physiology is much more limited than that of apoA-I. |
| 591 | 11714842 | The increased concentration of apoB-containing lipoproteins present in apoA-II transgenic mice explains, in part, why these animals present increased atherosclerosis susceptibility. |
| 592 | 11714842 | We suggest that the existence of apoA-II or apoA-I in HDL could be an important signal for specific interaction with HDL receptors such as cubilin or heat shock protein 60. |
| 593 | 11738396 | The plasma parameter log (TG/HDL-C) as an atherogenic index: correlation with lipoprotein particle size and esterification rate in apoB-lipoprotein-depleted plasma (FER(HDL)). |
| 594 | 11768156 | As for lipoprotein analyses, the number of apolipoprotein B100 (ApoB100) particles is not significantly different between the two groups, and the higher content of triglycerides in NASH very low density lipoproteins (VLDL) increases the triglyceride-to-ApoB ratio and the particle size. |
| 595 | 11768156 | A decreased enzymatic activity of LPL or a defective assembly and secretion of VLDL from hepatocytes due to a moderate reduction in microsomal triglyceride transfer protein could be involved in the overloading of VLDL. |
| 596 | 11893772 | ApoE found in the LDL fraction of RLP resides on pre-beta lipoproteins that lack apoA-I as well as apoB. |
| 597 | 11916950 | Recent results have established that microsomal triglyceride transfer protein (MTP) is rate limiting for the assembly and secretion of apoB-containing lipoproteins. |
| 598 | 11932277 | Total cholesterol (TC), triglyceride, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol (LDLc), apolipoprotein A(1), apolipoprotein B, and lipoprotein (a) [Lp(a)] were measured after an overnight fast. |
| 599 | 11934682 | Effect of IGF-I therapy on VLDL apolipoprotein B100 metabolism in type 1 diabetes mellitus. |
| 600 | 11934682 | Secretion and clearance rates of very low density lipoprotein (VLDL) apolipoprotein B100 (apoB) determine plasma lipid concentrations. |
| 601 | 11934682 | Type 1 diabetes is characterized by increased growth hormone (GH) secretion and decreased insulin-like growth factor (IGF) I concentrations. |
| 602 | 11934682 | This study examined the effect of low-dose (40 microg.kg(-1).day(-1)) IGF-I therapy on VLDL apoB metabolism, VLDL composition, and the GH-IGF-I axis during euglycemia in type 1 diabetes. |
| 603 | 11934682 | Using a stable isotope technique, VLDL apoB kinetics were estimated before and after 1 wk of IGF-I therapy in 12 patients with type 1 diabetes in a double-blind, placebo-controlled trial. |
| 604 | 11934682 | Fasting plasma triglyceride (P < 0.03), VLDL-triglyceride concentrations (P < 0.05), and the VLDL-triglyceride-to-VLDL apoB ratio (P < 0.002) significantly decreased after IGF-I therapy, whereas VLDL apoB kinetics were not significantly affected by IGF-I therapy. |
| 605 | 11934682 | The mean overnight insulin concentrations during euglycemia decreased by 25% after IGF-I therapy. |
| 606 | 11934682 | IGF-I therapy changes fasting triglyceride concentrations and VLDL composition probably because of an increase in insulin sensitivity. |
| 607 | 11934682 | Effect of IGF-I therapy on VLDL apolipoprotein B100 metabolism in type 1 diabetes mellitus. |
| 608 | 11934682 | Secretion and clearance rates of very low density lipoprotein (VLDL) apolipoprotein B100 (apoB) determine plasma lipid concentrations. |
| 609 | 11934682 | Type 1 diabetes is characterized by increased growth hormone (GH) secretion and decreased insulin-like growth factor (IGF) I concentrations. |
| 610 | 11934682 | This study examined the effect of low-dose (40 microg.kg(-1).day(-1)) IGF-I therapy on VLDL apoB metabolism, VLDL composition, and the GH-IGF-I axis during euglycemia in type 1 diabetes. |
| 611 | 11934682 | Using a stable isotope technique, VLDL apoB kinetics were estimated before and after 1 wk of IGF-I therapy in 12 patients with type 1 diabetes in a double-blind, placebo-controlled trial. |
| 612 | 11934682 | Fasting plasma triglyceride (P < 0.03), VLDL-triglyceride concentrations (P < 0.05), and the VLDL-triglyceride-to-VLDL apoB ratio (P < 0.002) significantly decreased after IGF-I therapy, whereas VLDL apoB kinetics were not significantly affected by IGF-I therapy. |
| 613 | 11934682 | The mean overnight insulin concentrations during euglycemia decreased by 25% after IGF-I therapy. |
| 614 | 11934682 | IGF-I therapy changes fasting triglyceride concentrations and VLDL composition probably because of an increase in insulin sensitivity. |
| 615 | 11934682 | Effect of IGF-I therapy on VLDL apolipoprotein B100 metabolism in type 1 diabetes mellitus. |
| 616 | 11934682 | Secretion and clearance rates of very low density lipoprotein (VLDL) apolipoprotein B100 (apoB) determine plasma lipid concentrations. |
| 617 | 11934682 | Type 1 diabetes is characterized by increased growth hormone (GH) secretion and decreased insulin-like growth factor (IGF) I concentrations. |
| 618 | 11934682 | This study examined the effect of low-dose (40 microg.kg(-1).day(-1)) IGF-I therapy on VLDL apoB metabolism, VLDL composition, and the GH-IGF-I axis during euglycemia in type 1 diabetes. |
| 619 | 11934682 | Using a stable isotope technique, VLDL apoB kinetics were estimated before and after 1 wk of IGF-I therapy in 12 patients with type 1 diabetes in a double-blind, placebo-controlled trial. |
| 620 | 11934682 | Fasting plasma triglyceride (P < 0.03), VLDL-triglyceride concentrations (P < 0.05), and the VLDL-triglyceride-to-VLDL apoB ratio (P < 0.002) significantly decreased after IGF-I therapy, whereas VLDL apoB kinetics were not significantly affected by IGF-I therapy. |
| 621 | 11934682 | The mean overnight insulin concentrations during euglycemia decreased by 25% after IGF-I therapy. |
| 622 | 11934682 | IGF-I therapy changes fasting triglyceride concentrations and VLDL composition probably because of an increase in insulin sensitivity. |
| 623 | 11934682 | Effect of IGF-I therapy on VLDL apolipoprotein B100 metabolism in type 1 diabetes mellitus. |
| 624 | 11934682 | Secretion and clearance rates of very low density lipoprotein (VLDL) apolipoprotein B100 (apoB) determine plasma lipid concentrations. |
| 625 | 11934682 | Type 1 diabetes is characterized by increased growth hormone (GH) secretion and decreased insulin-like growth factor (IGF) I concentrations. |
| 626 | 11934682 | This study examined the effect of low-dose (40 microg.kg(-1).day(-1)) IGF-I therapy on VLDL apoB metabolism, VLDL composition, and the GH-IGF-I axis during euglycemia in type 1 diabetes. |
| 627 | 11934682 | Using a stable isotope technique, VLDL apoB kinetics were estimated before and after 1 wk of IGF-I therapy in 12 patients with type 1 diabetes in a double-blind, placebo-controlled trial. |
| 628 | 11934682 | Fasting plasma triglyceride (P < 0.03), VLDL-triglyceride concentrations (P < 0.05), and the VLDL-triglyceride-to-VLDL apoB ratio (P < 0.002) significantly decreased after IGF-I therapy, whereas VLDL apoB kinetics were not significantly affected by IGF-I therapy. |
| 629 | 11934682 | The mean overnight insulin concentrations during euglycemia decreased by 25% after IGF-I therapy. |
| 630 | 11934682 | IGF-I therapy changes fasting triglyceride concentrations and VLDL composition probably because of an increase in insulin sensitivity. |
| 631 | 11960511 | Estimation of apolipoprotein B and/or apolipoprotein E genotype can improve prediction. |
| 632 | 11996942 | The following subjects are reviewed: (1) methodology; (2) normal individuals and the effects of aging; (3) diet; (4) hereditary dyslipidemias: familial hypercholesterolemia, familial combined hyperlipidemia, cholesteryl ester storage disease, cholesteryl ester transfer protein deficiency, lipoprotein lipase deficiency, familial hypobetalipoproteinemia, and truncated forms of apoB; (5) hormonal perturbations: estrogen, insulin, diabetes, obesity, and growth hormone; (6) the nephrotic syndrome; and (7) the effects of the statin class of drugs. |
| 633 | 11996958 | Coronary artery disease is associated with the ratio of apolipoprotein A-I/B and serum concentration of apolipoprotein B, but not with paraoxonase enzyme activity in Iranian subjects. |
| 634 | 11996958 | To determine the association of serum apolipoprotein (apo) A-I and B concentrations, and paraoxonase (PON) high-density lipoprotein (HDL) associated enzyme activity with angiographically determined coronary artery disease (CAD) in Iranian diabetic and non-diabetic CAD patients and non-diabetic control subjects, 251 subjects aged 30-70 years, who underwent their first coronary angiography were matched and randomly assigned into three groups: CAD(+)DM(+), CAD(+)DM(-), and CAD(-)DM(-) (control). |
| 635 | 11996958 | Apolipoprotein concentrations were measured in a fasting serum sample by immunoturbidometric assay and paraoxonase/arylesterase activities by spectrophotometric assay of p-nitrophenol/phenol production following addition of paraoxon/phenylacetate. |
| 636 | 12023854 | We have described previously the ability of a peptide derived from the apolipoprotein B100 (apoB100) moiety of low-density lipoproteins (KRAD14) to inhibit the procoagulant function of TF. |
| 637 | 12032161 | Lipoprotein lipase deficiency and CETP in streptozotocin-treated apoB-expressing mice. |
| 638 | 12032161 | To study the effects of diabetes on lipoprotein profiles and atherosclerosis in a rodent model, we crossed mice that express human apolipoprotein B (HuB), mice that have a heterozygous deletion of lipoprotein lipase (LPL1), and transgenic mice expressing human cholesteryl ester transfer protein (CETP). |
| 639 | 12032161 | Fast-protein liquid chromatography analysis of plasma samples showed that HuB/LPL1 mice had increased VLDL triglyceride, and HuB/LPL1/CETP mice had decreased HDL and increased VLDL and IDL/LDL. |
| 640 | 12032161 | All strains of mice were made diabetic using streptozotocin (STZ); diabetes did not alter lipid profiles or atherosclerosis in HuB or HuB/LPL1/CETP mice. |
| 641 | 12032161 | In contrast, STZ-treated HuB/LPL1 mice were more diabetic, severely hyperlipidemic due to increased cholesterol and triglyceride in VLDL and IDL/LDL, and had more atherosclerosis. |
| 642 | 12032161 | Lipoprotein lipase deficiency and CETP in streptozotocin-treated apoB-expressing mice. |
| 643 | 12032161 | To study the effects of diabetes on lipoprotein profiles and atherosclerosis in a rodent model, we crossed mice that express human apolipoprotein B (HuB), mice that have a heterozygous deletion of lipoprotein lipase (LPL1), and transgenic mice expressing human cholesteryl ester transfer protein (CETP). |
| 644 | 12032161 | Fast-protein liquid chromatography analysis of plasma samples showed that HuB/LPL1 mice had increased VLDL triglyceride, and HuB/LPL1/CETP mice had decreased HDL and increased VLDL and IDL/LDL. |
| 645 | 12032161 | All strains of mice were made diabetic using streptozotocin (STZ); diabetes did not alter lipid profiles or atherosclerosis in HuB or HuB/LPL1/CETP mice. |
| 646 | 12032161 | In contrast, STZ-treated HuB/LPL1 mice were more diabetic, severely hyperlipidemic due to increased cholesterol and triglyceride in VLDL and IDL/LDL, and had more atherosclerosis. |
| 647 | 12086920 | Phospholipid transfer protein (PLTP) is a member of the lipid transfer/lipopolysaccharide binding protein gene family. |
| 648 | 12086920 | The phenotype of PLTP transgenic and gene knock out mice indicates that PLTP plays a major role in the metabolism of high-density lipoprotein (HDL) and apoB-containing lipoproteins and thereby influences the concentration, apolipoprotein content, and size of lipoprotein particles in plasma. |
| 649 | 12086920 | At lease two underlined mechanisms are involved in the reduction of atherosclerosis in PLTP deficient status, 1) reduction of apoB-containing lipoprotein production and levels; and 2) increase of anti-oxidation potential. |
| 650 | 12086920 | Phospholipid transfer protein (PLTP) is a member of the lipid transfer/lipopolysaccharide binding protein gene family. |
| 651 | 12086920 | The phenotype of PLTP transgenic and gene knock out mice indicates that PLTP plays a major role in the metabolism of high-density lipoprotein (HDL) and apoB-containing lipoproteins and thereby influences the concentration, apolipoprotein content, and size of lipoprotein particles in plasma. |
| 652 | 12086920 | At lease two underlined mechanisms are involved in the reduction of atherosclerosis in PLTP deficient status, 1) reduction of apoB-containing lipoprotein production and levels; and 2) increase of anti-oxidation potential. |
| 653 | 12116231 | To identify genes that affect these traits and disorders, we looked for association between markers in candidate genes (apolipoprotein AII (apo AII), apolipoprotein AI-CIII-AIV gene cluster (apo AI-CIII-AIV), apolipoprotein E (apo E), cholesteryl ester transfer protein (CETP), cholesterol 7alpha-hydroxylase (CYP7a), hepatic lipase (HL), and microsomal triglyceride transfer protein (MTP)) and known risk factors (triglycerides (Tg), total cholesterol (TC), apolipoprotein AI (apo AI), apolipoprotein AII (apo AII), apolipoprotein B (apo B), body mass index (BMI), blood pressure (BP), leptin, and fasting blood sugar (FBS) levels.) |
| 654 | 12116231 | A total of 1,102 individuals from the Pacific island of Kosrae were genotyped for the following markers: Apo AII/MspI, Apo CIII/SstI, Apo AI/XmnI, Apo E/HhaI, CETP/TaqIB, CYP7a/BsaI, HL/DraI, and MTP/HhpI. |
| 655 | 12116231 | We also confirmed the following associations: 1) the apo AII/MspI with Tg level; 2) the apo CIII/SstI with Tg, TC, and apo B levels; 3) the Apo E/HhaI E2, E3, and E4 alleles with TC, apo AI, and apo B levels; and 4) the CETP/TaqIB with apo AI level. |
| 656 | 12126770 | Body-mass index (BMI), waist:hip ratio (WHR), urinary albumin excretion rate, presence or absence of hypertension, uric acid levels, and apoB(100) levels were assessed. |
| 657 | 12126770 | Both higher BMI and urinary albumin excretion rate were associated with higher apoB(100) levels (1.02 +/- 0.25 ( +/- S.D.) g/l in normal weight, 1.07 +/- 0.22 g/l in overweight and 1.14 +/- 0.25 g/l in obese individuals; P < 0.01; 1.09 +/- 0.23 g/l in normoalbuminuric patients, 1.06 +/- 0.22 g/l if urinary albumin excretion rate 20-50 microg/min and 1.17 +/- 0.27 g/l if urinary albumin excretion rate > 50 microg/min; P < 0.05). |
| 658 | 12126770 | Thus apoB(100) levels show an association with the metabolic syndrome and, hypothetically, to insulin-insensitivity in Type 2 diabetes. |
| 659 | 12126770 | Body-mass index (BMI), waist:hip ratio (WHR), urinary albumin excretion rate, presence or absence of hypertension, uric acid levels, and apoB(100) levels were assessed. |
| 660 | 12126770 | Both higher BMI and urinary albumin excretion rate were associated with higher apoB(100) levels (1.02 +/- 0.25 ( +/- S.D.) g/l in normal weight, 1.07 +/- 0.22 g/l in overweight and 1.14 +/- 0.25 g/l in obese individuals; P < 0.01; 1.09 +/- 0.23 g/l in normoalbuminuric patients, 1.06 +/- 0.22 g/l if urinary albumin excretion rate 20-50 microg/min and 1.17 +/- 0.27 g/l if urinary albumin excretion rate > 50 microg/min; P < 0.05). |
| 661 | 12126770 | Thus apoB(100) levels show an association with the metabolic syndrome and, hypothetically, to insulin-insensitivity in Type 2 diabetes. |
| 662 | 12126770 | Body-mass index (BMI), waist:hip ratio (WHR), urinary albumin excretion rate, presence or absence of hypertension, uric acid levels, and apoB(100) levels were assessed. |
| 663 | 12126770 | Both higher BMI and urinary albumin excretion rate were associated with higher apoB(100) levels (1.02 +/- 0.25 ( +/- S.D.) g/l in normal weight, 1.07 +/- 0.22 g/l in overweight and 1.14 +/- 0.25 g/l in obese individuals; P < 0.01; 1.09 +/- 0.23 g/l in normoalbuminuric patients, 1.06 +/- 0.22 g/l if urinary albumin excretion rate 20-50 microg/min and 1.17 +/- 0.27 g/l if urinary albumin excretion rate > 50 microg/min; P < 0.05). |
| 664 | 12126770 | Thus apoB(100) levels show an association with the metabolic syndrome and, hypothetically, to insulin-insensitivity in Type 2 diabetes. |
| 665 | 12145148 | Regulatory effects of HMG CoA reductase inhibitor and fish oils on apolipoprotein B-100 kinetics in insulin-resistant obese male subjects with dyslipidemia. |
| 666 | 12145148 | Hepatic accumulation of lipid substrates perturbs apolipoproteinB-100 (apoB) metabolism in insulin-resistant, obese subjects and may account for increased risk of cardiovascular disease. |
| 667 | 12145148 | The differential effects of atorvastatin and fish oils on apoB kinetics support their combined use in correcting defective apoB metabolism in obese, insulin-resistant subjects. |
| 668 | 12145148 | Regulatory effects of HMG CoA reductase inhibitor and fish oils on apolipoprotein B-100 kinetics in insulin-resistant obese male subjects with dyslipidemia. |
| 669 | 12145148 | Hepatic accumulation of lipid substrates perturbs apolipoproteinB-100 (apoB) metabolism in insulin-resistant, obese subjects and may account for increased risk of cardiovascular disease. |
| 670 | 12145148 | The differential effects of atorvastatin and fish oils on apoB kinetics support their combined use in correcting defective apoB metabolism in obese, insulin-resistant subjects. |
| 671 | 12145148 | Regulatory effects of HMG CoA reductase inhibitor and fish oils on apolipoprotein B-100 kinetics in insulin-resistant obese male subjects with dyslipidemia. |
| 672 | 12145148 | Hepatic accumulation of lipid substrates perturbs apolipoproteinB-100 (apoB) metabolism in insulin-resistant, obese subjects and may account for increased risk of cardiovascular disease. |
| 673 | 12145148 | The differential effects of atorvastatin and fish oils on apoB kinetics support their combined use in correcting defective apoB metabolism in obese, insulin-resistant subjects. |
| 674 | 12387587 | Simple correlation analysis showed that BChE activity was positively correlated with age, sex, body mass index, hypertension and DM, as well as with triglycerides (TGs), total cholesterol, low-density lipoprotein cholesterol and apolipoprotein B (Apo B). |
| 675 | 12401722 | Relationship of phospholipid transfer protein activity to HDL and apolipoprotein B-containing lipoproteins in subjects with and without type 1 diabetes. |
| 676 | 12401722 | Patients with type 1 diabetes have greatly increased phospholipid transfer protein (PLTP) activity and have an altered HDL subclass distribution. |
| 677 | 12401722 | In 195 patients with type 1 diabetes and in 194 men and women aged 30-55 years, we examined the relationship of PLTP activity to HDL and examined whether PLTP activity contributes to differences in HDL found in type 1 diabetes. |
| 678 | 12401722 | Higher PLTP activity was associated with more large HDL (P < 0.001) and less small HDL (P < 0.01), more apoAI and apoAII (both at P < 0.001), and more apoAI in both LpAI and LpAIAII (P = 0.02 and P < 0.001, respectively). |
| 679 | 12401722 | Adjusting for PLTP activity halved the difference between subjects with and without diabetes in apoA1 (from 10.1 mg/dl higher in subjects with diabetes to 4.6 mg/dl higher) and large HDL (2.4 micro mol/l higher to 1.2 micro mol/l higher) and reduced the difference in HDL size (from 0.31 nm higher to 0.26 nm higher). |
| 680 | 12401722 | PLTP activity was also positively associated with apoB, total VLDL and LDL particle number, and IDL level in subjects with diabetes. |
| 681 | 12401722 | These data support the idea that PLTP is a major factor in HDL conversion and remodeling in humans and that higher PLTP activity makes an important contribution to the higher apoAI levels and altered HDL subclass distribution in type 1 diabetes. |
| 682 | 12401722 | They also support a role for PLTP in the metabolism of apoB-containing lipoproteins. |
| 683 | 12401722 | Relationship of phospholipid transfer protein activity to HDL and apolipoprotein B-containing lipoproteins in subjects with and without type 1 diabetes. |
| 684 | 12401722 | Patients with type 1 diabetes have greatly increased phospholipid transfer protein (PLTP) activity and have an altered HDL subclass distribution. |
| 685 | 12401722 | In 195 patients with type 1 diabetes and in 194 men and women aged 30-55 years, we examined the relationship of PLTP activity to HDL and examined whether PLTP activity contributes to differences in HDL found in type 1 diabetes. |
| 686 | 12401722 | Higher PLTP activity was associated with more large HDL (P < 0.001) and less small HDL (P < 0.01), more apoAI and apoAII (both at P < 0.001), and more apoAI in both LpAI and LpAIAII (P = 0.02 and P < 0.001, respectively). |
| 687 | 12401722 | Adjusting for PLTP activity halved the difference between subjects with and without diabetes in apoA1 (from 10.1 mg/dl higher in subjects with diabetes to 4.6 mg/dl higher) and large HDL (2.4 micro mol/l higher to 1.2 micro mol/l higher) and reduced the difference in HDL size (from 0.31 nm higher to 0.26 nm higher). |
| 688 | 12401722 | PLTP activity was also positively associated with apoB, total VLDL and LDL particle number, and IDL level in subjects with diabetes. |
| 689 | 12401722 | These data support the idea that PLTP is a major factor in HDL conversion and remodeling in humans and that higher PLTP activity makes an important contribution to the higher apoAI levels and altered HDL subclass distribution in type 1 diabetes. |
| 690 | 12401722 | They also support a role for PLTP in the metabolism of apoB-containing lipoproteins. |
| 691 | 12401722 | Relationship of phospholipid transfer protein activity to HDL and apolipoprotein B-containing lipoproteins in subjects with and without type 1 diabetes. |
| 692 | 12401722 | Patients with type 1 diabetes have greatly increased phospholipid transfer protein (PLTP) activity and have an altered HDL subclass distribution. |
| 693 | 12401722 | In 195 patients with type 1 diabetes and in 194 men and women aged 30-55 years, we examined the relationship of PLTP activity to HDL and examined whether PLTP activity contributes to differences in HDL found in type 1 diabetes. |
| 694 | 12401722 | Higher PLTP activity was associated with more large HDL (P < 0.001) and less small HDL (P < 0.01), more apoAI and apoAII (both at P < 0.001), and more apoAI in both LpAI and LpAIAII (P = 0.02 and P < 0.001, respectively). |
| 695 | 12401722 | Adjusting for PLTP activity halved the difference between subjects with and without diabetes in apoA1 (from 10.1 mg/dl higher in subjects with diabetes to 4.6 mg/dl higher) and large HDL (2.4 micro mol/l higher to 1.2 micro mol/l higher) and reduced the difference in HDL size (from 0.31 nm higher to 0.26 nm higher). |
| 696 | 12401722 | PLTP activity was also positively associated with apoB, total VLDL and LDL particle number, and IDL level in subjects with diabetes. |
| 697 | 12401722 | These data support the idea that PLTP is a major factor in HDL conversion and remodeling in humans and that higher PLTP activity makes an important contribution to the higher apoAI levels and altered HDL subclass distribution in type 1 diabetes. |
| 698 | 12401722 | They also support a role for PLTP in the metabolism of apoB-containing lipoproteins. |
| 699 | 12486492 | After controlling for age and sex, multiple regression analyses showed significant associations of plasma tHcy concentration with glycated hemoglobin (p<0.05), plasma concentrations of creatinine (p<0.001) and apolipoprotein-B (p<0.05), but not with smoking, neuropathy or retinopathy. |
| 700 | 12486496 | Clinical features and fasting total cholesterol, triglyceride, HDL cholesterol, LDL cholesterol (LDLc, using Friedewald's equation and an alternative formula), apolipoprotein B (apoB), lipoprotein (a) and LDL particle size (on gradient polyacrylamide gel electrophoresis) were assessed. |
| 701 | 12486496 | Patients with phenotype B (36%) showed higher total cholesterol, triglyceride and apolipoprotein B, and lower HDL cholesterol and LDLc/apoB ratio. |
| 702 | 12486496 | Triglyceride was the best predictor of LDL particle size (r=-0.632, p<0.01), but an LDLc/apoB ratio below 1.297 mmol/g detected phenotype B best (sensitivity 65.9%, specificity 92.4%, kappa=0.611). |
| 703 | 12486496 | Clinical features and fasting total cholesterol, triglyceride, HDL cholesterol, LDL cholesterol (LDLc, using Friedewald's equation and an alternative formula), apolipoprotein B (apoB), lipoprotein (a) and LDL particle size (on gradient polyacrylamide gel electrophoresis) were assessed. |
| 704 | 12486496 | Patients with phenotype B (36%) showed higher total cholesterol, triglyceride and apolipoprotein B, and lower HDL cholesterol and LDLc/apoB ratio. |
| 705 | 12486496 | Triglyceride was the best predictor of LDL particle size (r=-0.632, p<0.01), but an LDLc/apoB ratio below 1.297 mmol/g detected phenotype B best (sensitivity 65.9%, specificity 92.4%, kappa=0.611). |
| 706 | 12486496 | Clinical features and fasting total cholesterol, triglyceride, HDL cholesterol, LDL cholesterol (LDLc, using Friedewald's equation and an alternative formula), apolipoprotein B (apoB), lipoprotein (a) and LDL particle size (on gradient polyacrylamide gel electrophoresis) were assessed. |
| 707 | 12486496 | Patients with phenotype B (36%) showed higher total cholesterol, triglyceride and apolipoprotein B, and lower HDL cholesterol and LDLc/apoB ratio. |
| 708 | 12486496 | Triglyceride was the best predictor of LDL particle size (r=-0.632, p<0.01), but an LDLc/apoB ratio below 1.297 mmol/g detected phenotype B best (sensitivity 65.9%, specificity 92.4%, kappa=0.611). |
| 709 | 12570165 | The ability of cells to secrete apolipoprotein B (apo-B) containing lipoproteins depends on expression of the apo-B and microsomal triglyceride transfer protein (MTP) genes. |
| 710 | 12606523 | The metabolic syndrome is characterized by insulin resistance and abnormal apolipoprotein AI (apoAI) and apolipoprotein B-100 (apoB) metabolism that may collectively accelerate atherosclerosis. |
| 711 | 12606523 | Both agents significantly lowered plasma triglycerides and apoCIII concentrations, but only atorvastatin significantly lowered (P < 0.001) plasma cholesteryl ester transfer protein activity. |
| 712 | 12639401 | The efficacy of Spirulina supplementation (2 g/day for 2 months) was determined using the preintervention and postintervention blood glucose levels, glycosylated hemoglobin (HbA(1c)) levels, and lipid profiles of the diabetic subjects. |
| 713 | 12639401 | The level of apolipoprotein B registered a significant fall together with a significant increment in the level of apolipoprotein A1. |
| 714 | 12684543 | Kinetics of apolipoprotein B100 (apoB100)-containing lipoproteins were determined before and after atorvastatin treatment and compared with data obtained in five normolipidemic volunteers. |
| 715 | 12691171 | In the field of lipoprotein metabolism and cardiovascular disease several gene polymorphisms for key proteins, such as apoproteins (apo) E, B, A-IV and C-III, LDL receptor, microsomal transfer protein (MTP), fatty acid-binding protein (FABP), cholesteryl ester transfer protein (CETP), lipoprotein lipase and hepatic lipase, have been identified and linked to variable responses to diets. |
| 716 | 12691171 | Among single nucleotide polymorphisms (SNP) already studied (apoE (epsilon2, epsilon3, epsilon4), apoB (-516C/T), apoC-III (SstI), apoA-IV (Ser347Thr), MTP (-493G/T), intestinal FABP (Ala54Thr), CETP (TaqIB) and hepatic lipase (-480C/T)), some SNP showed interactions with diets in relation to changes in particular variables after 3 months on the dietary regimens. |
| 717 | 12691171 | This was the case for apoE and LDL-cholesterol and triacylglycerols, apoA-IV and LDL-cholesterol, MTP and LDL-cholesterol, intestinal FABP and triacylglycerols. |
| 718 | 12714034 | It is now clear that HDL plays a pivotal role in cellular cholesterol efflux via the interaction of apolipoprotein A-I with the ATP binding cassette transporter A-1. |
| 719 | 12714034 | The cholesterol in HDL can either be transferred to apolipoprotein B-containing particles via CETP or delivered directly to the liver with the help of scavenger receptor B1. |
| 720 | 12716735 | Regulation of microsomal triglyceride transfer protein gene by insulin in HepG2 cells: roles of MAPKerk and MAPKp38. |
| 721 | 12716735 | Microsomal triglyceride transfer protein (MTP) is rate limiting for the assembly and secretion of apolipoprotein B-containing lipoproteins. |
| 722 | 12716735 | Elevated hepatic MTP mRNA level, presumably as a result of impaired insulin signaling, has been implicated in the pathophysiology of dyslipidemia associated with insulin resistance/type 2 diabetes. |
| 723 | 12716735 | In this study, we showed that insulin decreases MTP mRNA level mainly through transcriptional regulation in HepG2 cells. |
| 724 | 12716735 | We demonstrated that insulin inhibits MTP gene transcription through MAPK(erk) cascade but not through the PI 3-kinase pathway. |
| 725 | 12716735 | In addition, cellular MAPK(erk) and MAPK(p38) activities play a counterbalancing role in regulating the MTP gene transcription. |
| 726 | 12716736 | We investigated VLDL-triglyceride and -apolipoprotein (apo)-B production in relation to DNL and insulin sensitivity in female ob/ob mice. |
| 727 | 12716736 | No differences in hepatic expression of genes encoding apoB and microsomal triglyceride transfer protein were found. |
| 728 | 12818411 | Genetic variation in the microsomal triglyceride transfer protein (MTP) affects the secretion pattern and plasma concentration of apolipoprotein (aopB)-containing lipoproteins and a common functional -493 G/T polymorphism has been reported to influence plasma lipids levels. |
| 729 | 12818411 | Since type 2 diabetes is associated with obesity and insulin resistance, the present study investigated the effect of this polymorphism on plasma lipids, apoB and LDL subfractions in 281 Chinese type 2 diabetic subjects and 364 non-diabetic controls. |
| 730 | 12818412 | High apoCIII concentration in apoB lipoproteins is a prominent component of atherogenic dyslipidemia, and explains the risk of coronary heart disease (CHD) associated with high triglyceride (TG). |
| 731 | 12818412 | Using immunoaffinity chromatography and ultracentrifugation, we prepared large and small VLDL, IDL and LDL with or without apoCIII or apoE. |
| 732 | 12867534 | Platelet-activating factor acetylhydrolase (PAF-AH) is a phospholipase A2 associated with lipoproteins that hydrolyzes platelet-activating factor (PAF) and oxidized phospholipids. |
| 733 | 12867534 | In healthy subjects, plasma total PAF-AH concentration was positively correlated with PAF-AH activity and with plasma total cholesterol, triacylglycerol, LDL cholesterol and apolipoprotein B (apoB) concentrations (all P < 0.01). |
| 734 | 12867534 | Both hyperlipidemic and diabetic subjects had lower ratios of PAF-AH to apoB (P < 0.01) and higher ratios of PAF-AH to apoA-I (P < 0.01) than did controls. |
| 735 | 12867534 | Platelet-activating factor acetylhydrolase (PAF-AH) is a phospholipase A2 associated with lipoproteins that hydrolyzes platelet-activating factor (PAF) and oxidized phospholipids. |
| 736 | 12867534 | In healthy subjects, plasma total PAF-AH concentration was positively correlated with PAF-AH activity and with plasma total cholesterol, triacylglycerol, LDL cholesterol and apolipoprotein B (apoB) concentrations (all P < 0.01). |
| 737 | 12867534 | Both hyperlipidemic and diabetic subjects had lower ratios of PAF-AH to apoB (P < 0.01) and higher ratios of PAF-AH to apoA-I (P < 0.01) than did controls. |
| 738 | 12870170 | A double knockout (DKO) mouse (low-density lipoprotein receptor [LDLr] -/-; apolipoprotein B [apoB] mRNA editing catalytic polypeptide-1 [Apobec1] -/-) was studied. |
| 739 | 12898470 | To assess postprandial lipidemia in normotriglyceridaemic type 2 diabetic patients treated with diet only, 12 non-obese patients (8 males, hemoglobin A(1c) [HbA(1c)] 6.80 +/- 0.67%) and 14 controls of similar age, body mass index (BMI), and fasting triglyceride (Tg) were given a test meal (58 g fat, 100,000 IU vitamin A). |
| 740 | 12898470 | Fasting low-density lipoprotein (LDL) cholesterol (LDLc), high-density lipoprotein (HDL) cholesterol (HDLc), free fatty acids, and apolipoprotein B (apoB), and fasting and postprandial Tg, retinylpalmitate (RP), LDL size, glucose, and insulin were measured. |
| 741 | 12937310 | C-reactive protein, troponin T (TnT), total, HDL, LDL, and lipoprotein(a) cholesterol, apoA2, apoB, triglyceride, fibrinogen, D-dimer, albumin, and creatinine levels and clinical characteristics at the time of entry were recorded. |
| 742 | 12951628 | The regulation of hepatic VLDL secretion mainly depends on apolipoprotein (apo) B synthesis, on microsomal triglyceride transfer protein, insulin and the availability of triglycerides, free fatty acids (FFA) and cholesteryl ester. |
| 743 | 12951628 | On the other hand, the short-term addition of insulin has been shown to inhibit VLDL-triglyceride and apoB production in vitro. |
| 744 | 14514640 | Inhibition of net HepG2 cell apolipoprotein B secretion by the citrus flavonoid naringenin involves activation of phosphatidylinositol 3-kinase, independent of insulin receptor substrate-1 phosphorylation. |
| 745 | 14514640 | In HepG2 human hepatoma cells, naringenin inhibits apolipoprotein B (apoB) secretion primarily by inhibiting microsomal triglyceride transfer protein and enhances LDL receptor (LDLr)-mediated apoB-containing lipoprotein uptake. |
| 746 | 14514640 | Phosphatidylinositol 3-kinase (PI3K) activation by insulin increases sterol regulatory element-binding protein (SREBP)-1 and LDLr expression and inhibits apoB secretion in hepatocytes. |
| 747 | 14514640 | Insulin and naringenin induced PI3K-dependent increases in cytosolic and nuclear SREBP-1 and LDLr expression. |
| 748 | 14514640 | Similar PI3K-mediated increases in SREBP-1 were observed in McA-RH7777 rat hepatoma cells, which express predominantly SREBP-1c. |
| 749 | 14514640 | Reductions in HepG2 cell media apoB with naringenin were partially attenuated by wortmannin, whereas the effect of insulin was completely blocked. |
| 750 | 14514640 | Both treatments reduced apoB100 secretion in wild-type and LDLr(-/-) mouse hepatocytes to the same extent. |
| 751 | 14514640 | Insulin and naringenin increased HepG2 cell PI3K activity and decreased insulin receptor substrate (IRS)-2 levels. |
| 752 | 14514640 | In sharp contrast to insulin, naringenin did not induce tyrosine phosphorylation of IRS-1. |
| 753 | 14514640 | We conclude that naringenin increases LDLr expression in HepG2 cells via PI3K-mediated upregulation of SREBP-1, independent of IRS-1 phosphorylation. |
| 754 | 14514640 | Although this pathway may not regulate apoB secretion in primary hepatocytes, PI3K activation by this novel mechanism may explain the insulin-like effects of naringenin in vivo. |
| 755 | 14514640 | Inhibition of net HepG2 cell apolipoprotein B secretion by the citrus flavonoid naringenin involves activation of phosphatidylinositol 3-kinase, independent of insulin receptor substrate-1 phosphorylation. |
| 756 | 14514640 | In HepG2 human hepatoma cells, naringenin inhibits apolipoprotein B (apoB) secretion primarily by inhibiting microsomal triglyceride transfer protein and enhances LDL receptor (LDLr)-mediated apoB-containing lipoprotein uptake. |
| 757 | 14514640 | Phosphatidylinositol 3-kinase (PI3K) activation by insulin increases sterol regulatory element-binding protein (SREBP)-1 and LDLr expression and inhibits apoB secretion in hepatocytes. |
| 758 | 14514640 | Insulin and naringenin induced PI3K-dependent increases in cytosolic and nuclear SREBP-1 and LDLr expression. |
| 759 | 14514640 | Similar PI3K-mediated increases in SREBP-1 were observed in McA-RH7777 rat hepatoma cells, which express predominantly SREBP-1c. |
| 760 | 14514640 | Reductions in HepG2 cell media apoB with naringenin were partially attenuated by wortmannin, whereas the effect of insulin was completely blocked. |
| 761 | 14514640 | Both treatments reduced apoB100 secretion in wild-type and LDLr(-/-) mouse hepatocytes to the same extent. |
| 762 | 14514640 | Insulin and naringenin increased HepG2 cell PI3K activity and decreased insulin receptor substrate (IRS)-2 levels. |
| 763 | 14514640 | In sharp contrast to insulin, naringenin did not induce tyrosine phosphorylation of IRS-1. |
| 764 | 14514640 | We conclude that naringenin increases LDLr expression in HepG2 cells via PI3K-mediated upregulation of SREBP-1, independent of IRS-1 phosphorylation. |
| 765 | 14514640 | Although this pathway may not regulate apoB secretion in primary hepatocytes, PI3K activation by this novel mechanism may explain the insulin-like effects of naringenin in vivo. |
| 766 | 14514640 | Inhibition of net HepG2 cell apolipoprotein B secretion by the citrus flavonoid naringenin involves activation of phosphatidylinositol 3-kinase, independent of insulin receptor substrate-1 phosphorylation. |
| 767 | 14514640 | In HepG2 human hepatoma cells, naringenin inhibits apolipoprotein B (apoB) secretion primarily by inhibiting microsomal triglyceride transfer protein and enhances LDL receptor (LDLr)-mediated apoB-containing lipoprotein uptake. |
| 768 | 14514640 | Phosphatidylinositol 3-kinase (PI3K) activation by insulin increases sterol regulatory element-binding protein (SREBP)-1 and LDLr expression and inhibits apoB secretion in hepatocytes. |
| 769 | 14514640 | Insulin and naringenin induced PI3K-dependent increases in cytosolic and nuclear SREBP-1 and LDLr expression. |
| 770 | 14514640 | Similar PI3K-mediated increases in SREBP-1 were observed in McA-RH7777 rat hepatoma cells, which express predominantly SREBP-1c. |
| 771 | 14514640 | Reductions in HepG2 cell media apoB with naringenin were partially attenuated by wortmannin, whereas the effect of insulin was completely blocked. |
| 772 | 14514640 | Both treatments reduced apoB100 secretion in wild-type and LDLr(-/-) mouse hepatocytes to the same extent. |
| 773 | 14514640 | Insulin and naringenin increased HepG2 cell PI3K activity and decreased insulin receptor substrate (IRS)-2 levels. |
| 774 | 14514640 | In sharp contrast to insulin, naringenin did not induce tyrosine phosphorylation of IRS-1. |
| 775 | 14514640 | We conclude that naringenin increases LDLr expression in HepG2 cells via PI3K-mediated upregulation of SREBP-1, independent of IRS-1 phosphorylation. |
| 776 | 14514640 | Although this pathway may not regulate apoB secretion in primary hepatocytes, PI3K activation by this novel mechanism may explain the insulin-like effects of naringenin in vivo. |
| 777 | 14514640 | Inhibition of net HepG2 cell apolipoprotein B secretion by the citrus flavonoid naringenin involves activation of phosphatidylinositol 3-kinase, independent of insulin receptor substrate-1 phosphorylation. |
| 778 | 14514640 | In HepG2 human hepatoma cells, naringenin inhibits apolipoprotein B (apoB) secretion primarily by inhibiting microsomal triglyceride transfer protein and enhances LDL receptor (LDLr)-mediated apoB-containing lipoprotein uptake. |
| 779 | 14514640 | Phosphatidylinositol 3-kinase (PI3K) activation by insulin increases sterol regulatory element-binding protein (SREBP)-1 and LDLr expression and inhibits apoB secretion in hepatocytes. |
| 780 | 14514640 | Insulin and naringenin induced PI3K-dependent increases in cytosolic and nuclear SREBP-1 and LDLr expression. |
| 781 | 14514640 | Similar PI3K-mediated increases in SREBP-1 were observed in McA-RH7777 rat hepatoma cells, which express predominantly SREBP-1c. |
| 782 | 14514640 | Reductions in HepG2 cell media apoB with naringenin were partially attenuated by wortmannin, whereas the effect of insulin was completely blocked. |
| 783 | 14514640 | Both treatments reduced apoB100 secretion in wild-type and LDLr(-/-) mouse hepatocytes to the same extent. |
| 784 | 14514640 | Insulin and naringenin increased HepG2 cell PI3K activity and decreased insulin receptor substrate (IRS)-2 levels. |
| 785 | 14514640 | In sharp contrast to insulin, naringenin did not induce tyrosine phosphorylation of IRS-1. |
| 786 | 14514640 | We conclude that naringenin increases LDLr expression in HepG2 cells via PI3K-mediated upregulation of SREBP-1, independent of IRS-1 phosphorylation. |
| 787 | 14514640 | Although this pathway may not regulate apoB secretion in primary hepatocytes, PI3K activation by this novel mechanism may explain the insulin-like effects of naringenin in vivo. |
| 788 | 14514640 | Inhibition of net HepG2 cell apolipoprotein B secretion by the citrus flavonoid naringenin involves activation of phosphatidylinositol 3-kinase, independent of insulin receptor substrate-1 phosphorylation. |
| 789 | 14514640 | In HepG2 human hepatoma cells, naringenin inhibits apolipoprotein B (apoB) secretion primarily by inhibiting microsomal triglyceride transfer protein and enhances LDL receptor (LDLr)-mediated apoB-containing lipoprotein uptake. |
| 790 | 14514640 | Phosphatidylinositol 3-kinase (PI3K) activation by insulin increases sterol regulatory element-binding protein (SREBP)-1 and LDLr expression and inhibits apoB secretion in hepatocytes. |
| 791 | 14514640 | Insulin and naringenin induced PI3K-dependent increases in cytosolic and nuclear SREBP-1 and LDLr expression. |
| 792 | 14514640 | Similar PI3K-mediated increases in SREBP-1 were observed in McA-RH7777 rat hepatoma cells, which express predominantly SREBP-1c. |
| 793 | 14514640 | Reductions in HepG2 cell media apoB with naringenin were partially attenuated by wortmannin, whereas the effect of insulin was completely blocked. |
| 794 | 14514640 | Both treatments reduced apoB100 secretion in wild-type and LDLr(-/-) mouse hepatocytes to the same extent. |
| 795 | 14514640 | Insulin and naringenin increased HepG2 cell PI3K activity and decreased insulin receptor substrate (IRS)-2 levels. |
| 796 | 14514640 | In sharp contrast to insulin, naringenin did not induce tyrosine phosphorylation of IRS-1. |
| 797 | 14514640 | We conclude that naringenin increases LDLr expression in HepG2 cells via PI3K-mediated upregulation of SREBP-1, independent of IRS-1 phosphorylation. |
| 798 | 14514640 | Although this pathway may not regulate apoB secretion in primary hepatocytes, PI3K activation by this novel mechanism may explain the insulin-like effects of naringenin in vivo. |
| 799 | 14514640 | Inhibition of net HepG2 cell apolipoprotein B secretion by the citrus flavonoid naringenin involves activation of phosphatidylinositol 3-kinase, independent of insulin receptor substrate-1 phosphorylation. |
| 800 | 14514640 | In HepG2 human hepatoma cells, naringenin inhibits apolipoprotein B (apoB) secretion primarily by inhibiting microsomal triglyceride transfer protein and enhances LDL receptor (LDLr)-mediated apoB-containing lipoprotein uptake. |
| 801 | 14514640 | Phosphatidylinositol 3-kinase (PI3K) activation by insulin increases sterol regulatory element-binding protein (SREBP)-1 and LDLr expression and inhibits apoB secretion in hepatocytes. |
| 802 | 14514640 | Insulin and naringenin induced PI3K-dependent increases in cytosolic and nuclear SREBP-1 and LDLr expression. |
| 803 | 14514640 | Similar PI3K-mediated increases in SREBP-1 were observed in McA-RH7777 rat hepatoma cells, which express predominantly SREBP-1c. |
| 804 | 14514640 | Reductions in HepG2 cell media apoB with naringenin were partially attenuated by wortmannin, whereas the effect of insulin was completely blocked. |
| 805 | 14514640 | Both treatments reduced apoB100 secretion in wild-type and LDLr(-/-) mouse hepatocytes to the same extent. |
| 806 | 14514640 | Insulin and naringenin increased HepG2 cell PI3K activity and decreased insulin receptor substrate (IRS)-2 levels. |
| 807 | 14514640 | In sharp contrast to insulin, naringenin did not induce tyrosine phosphorylation of IRS-1. |
| 808 | 14514640 | We conclude that naringenin increases LDLr expression in HepG2 cells via PI3K-mediated upregulation of SREBP-1, independent of IRS-1 phosphorylation. |
| 809 | 14514640 | Although this pathway may not regulate apoB secretion in primary hepatocytes, PI3K activation by this novel mechanism may explain the insulin-like effects of naringenin in vivo. |
| 810 | 14613004 | However, even in the absence of the hyperglycaemic state which characterizes type 2 diabetic patients, non diabetic individuals with a specific form of obesity, named abdominal obesity, often show clustering metabolic abnormalities which include high triglyceride levels, increased apolipoprotein B, small dense low density lipoproteins and decreased high density lipoproteins-cholesterol levels, a hyperinsulinemic-insulin resistant state, alterations in coagulation factors as well as an inflammatory profile. |
| 811 | 14634011 | Apolipoprotein B production reduces lipotoxic cardiomyopathy: studies in heart-specific lipoprotein lipase transgenic mouse. |
| 812 | 14634011 | Transgenic mice expressing non-transferable lipoprotein lipase (LpL) with a glycosylated phosphatidyl-inositol (GPI) anchor in cardiomyocytes have dilated cardiomyopathy. |
| 813 | 14634011 | Hearts from 3-month-old mice expressing GPI-anchored human LpL (hLpLGPI) mice had increased fatty acid oxidation and heart failure genes and decreased glucose transporter genes. 6-month-old mice had increased mRNA expression and activation of the apoptosis marker caspase-3. |
| 814 | 14634011 | To test whether lipid accumulation in the hLpLGPI heart is reduced by cardiac expression of apoB, hLpLGPI mice were bred with transgenic human apoB (HuB)-expressing mice. |
| 815 | 14634011 | Hearts of HuB/hLpLGPI mice had less triglyceride (38%) and free fatty acids (19%), secreted more apoB, and expressed less atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) and more glucose transporter 4 (GLUT4). |
| 816 | 14634011 | Apolipoprotein B production reduces lipotoxic cardiomyopathy: studies in heart-specific lipoprotein lipase transgenic mouse. |
| 817 | 14634011 | Transgenic mice expressing non-transferable lipoprotein lipase (LpL) with a glycosylated phosphatidyl-inositol (GPI) anchor in cardiomyocytes have dilated cardiomyopathy. |
| 818 | 14634011 | Hearts from 3-month-old mice expressing GPI-anchored human LpL (hLpLGPI) mice had increased fatty acid oxidation and heart failure genes and decreased glucose transporter genes. 6-month-old mice had increased mRNA expression and activation of the apoptosis marker caspase-3. |
| 819 | 14634011 | To test whether lipid accumulation in the hLpLGPI heart is reduced by cardiac expression of apoB, hLpLGPI mice were bred with transgenic human apoB (HuB)-expressing mice. |
| 820 | 14634011 | Hearts of HuB/hLpLGPI mice had less triglyceride (38%) and free fatty acids (19%), secreted more apoB, and expressed less atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) and more glucose transporter 4 (GLUT4). |
| 821 | 14634011 | Apolipoprotein B production reduces lipotoxic cardiomyopathy: studies in heart-specific lipoprotein lipase transgenic mouse. |
| 822 | 14634011 | Transgenic mice expressing non-transferable lipoprotein lipase (LpL) with a glycosylated phosphatidyl-inositol (GPI) anchor in cardiomyocytes have dilated cardiomyopathy. |
| 823 | 14634011 | Hearts from 3-month-old mice expressing GPI-anchored human LpL (hLpLGPI) mice had increased fatty acid oxidation and heart failure genes and decreased glucose transporter genes. 6-month-old mice had increased mRNA expression and activation of the apoptosis marker caspase-3. |
| 824 | 14634011 | To test whether lipid accumulation in the hLpLGPI heart is reduced by cardiac expression of apoB, hLpLGPI mice were bred with transgenic human apoB (HuB)-expressing mice. |
| 825 | 14634011 | Hearts of HuB/hLpLGPI mice had less triglyceride (38%) and free fatty acids (19%), secreted more apoB, and expressed less atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) and more glucose transporter 4 (GLUT4). |
| 826 | 14729390 | In mediating the transfer of cholesteryl esters (CE) from antiatherogenic high density lipoprotein (HDL) to proatherogenic apolipoprotein (apo)-B-containing lipoprotein particles (including very low density lipoprotein [VLDL], VLDL remnants, intermediate density lipoprotein [IDL], and low density lipoprotein [LDL]), the CE transfer protein (CETP) plays a critical role not only in the reverse cholesterol transport (RCT) pathway but also in the intravascular remodeling and recycling of HDL particles. |
| 827 | 14729390 | In such states, CETP activity is elevated and contributes significantly to the cholesterol burden in atherogenic apoB-containing lipoproteins. |
| 828 | 14970003 | In vitro studies with hepatocytes derived from 10-wk ZDF rats showed minimal insulin dose effects on apoB secretion compared with the response and sensitivity of hepatocytes derived from 20-wk ZDF and control lean rats. |
| 829 | 15001601 | At baseline and at study end, PAF-AH activity was associated with the apolipoprotein B (apoB) content in dLDL (LDL-5 and LDL-6) (r = 0.447; P < 0.001 and r = 0.651; P < 0.001, respectively) and with non-HDL cholesterol at baseline (r = 0.485; P < 0.001). |
| 830 | 15001601 | However, after additional adjustment for apoB in dLDL and non-HDL cholesterol at baseline, the odds ratio increment for CAD across PAF-AH quartiles was 2.09 (95% confidence interval, 1.02-4.29; P = 0.043). |
| 831 | 15001601 | At baseline and at study end, PAF-AH activity was associated with the apolipoprotein B (apoB) content in dLDL (LDL-5 and LDL-6) (r = 0.447; P < 0.001 and r = 0.651; P < 0.001, respectively) and with non-HDL cholesterol at baseline (r = 0.485; P < 0.001). |
| 832 | 15001601 | However, after additional adjustment for apoB in dLDL and non-HDL cholesterol at baseline, the odds ratio increment for CAD across PAF-AH quartiles was 2.09 (95% confidence interval, 1.02-4.29; P = 0.043). |
| 833 | 15015140 | The genotype TT of -108C/T polymorphism in the promoter region of the PON1 gene, which is associated with decreased PON1 expression, showed a significantly higher Ox-LDL/apoB ratio than genotypes TC or CC (TT: 0.60 +/- 0.15, CT + CC: 0.55 +/- 0.11, P =.02). |
| 834 | 15015140 | Increased Ox-LDL/apoB may result, at least partly, from reduced serum antioxidant capacity in the diabetic state, including the attenuation of PON1 action. |
| 835 | 15015140 | The genotype TT of -108C/T polymorphism in the promoter region of the PON1 gene, which is associated with decreased PON1 expression, showed a significantly higher Ox-LDL/apoB ratio than genotypes TC or CC (TT: 0.60 +/- 0.15, CT + CC: 0.55 +/- 0.11, P =.02). |
| 836 | 15015140 | Increased Ox-LDL/apoB may result, at least partly, from reduced serum antioxidant capacity in the diabetic state, including the attenuation of PON1 action. |
| 837 | 15047487 | We showed a positive correlation between circulating interleukin (IL-6) levels and obesity and insulin resistance suggesting that IL-6 could be involved in insulin resistance in humans. |
| 838 | 15047487 | We found an inverse correlation between circulating adiponectin levels and both insulin resistance and cardiovascular risk factors such as CRP levels and apolipoprotein B/A1 ratio. |
| 839 | 15126535 | Before and over the 6 h after the meal, serial blood samples were taken for determination of glucose, insulin, lipids, lipoproteins, apolipoprotein B-48 (apo B-48), apo B-100, free fatty acids, and lipoprotein lipase activity. |
| 840 | 15161788 | Atorvastatin decreases apolipoprotein C-III in apolipoprotein B-containing lipoprotein and HDL in type 2 diabetes: a potential mechanism to lower plasma triglycerides. |
| 841 | 15223114 | The role of angiotensin-converting enzyme and apolipoprotein-E gene polymorphisms on lipid compositions in newborn infants with intrauterine growth restriction. |
| 842 | 15223114 | Several studies have shown that polymorphisms in angiotensin-converting enzyme (ACE) and apolipoprotein-E (Apo-E) are effective in developing the insulin resistance and also in increasing the risk of coronary heart disease. |
| 843 | 15223114 | In present study, the frequencies of ACE, Apo-E gene polymorphisms, apolipoprotein-B (Apo-B) mutation and lipid compositions were determined in full-term newborn infants with IUGR. |
| 844 | 15223114 | While total cholesterol (TC) and Apo-B concentrations in infants with IUGR was found to be significantly higher than that of the control group (p<0.05), triglyceride (TG), low-density lipoproteins (LDL), high-density lipoproteins (HDL) and Apo-A1 levels were similar (p>0.05). |
| 845 | 15223114 | The role of angiotensin-converting enzyme and apolipoprotein-E gene polymorphisms on lipid compositions in newborn infants with intrauterine growth restriction. |
| 846 | 15223114 | Several studies have shown that polymorphisms in angiotensin-converting enzyme (ACE) and apolipoprotein-E (Apo-E) are effective in developing the insulin resistance and also in increasing the risk of coronary heart disease. |
| 847 | 15223114 | In present study, the frequencies of ACE, Apo-E gene polymorphisms, apolipoprotein-B (Apo-B) mutation and lipid compositions were determined in full-term newborn infants with IUGR. |
| 848 | 15223114 | While total cholesterol (TC) and Apo-B concentrations in infants with IUGR was found to be significantly higher than that of the control group (p<0.05), triglyceride (TG), low-density lipoproteins (LDL), high-density lipoproteins (HDL) and Apo-A1 levels were similar (p>0.05). |
| 849 | 15306190 | Plasma triglycerides and the fractional esterification rate in apoB-depleted lipoproteins (FER(HDL)), an index of high-density lipoprotein (HDL) composition, were significantly higher (P = 0.01 and P = 0.001, respectively), and HDL cholesterol (HDL-C) was significantly lower (P = 0.03) in Caucasians with genotypes containing the minor allele of the -1131T>C polymorphism compared to the homozygotes for the major allele. |
| 850 | 15306190 | The relationship between APOA5 genotype or haplogenotype and FER(HDL) remained significant even after the addition of both HDL-C and triglyceride to the model. |
| 851 | 15375785 | Apolipoprotein C-III protein concentrations and gene polymorphisms in type 1 diabetes: associations with lipoprotein subclasses. |
| 852 | 15375785 | Serum apolipoprotein C-III (apoCIII) concentration and apoCIII gene polymorphisms have been shown to be a risk factor for cardiovascular disease; however, the underlying mechanisms remain unclear. |
| 853 | 15375785 | Higher apoCIII concentrations were associated (P < .0001) with increased triglycerides (r = 0.78), total (r = 0.61) and low-density lipoprotein (LDL) (r = 0.40) cholesterol, apoA-I (r = 0.26), and apoB (r = 0.50), and these relationships persisted after controlling for age, gender, body mass index (BMI), and hemoglobin A1c (HbA1c). |
| 854 | 15375785 | Neither the T(-455) --> C polymorphism affecting an insulin response element in the apoCIII gene promoter nor a SacI polymorphism in the 3'UTR were associated with any alterations in circulating apoCIII concentrations, serum lipids, apolipoprotein concentrations, lipoprotein composition, or parameters measured by NMR lipoprotein subclass analyses. |
| 855 | 15448094 | The present observations support a pathophysiological role of PLTP in decreasing the vitamin E content of apolipoprotein B-containing lipoproteins, but not of HDL in plasma of type 2 diabetic patients, contributing to a greater potential for LDL oxidation. |
| 856 | 15529616 | In addition, other components commonly aggregate with the major components: elevated apolipoprotein B, small LDL particles, insulin resistance and hyperinsulinemia, impaired glucose tolerance (IGT), elevated C-reactive protein (CRP), and variation in coagulation factors (plasminogen activator inhibitor [PAI]-I and fibrinogen). |
| 857 | 15541048 | Release of TNF-alpha from in vitro-stimulated monocytes is negatively associated with serum levels of apolipoprotein B in patients with type 2 diabetes. |
| 858 | 15541048 | The release of TNF-alpha from diabetic cells correlated negatively with serum levels of apolipoprotein B (apoB) (R = -0.755, P = 0.001), total plasma cholesterol (R = - 0.702, P = 0.002) and the presence of retinopathy (R = -0.572, P = 0.021). |
| 859 | 15541048 | In a multiple linear regression model, only the level of apoB and diabetes duration demonstrated significant effects on the release of TNF-alpha, with apoB alone accounting for 57% of the variation. |
| 860 | 15541048 | Release of TNF-alpha from in vitro-stimulated monocytes is negatively associated with serum levels of apolipoprotein B in patients with type 2 diabetes. |
| 861 | 15541048 | The release of TNF-alpha from diabetic cells correlated negatively with serum levels of apolipoprotein B (apoB) (R = -0.755, P = 0.001), total plasma cholesterol (R = - 0.702, P = 0.002) and the presence of retinopathy (R = -0.572, P = 0.021). |
| 862 | 15541048 | In a multiple linear regression model, only the level of apoB and diabetes duration demonstrated significant effects on the release of TNF-alpha, with apoB alone accounting for 57% of the variation. |
| 863 | 15541048 | Release of TNF-alpha from in vitro-stimulated monocytes is negatively associated with serum levels of apolipoprotein B in patients with type 2 diabetes. |
| 864 | 15541048 | The release of TNF-alpha from diabetic cells correlated negatively with serum levels of apolipoprotein B (apoB) (R = -0.755, P = 0.001), total plasma cholesterol (R = - 0.702, P = 0.002) and the presence of retinopathy (R = -0.572, P = 0.021). |
| 865 | 15541048 | In a multiple linear regression model, only the level of apoB and diabetes duration demonstrated significant effects on the release of TNF-alpha, with apoB alone accounting for 57% of the variation. |
| 866 | 15561934 | Hepatic PTP-1B expression regulates the assembly and secretion of apolipoprotein B-containing lipoproteins: evidence from protein tyrosine phosphatase-1B overexpression, knockout, and RNAi studies. |
| 867 | 15561934 | Protein tyrosine phosphatase-1B (PTP-1B) plays an important role in regulation of insulin signal transduction, and modulation of PTP-1B expression seems to have a profound effect on insulin sensitivity and diet-induced weight gain. |
| 868 | 15561934 | The molecular link between PTP-1B expression and metabolic dyslipidemia, a major complication of insulin resistance, was investigated in the present study using PTP-1B knockout mice as well as overexpression and suppression of PTP-1B. |
| 869 | 15561934 | Lipoprotein profile analysis of plasma from PTP-1B knockout mice revealed a significant reduction in apolipoprotein B (apoB100) lipoproteins, associated with reduced hepatic apoB100 secretion from isolated primary hepatocytes. |
| 870 | 15561934 | Conversely, adenoviral-mediated overexpression of PTP-1B in HepG2 cells downregulated the phosphorylation of insulin receptor and insulin receptor substrate-1 and caused increases in cellular and secreted apoB100 as a result of increased intracellular apoB100 stability. |
| 871 | 15561934 | Hepatic PTP-1B expression regulates the assembly and secretion of apolipoprotein B-containing lipoproteins: evidence from protein tyrosine phosphatase-1B overexpression, knockout, and RNAi studies. |
| 872 | 15561934 | Protein tyrosine phosphatase-1B (PTP-1B) plays an important role in regulation of insulin signal transduction, and modulation of PTP-1B expression seems to have a profound effect on insulin sensitivity and diet-induced weight gain. |
| 873 | 15561934 | The molecular link between PTP-1B expression and metabolic dyslipidemia, a major complication of insulin resistance, was investigated in the present study using PTP-1B knockout mice as well as overexpression and suppression of PTP-1B. |
| 874 | 15561934 | Lipoprotein profile analysis of plasma from PTP-1B knockout mice revealed a significant reduction in apolipoprotein B (apoB100) lipoproteins, associated with reduced hepatic apoB100 secretion from isolated primary hepatocytes. |
| 875 | 15561934 | Conversely, adenoviral-mediated overexpression of PTP-1B in HepG2 cells downregulated the phosphorylation of insulin receptor and insulin receptor substrate-1 and caused increases in cellular and secreted apoB100 as a result of increased intracellular apoB100 stability. |
| 876 | 15561934 | Hepatic PTP-1B expression regulates the assembly and secretion of apolipoprotein B-containing lipoproteins: evidence from protein tyrosine phosphatase-1B overexpression, knockout, and RNAi studies. |
| 877 | 15561934 | Protein tyrosine phosphatase-1B (PTP-1B) plays an important role in regulation of insulin signal transduction, and modulation of PTP-1B expression seems to have a profound effect on insulin sensitivity and diet-induced weight gain. |
| 878 | 15561934 | The molecular link between PTP-1B expression and metabolic dyslipidemia, a major complication of insulin resistance, was investigated in the present study using PTP-1B knockout mice as well as overexpression and suppression of PTP-1B. |
| 879 | 15561934 | Lipoprotein profile analysis of plasma from PTP-1B knockout mice revealed a significant reduction in apolipoprotein B (apoB100) lipoproteins, associated with reduced hepatic apoB100 secretion from isolated primary hepatocytes. |
| 880 | 15561934 | Conversely, adenoviral-mediated overexpression of PTP-1B in HepG2 cells downregulated the phosphorylation of insulin receptor and insulin receptor substrate-1 and caused increases in cellular and secreted apoB100 as a result of increased intracellular apoB100 stability. |
| 881 | 15646744 | These factors were 6 risk factors (dyslipidaemia characterized by high apoB/apoA1 ratio, smoking, hypertension, diabetes mellitus, abdominal obesity and stressful psychosocial factors) and 3 protective factors (daily consumption of fruits and vegetables, regular alcohol consumption, and regular physical activity). |
| 882 | 15671223 | We measured circulating total, LDL, and HDL cholesterol, triacylglycerol, lipoprotein(a), apolipoprotein (apo) A1, apoB, hemoglobin (Hb)A1c, insulin, C-peptide, and leptin concentrations. |
| 883 | 15671223 | Diets high in lignan intake may increase apoB-containing lipoproteins and decrease fasting insulin secretion, but these findings require confirmation. |
| 884 | 15671223 | We measured circulating total, LDL, and HDL cholesterol, triacylglycerol, lipoprotein(a), apolipoprotein (apo) A1, apoB, hemoglobin (Hb)A1c, insulin, C-peptide, and leptin concentrations. |
| 885 | 15671223 | Diets high in lignan intake may increase apoB-containing lipoproteins and decrease fasting insulin secretion, but these findings require confirmation. |
| 886 | 15719888 | By contrast, non-HDLC values were shown to be independent of TG, and better correlated to ApoB than LDLC values. |
| 887 | 15719888 | The ratio LDLC/ApoB was shown continuously to decrease with increasing TG concentrations, while the ratio non-HDLC/ApoB did not. |
| 888 | 15719888 | By contrast, non-HDLC values were shown to be independent of TG, and better correlated to ApoB than LDLC values. |
| 889 | 15719888 | The ratio LDLC/ApoB was shown continuously to decrease with increasing TG concentrations, while the ratio non-HDLC/ApoB did not. |
| 890 | 15734858 | Adipocytokines and VLDL metabolism: independent regulatory effects of adiponectin, insulin resistance, and fat compartments on VLDL apolipoprotein B-100 kinetics? |
| 891 | 15734858 | Plasma adiponectin, leptin, resistin, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) concentrations were measured using enzyme immunoassays and insulin resistance by homeostasis model assessment (HOMA) score in 41 men with BMI of 22-35 kg/m(2). |
| 892 | 15734858 | In univariate regression, plasma adiponectin and leptin concentrations were inversely and directly associated, respectively, with plasma triglyceride; HOMA score; and visceral, subcutaneous, and total ATMs. |
| 893 | 15734858 | Conversely, adiponectin and leptin were directly and inversely correlated, respectively, with VLDL apoB catabolism and HDL cholesterol concentration (P < 0.05). |
| 894 | 15734858 | Resistin, IL-6, and TNF-alpha were not significantly associated with any of these variables. |
| 895 | 15734858 | In multivariate regression, adiponectin was the most significant predictor of plasma VLDL apoB concentration (P = 0.001) and, together with total or subcutaneous ATM, was an independent predictor of VLDL apoB catabolism (P < 0.001); HOMA score was the most significant predictor of VLDL apoB hepatic secretion (P < 0.05). |
| 896 | 15734858 | Leptin was not an independent predictor of VLDL apoB kinetics. |
| 897 | 15734858 | In conclusion, plasma VLDL apoB kinetics may be differentially controlled by adiponectin and insulin resistance, with adiponectin regulating catabolism and insulin resistance regulating hepatic secretion in men. |
| 898 | 15734858 | Total body fat may also independently determine the rate of VLDL catabolism, but leptin, resistin, IL-6, and TNF-alpha do not have a significant effect in regulating apoB kinetics. |
| 899 | 15734858 | Adipocytokines and VLDL metabolism: independent regulatory effects of adiponectin, insulin resistance, and fat compartments on VLDL apolipoprotein B-100 kinetics? |
| 900 | 15734858 | Plasma adiponectin, leptin, resistin, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) concentrations were measured using enzyme immunoassays and insulin resistance by homeostasis model assessment (HOMA) score in 41 men with BMI of 22-35 kg/m(2). |
| 901 | 15734858 | In univariate regression, plasma adiponectin and leptin concentrations were inversely and directly associated, respectively, with plasma triglyceride; HOMA score; and visceral, subcutaneous, and total ATMs. |
| 902 | 15734858 | Conversely, adiponectin and leptin were directly and inversely correlated, respectively, with VLDL apoB catabolism and HDL cholesterol concentration (P < 0.05). |
| 903 | 15734858 | Resistin, IL-6, and TNF-alpha were not significantly associated with any of these variables. |
| 904 | 15734858 | In multivariate regression, adiponectin was the most significant predictor of plasma VLDL apoB concentration (P = 0.001) and, together with total or subcutaneous ATM, was an independent predictor of VLDL apoB catabolism (P < 0.001); HOMA score was the most significant predictor of VLDL apoB hepatic secretion (P < 0.05). |
| 905 | 15734858 | Leptin was not an independent predictor of VLDL apoB kinetics. |
| 906 | 15734858 | In conclusion, plasma VLDL apoB kinetics may be differentially controlled by adiponectin and insulin resistance, with adiponectin regulating catabolism and insulin resistance regulating hepatic secretion in men. |
| 907 | 15734858 | Total body fat may also independently determine the rate of VLDL catabolism, but leptin, resistin, IL-6, and TNF-alpha do not have a significant effect in regulating apoB kinetics. |
| 908 | 15734858 | Adipocytokines and VLDL metabolism: independent regulatory effects of adiponectin, insulin resistance, and fat compartments on VLDL apolipoprotein B-100 kinetics? |
| 909 | 15734858 | Plasma adiponectin, leptin, resistin, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) concentrations were measured using enzyme immunoassays and insulin resistance by homeostasis model assessment (HOMA) score in 41 men with BMI of 22-35 kg/m(2). |
| 910 | 15734858 | In univariate regression, plasma adiponectin and leptin concentrations were inversely and directly associated, respectively, with plasma triglyceride; HOMA score; and visceral, subcutaneous, and total ATMs. |
| 911 | 15734858 | Conversely, adiponectin and leptin were directly and inversely correlated, respectively, with VLDL apoB catabolism and HDL cholesterol concentration (P < 0.05). |
| 912 | 15734858 | Resistin, IL-6, and TNF-alpha were not significantly associated with any of these variables. |
| 913 | 15734858 | In multivariate regression, adiponectin was the most significant predictor of plasma VLDL apoB concentration (P = 0.001) and, together with total or subcutaneous ATM, was an independent predictor of VLDL apoB catabolism (P < 0.001); HOMA score was the most significant predictor of VLDL apoB hepatic secretion (P < 0.05). |
| 914 | 15734858 | Leptin was not an independent predictor of VLDL apoB kinetics. |
| 915 | 15734858 | In conclusion, plasma VLDL apoB kinetics may be differentially controlled by adiponectin and insulin resistance, with adiponectin regulating catabolism and insulin resistance regulating hepatic secretion in men. |
| 916 | 15734858 | Total body fat may also independently determine the rate of VLDL catabolism, but leptin, resistin, IL-6, and TNF-alpha do not have a significant effect in regulating apoB kinetics. |
| 917 | 15734858 | Adipocytokines and VLDL metabolism: independent regulatory effects of adiponectin, insulin resistance, and fat compartments on VLDL apolipoprotein B-100 kinetics? |
| 918 | 15734858 | Plasma adiponectin, leptin, resistin, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) concentrations were measured using enzyme immunoassays and insulin resistance by homeostasis model assessment (HOMA) score in 41 men with BMI of 22-35 kg/m(2). |
| 919 | 15734858 | In univariate regression, plasma adiponectin and leptin concentrations were inversely and directly associated, respectively, with plasma triglyceride; HOMA score; and visceral, subcutaneous, and total ATMs. |
| 920 | 15734858 | Conversely, adiponectin and leptin were directly and inversely correlated, respectively, with VLDL apoB catabolism and HDL cholesterol concentration (P < 0.05). |
| 921 | 15734858 | Resistin, IL-6, and TNF-alpha were not significantly associated with any of these variables. |
| 922 | 15734858 | In multivariate regression, adiponectin was the most significant predictor of plasma VLDL apoB concentration (P = 0.001) and, together with total or subcutaneous ATM, was an independent predictor of VLDL apoB catabolism (P < 0.001); HOMA score was the most significant predictor of VLDL apoB hepatic secretion (P < 0.05). |
| 923 | 15734858 | Leptin was not an independent predictor of VLDL apoB kinetics. |
| 924 | 15734858 | In conclusion, plasma VLDL apoB kinetics may be differentially controlled by adiponectin and insulin resistance, with adiponectin regulating catabolism and insulin resistance regulating hepatic secretion in men. |
| 925 | 15734858 | Total body fat may also independently determine the rate of VLDL catabolism, but leptin, resistin, IL-6, and TNF-alpha do not have a significant effect in regulating apoB kinetics. |
| 926 | 15734858 | Adipocytokines and VLDL metabolism: independent regulatory effects of adiponectin, insulin resistance, and fat compartments on VLDL apolipoprotein B-100 kinetics? |
| 927 | 15734858 | Plasma adiponectin, leptin, resistin, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) concentrations were measured using enzyme immunoassays and insulin resistance by homeostasis model assessment (HOMA) score in 41 men with BMI of 22-35 kg/m(2). |
| 928 | 15734858 | In univariate regression, plasma adiponectin and leptin concentrations were inversely and directly associated, respectively, with plasma triglyceride; HOMA score; and visceral, subcutaneous, and total ATMs. |
| 929 | 15734858 | Conversely, adiponectin and leptin were directly and inversely correlated, respectively, with VLDL apoB catabolism and HDL cholesterol concentration (P < 0.05). |
| 930 | 15734858 | Resistin, IL-6, and TNF-alpha were not significantly associated with any of these variables. |
| 931 | 15734858 | In multivariate regression, adiponectin was the most significant predictor of plasma VLDL apoB concentration (P = 0.001) and, together with total or subcutaneous ATM, was an independent predictor of VLDL apoB catabolism (P < 0.001); HOMA score was the most significant predictor of VLDL apoB hepatic secretion (P < 0.05). |
| 932 | 15734858 | Leptin was not an independent predictor of VLDL apoB kinetics. |
| 933 | 15734858 | In conclusion, plasma VLDL apoB kinetics may be differentially controlled by adiponectin and insulin resistance, with adiponectin regulating catabolism and insulin resistance regulating hepatic secretion in men. |
| 934 | 15734858 | Total body fat may also independently determine the rate of VLDL catabolism, but leptin, resistin, IL-6, and TNF-alpha do not have a significant effect in regulating apoB kinetics. |
| 935 | 15734858 | Adipocytokines and VLDL metabolism: independent regulatory effects of adiponectin, insulin resistance, and fat compartments on VLDL apolipoprotein B-100 kinetics? |
| 936 | 15734858 | Plasma adiponectin, leptin, resistin, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) concentrations were measured using enzyme immunoassays and insulin resistance by homeostasis model assessment (HOMA) score in 41 men with BMI of 22-35 kg/m(2). |
| 937 | 15734858 | In univariate regression, plasma adiponectin and leptin concentrations were inversely and directly associated, respectively, with plasma triglyceride; HOMA score; and visceral, subcutaneous, and total ATMs. |
| 938 | 15734858 | Conversely, adiponectin and leptin were directly and inversely correlated, respectively, with VLDL apoB catabolism and HDL cholesterol concentration (P < 0.05). |
| 939 | 15734858 | Resistin, IL-6, and TNF-alpha were not significantly associated with any of these variables. |
| 940 | 15734858 | In multivariate regression, adiponectin was the most significant predictor of plasma VLDL apoB concentration (P = 0.001) and, together with total or subcutaneous ATM, was an independent predictor of VLDL apoB catabolism (P < 0.001); HOMA score was the most significant predictor of VLDL apoB hepatic secretion (P < 0.05). |
| 941 | 15734858 | Leptin was not an independent predictor of VLDL apoB kinetics. |
| 942 | 15734858 | In conclusion, plasma VLDL apoB kinetics may be differentially controlled by adiponectin and insulin resistance, with adiponectin regulating catabolism and insulin resistance regulating hepatic secretion in men. |
| 943 | 15734858 | Total body fat may also independently determine the rate of VLDL catabolism, but leptin, resistin, IL-6, and TNF-alpha do not have a significant effect in regulating apoB kinetics. |
| 944 | 15823289 | Association between insulin resistance and apolipoprotein B in normoglycemic Koreans. |
| 945 | 15856946 | The aim of this study was the search of association with diabetic polyneuropathy of the polymorphic markers epsilon2/epsilon3/epsilon4 of apolipoprotein E (APOE) and I/D of apolipoprotein B (APOB) genes in groups of type 1 diabetes patients with diabetic polyneuropathy (n = 86) and without its clinical signs (n = 94). |
| 946 | 15877301 | Intestinal assembly and secretion of highly dense/lipid-poor apolipoprotein B48-containing lipoprotein particles in the fasting state: evidence for induction by insulin resistance and exogenous fatty acids. |
| 947 | 15877301 | Emerging evidence suggests that overproduction of intestinally derived apolipoprotein (apo) B48-containing lipoprotein particles may be an important contributor to both fasting and postprandial dyslipidemia in insulin-resistant states. |
| 948 | 15877301 | Mechanisms regulating the assembly and secretion of apoB48-containing lipoproteins are not fully understood particularly in the diabetic/insulin-resistant intestine. |
| 949 | 15877301 | Both intracellular and secreted apoB48 particles were examined in intestinal enterocytes isolated from normal or insulin-resistant fructose-fed hamsters, as well as in enterocytes treated with exogenous oleic acid. |
| 950 | 15877301 | A marked enhancement in assembly of apoB48-containing lipoproteins was also observed in the microsomal lumen of fructose-fed hamster enterocytes, suggesting facilitated assembly and secretion of dense intestinal lipoprotein particles in insulin-resistant states. |
| 951 | 15877301 | The production of these small, dense, and potentially atherogenic apoB48 particles can be stimulated by increased free fatty acid flux as well as in insulin-resistant diabetes. |
| 952 | 15877301 | Intestinal assembly and secretion of highly dense/lipid-poor apolipoprotein B48-containing lipoprotein particles in the fasting state: evidence for induction by insulin resistance and exogenous fatty acids. |
| 953 | 15877301 | Emerging evidence suggests that overproduction of intestinally derived apolipoprotein (apo) B48-containing lipoprotein particles may be an important contributor to both fasting and postprandial dyslipidemia in insulin-resistant states. |
| 954 | 15877301 | Mechanisms regulating the assembly and secretion of apoB48-containing lipoproteins are not fully understood particularly in the diabetic/insulin-resistant intestine. |
| 955 | 15877301 | Both intracellular and secreted apoB48 particles were examined in intestinal enterocytes isolated from normal or insulin-resistant fructose-fed hamsters, as well as in enterocytes treated with exogenous oleic acid. |
| 956 | 15877301 | A marked enhancement in assembly of apoB48-containing lipoproteins was also observed in the microsomal lumen of fructose-fed hamster enterocytes, suggesting facilitated assembly and secretion of dense intestinal lipoprotein particles in insulin-resistant states. |
| 957 | 15877301 | The production of these small, dense, and potentially atherogenic apoB48 particles can be stimulated by increased free fatty acid flux as well as in insulin-resistant diabetes. |
| 958 | 15877301 | Intestinal assembly and secretion of highly dense/lipid-poor apolipoprotein B48-containing lipoprotein particles in the fasting state: evidence for induction by insulin resistance and exogenous fatty acids. |
| 959 | 15877301 | Emerging evidence suggests that overproduction of intestinally derived apolipoprotein (apo) B48-containing lipoprotein particles may be an important contributor to both fasting and postprandial dyslipidemia in insulin-resistant states. |
| 960 | 15877301 | Mechanisms regulating the assembly and secretion of apoB48-containing lipoproteins are not fully understood particularly in the diabetic/insulin-resistant intestine. |
| 961 | 15877301 | Both intracellular and secreted apoB48 particles were examined in intestinal enterocytes isolated from normal or insulin-resistant fructose-fed hamsters, as well as in enterocytes treated with exogenous oleic acid. |
| 962 | 15877301 | A marked enhancement in assembly of apoB48-containing lipoproteins was also observed in the microsomal lumen of fructose-fed hamster enterocytes, suggesting facilitated assembly and secretion of dense intestinal lipoprotein particles in insulin-resistant states. |
| 963 | 15877301 | The production of these small, dense, and potentially atherogenic apoB48 particles can be stimulated by increased free fatty acid flux as well as in insulin-resistant diabetes. |
| 964 | 15877301 | Intestinal assembly and secretion of highly dense/lipid-poor apolipoprotein B48-containing lipoprotein particles in the fasting state: evidence for induction by insulin resistance and exogenous fatty acids. |
| 965 | 15877301 | Emerging evidence suggests that overproduction of intestinally derived apolipoprotein (apo) B48-containing lipoprotein particles may be an important contributor to both fasting and postprandial dyslipidemia in insulin-resistant states. |
| 966 | 15877301 | Mechanisms regulating the assembly and secretion of apoB48-containing lipoproteins are not fully understood particularly in the diabetic/insulin-resistant intestine. |
| 967 | 15877301 | Both intracellular and secreted apoB48 particles were examined in intestinal enterocytes isolated from normal or insulin-resistant fructose-fed hamsters, as well as in enterocytes treated with exogenous oleic acid. |
| 968 | 15877301 | A marked enhancement in assembly of apoB48-containing lipoproteins was also observed in the microsomal lumen of fructose-fed hamster enterocytes, suggesting facilitated assembly and secretion of dense intestinal lipoprotein particles in insulin-resistant states. |
| 969 | 15877301 | The production of these small, dense, and potentially atherogenic apoB48 particles can be stimulated by increased free fatty acid flux as well as in insulin-resistant diabetes. |
| 970 | 15877301 | Intestinal assembly and secretion of highly dense/lipid-poor apolipoprotein B48-containing lipoprotein particles in the fasting state: evidence for induction by insulin resistance and exogenous fatty acids. |
| 971 | 15877301 | Emerging evidence suggests that overproduction of intestinally derived apolipoprotein (apo) B48-containing lipoprotein particles may be an important contributor to both fasting and postprandial dyslipidemia in insulin-resistant states. |
| 972 | 15877301 | Mechanisms regulating the assembly and secretion of apoB48-containing lipoproteins are not fully understood particularly in the diabetic/insulin-resistant intestine. |
| 973 | 15877301 | Both intracellular and secreted apoB48 particles were examined in intestinal enterocytes isolated from normal or insulin-resistant fructose-fed hamsters, as well as in enterocytes treated with exogenous oleic acid. |
| 974 | 15877301 | A marked enhancement in assembly of apoB48-containing lipoproteins was also observed in the microsomal lumen of fructose-fed hamster enterocytes, suggesting facilitated assembly and secretion of dense intestinal lipoprotein particles in insulin-resistant states. |
| 975 | 15877301 | The production of these small, dense, and potentially atherogenic apoB48 particles can be stimulated by increased free fatty acid flux as well as in insulin-resistant diabetes. |
| 976 | 15919788 | Inhibition of microsomal triglyceride transfer protein expression and apolipoprotein B100 secretion by the citrus flavonoid naringenin and by insulin involves activation of the mitogen-activated protein kinase pathway in hepatocytes. |
| 977 | 15919788 | Microsomal triglyceride transfer protein (MTP) is necessary for hepatocyte assembly and secretion of apolipoprotein (apo)B100-containing lipoproteins. |
| 978 | 15919788 | The citrus flavonoid naringenin, like insulin, decreased MTP expression in HepG2 cells, resulting in inhibition of apoB100 secretion; however, the mechanism for naringenin is independent of insulin receptor substrate-1/2. |
| 979 | 15919788 | Recently, it was reported that insulin decreased MTP expression in HepG2 cells via the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) (MAPK(erk)) pathway. |
| 980 | 15919788 | Inhibition of MAPK kinase (MEK) 1/2 in HepG2 cells significantly attenuated the naringenin- and insulin-induced reduction in MTP expression. |
| 981 | 15919788 | Both naringenin and insulin increased ERK1/2 phosphorylation, which was completely inhibited by MEK1/2 inhibition and enhanced by inhibition of MAPK(p38), a negative regulator of MAPK(erk) activity. |
| 982 | 15919788 | Inhibition of MEK1/2 significantly attenuated both the naringenin- and insulin-induced decrease in apoB100 secretion demonstrating a direct link between MAPK(erk) activation and apoB100 secretion. |
| 983 | 15919788 | Furthermore, both compounds increased MAPK(p38) activation, and therefore inhibition of MAPK(p38) amplified thenaringenin- and insulin-induced decrease in apoB100 secretion. |
| 984 | 15919788 | We conclude that MAPK(erk) signaling in hepatocytes is critical for inhibition of apoB100 secretion by naringenin and insulin. |
| 985 | 15919788 | Inhibition of microsomal triglyceride transfer protein expression and apolipoprotein B100 secretion by the citrus flavonoid naringenin and by insulin involves activation of the mitogen-activated protein kinase pathway in hepatocytes. |
| 986 | 15919788 | Microsomal triglyceride transfer protein (MTP) is necessary for hepatocyte assembly and secretion of apolipoprotein (apo)B100-containing lipoproteins. |
| 987 | 15919788 | The citrus flavonoid naringenin, like insulin, decreased MTP expression in HepG2 cells, resulting in inhibition of apoB100 secretion; however, the mechanism for naringenin is independent of insulin receptor substrate-1/2. |
| 988 | 15919788 | Recently, it was reported that insulin decreased MTP expression in HepG2 cells via the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) (MAPK(erk)) pathway. |
| 989 | 15919788 | Inhibition of MAPK kinase (MEK) 1/2 in HepG2 cells significantly attenuated the naringenin- and insulin-induced reduction in MTP expression. |
| 990 | 15919788 | Both naringenin and insulin increased ERK1/2 phosphorylation, which was completely inhibited by MEK1/2 inhibition and enhanced by inhibition of MAPK(p38), a negative regulator of MAPK(erk) activity. |
| 991 | 15919788 | Inhibition of MEK1/2 significantly attenuated both the naringenin- and insulin-induced decrease in apoB100 secretion demonstrating a direct link between MAPK(erk) activation and apoB100 secretion. |
| 992 | 15919788 | Furthermore, both compounds increased MAPK(p38) activation, and therefore inhibition of MAPK(p38) amplified thenaringenin- and insulin-induced decrease in apoB100 secretion. |
| 993 | 15919788 | We conclude that MAPK(erk) signaling in hepatocytes is critical for inhibition of apoB100 secretion by naringenin and insulin. |
| 994 | 15919788 | Inhibition of microsomal triglyceride transfer protein expression and apolipoprotein B100 secretion by the citrus flavonoid naringenin and by insulin involves activation of the mitogen-activated protein kinase pathway in hepatocytes. |
| 995 | 15919788 | Microsomal triglyceride transfer protein (MTP) is necessary for hepatocyte assembly and secretion of apolipoprotein (apo)B100-containing lipoproteins. |
| 996 | 15919788 | The citrus flavonoid naringenin, like insulin, decreased MTP expression in HepG2 cells, resulting in inhibition of apoB100 secretion; however, the mechanism for naringenin is independent of insulin receptor substrate-1/2. |
| 997 | 15919788 | Recently, it was reported that insulin decreased MTP expression in HepG2 cells via the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) (MAPK(erk)) pathway. |
| 998 | 15919788 | Inhibition of MAPK kinase (MEK) 1/2 in HepG2 cells significantly attenuated the naringenin- and insulin-induced reduction in MTP expression. |
| 999 | 15919788 | Both naringenin and insulin increased ERK1/2 phosphorylation, which was completely inhibited by MEK1/2 inhibition and enhanced by inhibition of MAPK(p38), a negative regulator of MAPK(erk) activity. |
| 1000 | 15919788 | Inhibition of MEK1/2 significantly attenuated both the naringenin- and insulin-induced decrease in apoB100 secretion demonstrating a direct link between MAPK(erk) activation and apoB100 secretion. |
| 1001 | 15919788 | Furthermore, both compounds increased MAPK(p38) activation, and therefore inhibition of MAPK(p38) amplified thenaringenin- and insulin-induced decrease in apoB100 secretion. |
| 1002 | 15919788 | We conclude that MAPK(erk) signaling in hepatocytes is critical for inhibition of apoB100 secretion by naringenin and insulin. |
| 1003 | 15919788 | Inhibition of microsomal triglyceride transfer protein expression and apolipoprotein B100 secretion by the citrus flavonoid naringenin and by insulin involves activation of the mitogen-activated protein kinase pathway in hepatocytes. |
| 1004 | 15919788 | Microsomal triglyceride transfer protein (MTP) is necessary for hepatocyte assembly and secretion of apolipoprotein (apo)B100-containing lipoproteins. |
| 1005 | 15919788 | The citrus flavonoid naringenin, like insulin, decreased MTP expression in HepG2 cells, resulting in inhibition of apoB100 secretion; however, the mechanism for naringenin is independent of insulin receptor substrate-1/2. |
| 1006 | 15919788 | Recently, it was reported that insulin decreased MTP expression in HepG2 cells via the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) (MAPK(erk)) pathway. |
| 1007 | 15919788 | Inhibition of MAPK kinase (MEK) 1/2 in HepG2 cells significantly attenuated the naringenin- and insulin-induced reduction in MTP expression. |
| 1008 | 15919788 | Both naringenin and insulin increased ERK1/2 phosphorylation, which was completely inhibited by MEK1/2 inhibition and enhanced by inhibition of MAPK(p38), a negative regulator of MAPK(erk) activity. |
| 1009 | 15919788 | Inhibition of MEK1/2 significantly attenuated both the naringenin- and insulin-induced decrease in apoB100 secretion demonstrating a direct link between MAPK(erk) activation and apoB100 secretion. |
| 1010 | 15919788 | Furthermore, both compounds increased MAPK(p38) activation, and therefore inhibition of MAPK(p38) amplified thenaringenin- and insulin-induced decrease in apoB100 secretion. |
| 1011 | 15919788 | We conclude that MAPK(erk) signaling in hepatocytes is critical for inhibition of apoB100 secretion by naringenin and insulin. |
| 1012 | 15983229 | We investigated the associations between the hepatic lipase gene (LIPC) -514C>T polymorphism and lipases, lipoproteins, and insulin sensitivity (Si) responses to exercise training. |
| 1013 | 15983229 | Black CC homozygotes had lower baseline lipoprotein lipase activity, HDL cholesterol, HDL3, and apolipoprotein (apo)A-1 concentrations. |
| 1014 | 15983229 | White CC homozygotes had lower baseline HDL cholesterol, apoA-1, LDL cholesterol, and apoB levels that remained low post-exercise training. |
| 1015 | 16152798 | In groups of type 1 diabetes mellitus patients with and without clinical signs of diabetic nephropathy (n = 62 and n = 68, respectively), a search was made for associations between diabetic nephropathy and the polymorphic marker epsilon2/epsilon3/epsilon4 of apolipoprotein E gene (APOE), I/D marker of apolipoprotein B gene (APOB), and Ser447Ter marker of lipoprotein lipase-encoding gene (LPL). |
| 1016 | 16152798 | The risk of diabetic nephropathy was higher in the carriers of allele epsilon3 and genotype epsilon3/epsilon3 of the polymorphic marker epsilon2/epsilon3/epsilon4 of APOE gene as well as in the carriers of allele 1 and APOB genotype/gene (OR = 2.08 and 2.16; 1.91 and 2.11, respectively). |
| 1017 | 16152798 | In groups of type 1 diabetes mellitus patients with and without clinical signs of diabetic nephropathy (n = 62 and n = 68, respectively), a search was made for associations between diabetic nephropathy and the polymorphic marker epsilon2/epsilon3/epsilon4 of apolipoprotein E gene (APOE), I/D marker of apolipoprotein B gene (APOB), and Ser447Ter marker of lipoprotein lipase-encoding gene (LPL). |
| 1018 | 16152798 | The risk of diabetic nephropathy was higher in the carriers of allele epsilon3 and genotype epsilon3/epsilon3 of the polymorphic marker epsilon2/epsilon3/epsilon4 of APOE gene as well as in the carriers of allele 1 and APOB genotype/gene (OR = 2.08 and 2.16; 1.91 and 2.11, respectively). |
| 1019 | 16176140 | Serum total cholesterol was moderately (P < .1) decreased in the C. tora group compared with the age- and gender-matched placebo group, as was the ratio of apolipoprotein B to apolipoprotein A1 (P < .1). |
| 1020 | 16176140 | Fasting blood glucose, hemoglobin A1c, blood urea nitrogen, creatinine, and activities of serum aspartate aminotransferase and alanine aminotransferase were not changed by the fiber supplement. |
| 1021 | 16343038 | To evaluate the influence of cholesterol ester transfer protein (CETP) TaqIB polymorphism, lipoprotein lipase (LPL) PvuII and HindIII polymorphisms, hepatic lipase (LIPC) G-250A polymorphism and apolipoprotein C-III (APOC3) SstI gene polymorphism on lipid levels in dyslipidemia of the metabolic syndrome, 150 patients with dyslipidemia of metabolic syndrome were included. 96 % of patients had type 2 diabetes. |
| 1022 | 16343038 | The apoB level was significantly higher in patients with S1S1 genotype of APOC3 SstI polymorphism when compared with S1S2 group (1.10+/-0.26 vs. 0.98+/-0.21 g/l, p=0.02). |
| 1023 | 16343038 | Similarly, patients with H-H- genotype of LPL HindIII polymorphism had significantly higher mean apoB, compared with H+H- and H+H+ group (1.35+/-0.30 vs. 1.10+/-0.26 g/l, p=0.02). |
| 1024 | 16343038 | In the multiple stepwise linear regression analysis, apoB level seemed to be influenced by APOC3 SstI genotype, which explained 6 % of its variance. |
| 1025 | 16343038 | The present study has shown that the S1 allele of APOC3 SstI polymorphism and the H- allele of LPL HindIII polymorphism might have a small effect on apoB levels in the Central European Caucasian population with dyslipidemia of metabolic syndrome. |
| 1026 | 16343038 | To evaluate the influence of cholesterol ester transfer protein (CETP) TaqIB polymorphism, lipoprotein lipase (LPL) PvuII and HindIII polymorphisms, hepatic lipase (LIPC) G-250A polymorphism and apolipoprotein C-III (APOC3) SstI gene polymorphism on lipid levels in dyslipidemia of the metabolic syndrome, 150 patients with dyslipidemia of metabolic syndrome were included. 96 % of patients had type 2 diabetes. |
| 1027 | 16343038 | The apoB level was significantly higher in patients with S1S1 genotype of APOC3 SstI polymorphism when compared with S1S2 group (1.10+/-0.26 vs. 0.98+/-0.21 g/l, p=0.02). |
| 1028 | 16343038 | Similarly, patients with H-H- genotype of LPL HindIII polymorphism had significantly higher mean apoB, compared with H+H- and H+H+ group (1.35+/-0.30 vs. 1.10+/-0.26 g/l, p=0.02). |
| 1029 | 16343038 | In the multiple stepwise linear regression analysis, apoB level seemed to be influenced by APOC3 SstI genotype, which explained 6 % of its variance. |
| 1030 | 16343038 | The present study has shown that the S1 allele of APOC3 SstI polymorphism and the H- allele of LPL HindIII polymorphism might have a small effect on apoB levels in the Central European Caucasian population with dyslipidemia of metabolic syndrome. |
| 1031 | 16343038 | To evaluate the influence of cholesterol ester transfer protein (CETP) TaqIB polymorphism, lipoprotein lipase (LPL) PvuII and HindIII polymorphisms, hepatic lipase (LIPC) G-250A polymorphism and apolipoprotein C-III (APOC3) SstI gene polymorphism on lipid levels in dyslipidemia of the metabolic syndrome, 150 patients with dyslipidemia of metabolic syndrome were included. 96 % of patients had type 2 diabetes. |
| 1032 | 16343038 | The apoB level was significantly higher in patients with S1S1 genotype of APOC3 SstI polymorphism when compared with S1S2 group (1.10+/-0.26 vs. 0.98+/-0.21 g/l, p=0.02). |
| 1033 | 16343038 | Similarly, patients with H-H- genotype of LPL HindIII polymorphism had significantly higher mean apoB, compared with H+H- and H+H+ group (1.35+/-0.30 vs. 1.10+/-0.26 g/l, p=0.02). |
| 1034 | 16343038 | In the multiple stepwise linear regression analysis, apoB level seemed to be influenced by APOC3 SstI genotype, which explained 6 % of its variance. |
| 1035 | 16343038 | The present study has shown that the S1 allele of APOC3 SstI polymorphism and the H- allele of LPL HindIII polymorphism might have a small effect on apoB levels in the Central European Caucasian population with dyslipidemia of metabolic syndrome. |
| 1036 | 16343038 | To evaluate the influence of cholesterol ester transfer protein (CETP) TaqIB polymorphism, lipoprotein lipase (LPL) PvuII and HindIII polymorphisms, hepatic lipase (LIPC) G-250A polymorphism and apolipoprotein C-III (APOC3) SstI gene polymorphism on lipid levels in dyslipidemia of the metabolic syndrome, 150 patients with dyslipidemia of metabolic syndrome were included. 96 % of patients had type 2 diabetes. |
| 1037 | 16343038 | The apoB level was significantly higher in patients with S1S1 genotype of APOC3 SstI polymorphism when compared with S1S2 group (1.10+/-0.26 vs. 0.98+/-0.21 g/l, p=0.02). |
| 1038 | 16343038 | Similarly, patients with H-H- genotype of LPL HindIII polymorphism had significantly higher mean apoB, compared with H+H- and H+H+ group (1.35+/-0.30 vs. 1.10+/-0.26 g/l, p=0.02). |
| 1039 | 16343038 | In the multiple stepwise linear regression analysis, apoB level seemed to be influenced by APOC3 SstI genotype, which explained 6 % of its variance. |
| 1040 | 16343038 | The present study has shown that the S1 allele of APOC3 SstI polymorphism and the H- allele of LPL HindIII polymorphism might have a small effect on apoB levels in the Central European Caucasian population with dyslipidemia of metabolic syndrome. |
| 1041 | 16353062 | High intensity exercise provoked development of atherogenic dyslipidemia: elevation of levels of total cholesterol, low density lipoprotein cholesterol, triglycerides, apolipoprotein B and apolipoprotein B/A1 ratio, and lowering of levels of high density lipoprotein cholesterol and apolipoprotein A1. |
| 1042 | 16356114 | In vitro studies revealed that apoB-100 proline and arginine residues are not oxidized to HAVA by HOCl or the myeloperoxidase/hydrogen peroxide (H(2)O(2)) oxidation system. |
| 1043 | 16375584 | Multiple logistic regression analysis showed strong and significant association between diabetes mellitus (odds ratio, OR = 5.24, p < or = 0.0001), male gender (OR = 8.84, p < or =0.0001), Lp(a) (OR = 1.014, p < or =0.006), hypertension (OR = 2.61, p < or =0.02), apoB (OR = 1.031, p < or =0.001), age (OR = 1.055, p < or =0.003), phosphorus (OR = 2.438, p < or =0.01), albumin-adjusted calcium (OR = 1.532, p < or =0.05), cholesterol (OR = 1.009, p < or =0.05) and the occurrence of CHD. |
| 1044 | 16375584 | On the basis of bivariate correlation analysis, serum-adjusted calcium was positively correlated with the levels of cholesterol (r = 0.285, p < or =0.0001), LDL-C (r = 0.320, p < or =0.0001), Lp(a) (r = 0.173, p < or = 0.005), apoB (r = 0.237, p < or =0.0001), LDL-C/apoB ratio (r = 0.180, p < or= 0.007), apoAI (r = 0.181, p < or =0.003) and inversely to HDL-C (r = -0.146, p < or =0.02) and HDL-C/apoAI ratio (r = -0.263, p < or =0.0001). |
| 1045 | 16375584 | Multiple logistic regression analysis showed strong and significant association between diabetes mellitus (odds ratio, OR = 5.24, p < or = 0.0001), male gender (OR = 8.84, p < or =0.0001), Lp(a) (OR = 1.014, p < or =0.006), hypertension (OR = 2.61, p < or =0.02), apoB (OR = 1.031, p < or =0.001), age (OR = 1.055, p < or =0.003), phosphorus (OR = 2.438, p < or =0.01), albumin-adjusted calcium (OR = 1.532, p < or =0.05), cholesterol (OR = 1.009, p < or =0.05) and the occurrence of CHD. |
| 1046 | 16375584 | On the basis of bivariate correlation analysis, serum-adjusted calcium was positively correlated with the levels of cholesterol (r = 0.285, p < or =0.0001), LDL-C (r = 0.320, p < or =0.0001), Lp(a) (r = 0.173, p < or = 0.005), apoB (r = 0.237, p < or =0.0001), LDL-C/apoB ratio (r = 0.180, p < or= 0.007), apoAI (r = 0.181, p < or =0.003) and inversely to HDL-C (r = -0.146, p < or =0.02) and HDL-C/apoAI ratio (r = -0.263, p < or =0.0001). |
| 1047 | 16459311 | Coactivation of Foxa2 through Pgc-1beta promotes liver fatty acid oxidation and triglyceride/VLDL secretion. |
| 1048 | 16459311 | Adenoviral expression of Foxa2 and Pgc-1beta in livers of ob/ob mice results in decreased hepatic TAG content and increased plasma TAG concentrations. |
| 1049 | 16459311 | In addition, the concerted action of Foxa2/Pgc-1beta activates genes in mitochondrial beta oxidation and enhances fatty acid metabolism. |
| 1050 | 16459311 | Furthermore, Foxa2/Pgc-1beta induce the expression of microsomal transfer protein, thereby increasing apoB-containing VLDL secretion. |
| 1051 | 16459311 | These data demonstrate that Foxa2/Pgc-1beta regulate hepatic lipid homeostasis by affecting the clearance rate of fatty acids through oxidation and/or secretion of lipids in response to insulin. |
| 1052 | 16510370 | After fluvastatin therapy, LDL (-51%; P<.01), apolipoprotein B (ApoB; -33%; P<.01), intermediate-density LDL (idLDL) (-14.3%; P<.05), sdLDL (-45%; P<.01), and triglycerides (-38%; P<.01) were significantly decreased, and HDL (+14.3%; P<.05) and apolipoprotein A-I (ApoA-I; +7%; P<.05) were increased; large buoyant (lb) LDL did not change (P=NS). |
| 1053 | 16523413 | Serum alanine aminotransferase is associated with serum adiponectin, C-reactive protein and apolipoprotein B in young healthy men. |
| 1054 | 16523413 | We therefore examined the relationship between ALT and AST on the one hand, and serum adiponectin and highly sensitive CRP on the other, both of which have been reported to be associated with prospective risk of type 2 diabetes; we also tested for variable components of metabolic syndrome in 198 male college students aged 18-20 years. |
| 1055 | 16523413 | ALT showed a positive relationship with percentage body fat (r = 0.19, p = 0.02), serum leptin (r = 0.21, p = 0.01), LDL cholesterol (r = 0.29, p = 0.0003), triglyceride (r = 0.28, p = 0.0004) and apolipoprotein B (r = 0.35, p < 0.0001) even after adjustment for body mass index (BMI). |
| 1056 | 16523413 | Although there was a significant relationship with serum insulin, adiponectin (inversely), homeostasis model assessment of insulin resistance, systolic and diastolic blood pressure, HDL cholesterol (inversely) and LDL particle diameter in simple regression analysis, significance disappeared after adjustment for BMI. |
| 1057 | 16523413 | In a model including lipid variables, apolipoprotein B emerged as an independent predictor of ALT in addition to adiponectin and percentage body fat. |
| 1058 | 16523413 | In conclusion, serum ALT levels were associated with leptin and CRP as well as many components of the insulin resistance syndrome in young healthy men. |
| 1059 | 16523413 | Adiponectin, apolipoprotein B and percentage body fat emerged as significant and independent predictors of ALT. |
| 1060 | 16523413 | Since adiponectin and chronic subclinical inflammation have been reported to predict the development of type 2 diabetes and since abnormalities in apolipoprotein B metabolism occur in the early course of insulin resistance, these findings may be compatible with the association between liver markers and risk of diabetes. |
| 1061 | 16523413 | Serum alanine aminotransferase is associated with serum adiponectin, C-reactive protein and apolipoprotein B in young healthy men. |
| 1062 | 16523413 | We therefore examined the relationship between ALT and AST on the one hand, and serum adiponectin and highly sensitive CRP on the other, both of which have been reported to be associated with prospective risk of type 2 diabetes; we also tested for variable components of metabolic syndrome in 198 male college students aged 18-20 years. |
| 1063 | 16523413 | ALT showed a positive relationship with percentage body fat (r = 0.19, p = 0.02), serum leptin (r = 0.21, p = 0.01), LDL cholesterol (r = 0.29, p = 0.0003), triglyceride (r = 0.28, p = 0.0004) and apolipoprotein B (r = 0.35, p < 0.0001) even after adjustment for body mass index (BMI). |
| 1064 | 16523413 | Although there was a significant relationship with serum insulin, adiponectin (inversely), homeostasis model assessment of insulin resistance, systolic and diastolic blood pressure, HDL cholesterol (inversely) and LDL particle diameter in simple regression analysis, significance disappeared after adjustment for BMI. |
| 1065 | 16523413 | In a model including lipid variables, apolipoprotein B emerged as an independent predictor of ALT in addition to adiponectin and percentage body fat. |
| 1066 | 16523413 | In conclusion, serum ALT levels were associated with leptin and CRP as well as many components of the insulin resistance syndrome in young healthy men. |
| 1067 | 16523413 | Adiponectin, apolipoprotein B and percentage body fat emerged as significant and independent predictors of ALT. |
| 1068 | 16523413 | Since adiponectin and chronic subclinical inflammation have been reported to predict the development of type 2 diabetes and since abnormalities in apolipoprotein B metabolism occur in the early course of insulin resistance, these findings may be compatible with the association between liver markers and risk of diabetes. |
| 1069 | 16523413 | Serum alanine aminotransferase is associated with serum adiponectin, C-reactive protein and apolipoprotein B in young healthy men. |
| 1070 | 16523413 | We therefore examined the relationship between ALT and AST on the one hand, and serum adiponectin and highly sensitive CRP on the other, both of which have been reported to be associated with prospective risk of type 2 diabetes; we also tested for variable components of metabolic syndrome in 198 male college students aged 18-20 years. |
| 1071 | 16523413 | ALT showed a positive relationship with percentage body fat (r = 0.19, p = 0.02), serum leptin (r = 0.21, p = 0.01), LDL cholesterol (r = 0.29, p = 0.0003), triglyceride (r = 0.28, p = 0.0004) and apolipoprotein B (r = 0.35, p < 0.0001) even after adjustment for body mass index (BMI). |
| 1072 | 16523413 | Although there was a significant relationship with serum insulin, adiponectin (inversely), homeostasis model assessment of insulin resistance, systolic and diastolic blood pressure, HDL cholesterol (inversely) and LDL particle diameter in simple regression analysis, significance disappeared after adjustment for BMI. |
| 1073 | 16523413 | In a model including lipid variables, apolipoprotein B emerged as an independent predictor of ALT in addition to adiponectin and percentage body fat. |
| 1074 | 16523413 | In conclusion, serum ALT levels were associated with leptin and CRP as well as many components of the insulin resistance syndrome in young healthy men. |
| 1075 | 16523413 | Adiponectin, apolipoprotein B and percentage body fat emerged as significant and independent predictors of ALT. |
| 1076 | 16523413 | Since adiponectin and chronic subclinical inflammation have been reported to predict the development of type 2 diabetes and since abnormalities in apolipoprotein B metabolism occur in the early course of insulin resistance, these findings may be compatible with the association between liver markers and risk of diabetes. |
| 1077 | 16523413 | Serum alanine aminotransferase is associated with serum adiponectin, C-reactive protein and apolipoprotein B in young healthy men. |
| 1078 | 16523413 | We therefore examined the relationship between ALT and AST on the one hand, and serum adiponectin and highly sensitive CRP on the other, both of which have been reported to be associated with prospective risk of type 2 diabetes; we also tested for variable components of metabolic syndrome in 198 male college students aged 18-20 years. |
| 1079 | 16523413 | ALT showed a positive relationship with percentage body fat (r = 0.19, p = 0.02), serum leptin (r = 0.21, p = 0.01), LDL cholesterol (r = 0.29, p = 0.0003), triglyceride (r = 0.28, p = 0.0004) and apolipoprotein B (r = 0.35, p < 0.0001) even after adjustment for body mass index (BMI). |
| 1080 | 16523413 | Although there was a significant relationship with serum insulin, adiponectin (inversely), homeostasis model assessment of insulin resistance, systolic and diastolic blood pressure, HDL cholesterol (inversely) and LDL particle diameter in simple regression analysis, significance disappeared after adjustment for BMI. |
| 1081 | 16523413 | In a model including lipid variables, apolipoprotein B emerged as an independent predictor of ALT in addition to adiponectin and percentage body fat. |
| 1082 | 16523413 | In conclusion, serum ALT levels were associated with leptin and CRP as well as many components of the insulin resistance syndrome in young healthy men. |
| 1083 | 16523413 | Adiponectin, apolipoprotein B and percentage body fat emerged as significant and independent predictors of ALT. |
| 1084 | 16523413 | Since adiponectin and chronic subclinical inflammation have been reported to predict the development of type 2 diabetes and since abnormalities in apolipoprotein B metabolism occur in the early course of insulin resistance, these findings may be compatible with the association between liver markers and risk of diabetes. |
| 1085 | 16523413 | Serum alanine aminotransferase is associated with serum adiponectin, C-reactive protein and apolipoprotein B in young healthy men. |
| 1086 | 16523413 | We therefore examined the relationship between ALT and AST on the one hand, and serum adiponectin and highly sensitive CRP on the other, both of which have been reported to be associated with prospective risk of type 2 diabetes; we also tested for variable components of metabolic syndrome in 198 male college students aged 18-20 years. |
| 1087 | 16523413 | ALT showed a positive relationship with percentage body fat (r = 0.19, p = 0.02), serum leptin (r = 0.21, p = 0.01), LDL cholesterol (r = 0.29, p = 0.0003), triglyceride (r = 0.28, p = 0.0004) and apolipoprotein B (r = 0.35, p < 0.0001) even after adjustment for body mass index (BMI). |
| 1088 | 16523413 | Although there was a significant relationship with serum insulin, adiponectin (inversely), homeostasis model assessment of insulin resistance, systolic and diastolic blood pressure, HDL cholesterol (inversely) and LDL particle diameter in simple regression analysis, significance disappeared after adjustment for BMI. |
| 1089 | 16523413 | In a model including lipid variables, apolipoprotein B emerged as an independent predictor of ALT in addition to adiponectin and percentage body fat. |
| 1090 | 16523413 | In conclusion, serum ALT levels were associated with leptin and CRP as well as many components of the insulin resistance syndrome in young healthy men. |
| 1091 | 16523413 | Adiponectin, apolipoprotein B and percentage body fat emerged as significant and independent predictors of ALT. |
| 1092 | 16523413 | Since adiponectin and chronic subclinical inflammation have been reported to predict the development of type 2 diabetes and since abnormalities in apolipoprotein B metabolism occur in the early course of insulin resistance, these findings may be compatible with the association between liver markers and risk of diabetes. |
| 1093 | 16537441 | This protocol was used to map a set of metabolic traits, including plasma leptin to chromosome region 5q35; systolic blood pressure to 20p12; total cholesterol to 19p13, 12q24, and 16qter; hip circumference to 10q25 and 4q23; body mass index to 18p11 and 20q13; apolipoprotein B to 2p24-25; weight to 18q21; and fasting blood sugar to 1q31-1q43. |
| 1094 | 16546474 | The nonconcordant IR/NoMS group was less common than the MS/NoIR group and was distinct from the latter in having significantly lower waist girth, blood pressure, apolipoprotein B and triglyceride levels, and higher high-density lipoprotein cholesterol, glucose, and insulin levels and physical activity in both sexes. |
| 1095 | 16546474 | The IR/NoMS group had a 2.2-fold (95% confidence interval, 0.97-5.11) CVD likelihood compared with the large insulin-sensitive group, after adjustment for age, sex, log C-reactive protein, low-density lipoprotein cholesterol, smoking status, physical activity, and the 2 groups of MS with or without IR. |
| 1096 | 16596812 | Apolipoprotein (apo)B that constitutes the essential structural protein of these lipoproteins exists in two forms, the full length form apoB-100 and the carboxy-terminal truncated apoB-48. |
| 1097 | 16598898 | However, even in the absence of the hyperglycaemic state which characterizes type 2 diabetic patients, non diabetic individuals with a specific form of obesity, named abdominal obesity, often show clustering metabolic abnormalities which include high triglyceride levels, increased apolipoprotein B, small dense low dendity lipoproteins and decreased high density lipoproteins-cholesterol levels, a hyperinsulinemic-insulin resistant state, alterations in coagulation factors as well as an inflammatory profile. |
| 1098 | 16624317 | Impaired postprandial apolipoprotein-B48 metabolism in the obese, insulin-resistant JCR:LA-cp rat: increased atherogenicity for the metabolic syndrome. |
| 1099 | 16629852 | Defining the therapeutic target of statin therapy in terms of serum apolipoprotein B (apo B) rather than LDL cholesterol could also help to optimize statin treatment. |
| 1100 | 16634094 | Apolipoprotein B gene variants are involved in the determination of blood glucose and lipid levels in patients with non-insulin dependent diabetes mellitus. |
| 1101 | 16634094 | We have examined the frequency of the EcoRI, XbaI and MspI RFLPs of the apolipoprotein B (apo B) gene in 110 type 2 diabetic patients and 91 healthy control subjects in order to ascertain whether variation in this gene may influence the development of non-insulin dependent diabetes mellitus (type 2 diabetes). |
| 1102 | 16634094 | Serum lipids including total-cholesterol (T-Chol), triacylglycerol (TAG), apolipoprotein E (apo E), apolipoprotein AI (apo AI), apolipoprotein B and lipoprotein (a) (Lp(a)) were analysed. |
| 1103 | 16634094 | Apolipoprotein B gene variants are involved in the determination of blood glucose and lipid levels in patients with non-insulin dependent diabetes mellitus. |
| 1104 | 16634094 | We have examined the frequency of the EcoRI, XbaI and MspI RFLPs of the apolipoprotein B (apo B) gene in 110 type 2 diabetic patients and 91 healthy control subjects in order to ascertain whether variation in this gene may influence the development of non-insulin dependent diabetes mellitus (type 2 diabetes). |
| 1105 | 16634094 | Serum lipids including total-cholesterol (T-Chol), triacylglycerol (TAG), apolipoprotein E (apo E), apolipoprotein AI (apo AI), apolipoprotein B and lipoprotein (a) (Lp(a)) were analysed. |
| 1106 | 16634094 | Apolipoprotein B gene variants are involved in the determination of blood glucose and lipid levels in patients with non-insulin dependent diabetes mellitus. |
| 1107 | 16634094 | We have examined the frequency of the EcoRI, XbaI and MspI RFLPs of the apolipoprotein B (apo B) gene in 110 type 2 diabetic patients and 91 healthy control subjects in order to ascertain whether variation in this gene may influence the development of non-insulin dependent diabetes mellitus (type 2 diabetes). |
| 1108 | 16634094 | Serum lipids including total-cholesterol (T-Chol), triacylglycerol (TAG), apolipoprotein E (apo E), apolipoprotein AI (apo AI), apolipoprotein B and lipoprotein (a) (Lp(a)) were analysed. |
| 1109 | 16644688 | Intestinal insulin resistance and aberrant production of apolipoprotein B48 lipoproteins in an animal model of insulin resistance and metabolic dyslipidemia: evidence for activation of protein tyrosine phosphatase-1B, extracellular signal-related kinase, and sterol regulatory element-binding protein-1c in the fructose-fed hamster intestine. |
| 1110 | 16644688 | Intestinal lipoprotein production in chow-fed hamsters was responsive to the inhibitory effects of insulin, and a decrease in circulating levels of triglyceride-rich apolipoprotein (apo)B48-containing lipoproteins occurred 60 min after insulin administration. |
| 1111 | 16644688 | However, fructose-fed hamster intestine was not responsive to the insulin-induced downregulation of apoB48-lipoprotein production, suggesting insulin insensitivity at the level of the intestine. |
| 1112 | 16644688 | Enterocytes from the fructose-fed hamster exhibited normal activity of the insulin receptor but reduced levels of insulin receptor substrate-1 phosphorylation and mass and Akt protein mass. |
| 1113 | 16644688 | Conversely, the protein mass of the p110 subunit of phosphatidylinositol 3-kinase, protein tyrosine phosphatase-1B, and basal levels of phosphorylated extracellular signal-related kinase (ERK) were significantly increased in the fructose-fed hamster intestine. |
| 1114 | 16644688 | Modulating the ERK pathway through in vivo inhibition of mitogen-activated protein/ERK kinase 1/2, the upstream activator of ERK1/2, we observed a significant decrease in intestinal apoB48 synthesis and secretion. |
| 1115 | 16644688 | Interestingly, enhanced basal ERK activity in the fructose-fed hamster intestine was accompanied by an increased activation of sterol regulatory element-binding protein. |
| 1116 | 16644688 | In summary, these data suggest that insulin insensitivity at the level of the intestine and aberrant insulin signaling are important underlying factors in intestinal overproduction of highly atherogenic apoB48-containing lipoproteins in the insulin-resistant state. |
| 1117 | 16644688 | Basal activation of the ERK pathway may be an important contributor to the aberrant insulin signaling and lipoprotein overproduction in this model. |
| 1118 | 16644688 | Intestinal insulin resistance and aberrant production of apolipoprotein B48 lipoproteins in an animal model of insulin resistance and metabolic dyslipidemia: evidence for activation of protein tyrosine phosphatase-1B, extracellular signal-related kinase, and sterol regulatory element-binding protein-1c in the fructose-fed hamster intestine. |
| 1119 | 16644688 | Intestinal lipoprotein production in chow-fed hamsters was responsive to the inhibitory effects of insulin, and a decrease in circulating levels of triglyceride-rich apolipoprotein (apo)B48-containing lipoproteins occurred 60 min after insulin administration. |
| 1120 | 16644688 | However, fructose-fed hamster intestine was not responsive to the insulin-induced downregulation of apoB48-lipoprotein production, suggesting insulin insensitivity at the level of the intestine. |
| 1121 | 16644688 | Enterocytes from the fructose-fed hamster exhibited normal activity of the insulin receptor but reduced levels of insulin receptor substrate-1 phosphorylation and mass and Akt protein mass. |
| 1122 | 16644688 | Conversely, the protein mass of the p110 subunit of phosphatidylinositol 3-kinase, protein tyrosine phosphatase-1B, and basal levels of phosphorylated extracellular signal-related kinase (ERK) were significantly increased in the fructose-fed hamster intestine. |
| 1123 | 16644688 | Modulating the ERK pathway through in vivo inhibition of mitogen-activated protein/ERK kinase 1/2, the upstream activator of ERK1/2, we observed a significant decrease in intestinal apoB48 synthesis and secretion. |
| 1124 | 16644688 | Interestingly, enhanced basal ERK activity in the fructose-fed hamster intestine was accompanied by an increased activation of sterol regulatory element-binding protein. |
| 1125 | 16644688 | In summary, these data suggest that insulin insensitivity at the level of the intestine and aberrant insulin signaling are important underlying factors in intestinal overproduction of highly atherogenic apoB48-containing lipoproteins in the insulin-resistant state. |
| 1126 | 16644688 | Basal activation of the ERK pathway may be an important contributor to the aberrant insulin signaling and lipoprotein overproduction in this model. |
| 1127 | 16644688 | Intestinal insulin resistance and aberrant production of apolipoprotein B48 lipoproteins in an animal model of insulin resistance and metabolic dyslipidemia: evidence for activation of protein tyrosine phosphatase-1B, extracellular signal-related kinase, and sterol regulatory element-binding protein-1c in the fructose-fed hamster intestine. |
| 1128 | 16644688 | Intestinal lipoprotein production in chow-fed hamsters was responsive to the inhibitory effects of insulin, and a decrease in circulating levels of triglyceride-rich apolipoprotein (apo)B48-containing lipoproteins occurred 60 min after insulin administration. |
| 1129 | 16644688 | However, fructose-fed hamster intestine was not responsive to the insulin-induced downregulation of apoB48-lipoprotein production, suggesting insulin insensitivity at the level of the intestine. |
| 1130 | 16644688 | Enterocytes from the fructose-fed hamster exhibited normal activity of the insulin receptor but reduced levels of insulin receptor substrate-1 phosphorylation and mass and Akt protein mass. |
| 1131 | 16644688 | Conversely, the protein mass of the p110 subunit of phosphatidylinositol 3-kinase, protein tyrosine phosphatase-1B, and basal levels of phosphorylated extracellular signal-related kinase (ERK) were significantly increased in the fructose-fed hamster intestine. |
| 1132 | 16644688 | Modulating the ERK pathway through in vivo inhibition of mitogen-activated protein/ERK kinase 1/2, the upstream activator of ERK1/2, we observed a significant decrease in intestinal apoB48 synthesis and secretion. |
| 1133 | 16644688 | Interestingly, enhanced basal ERK activity in the fructose-fed hamster intestine was accompanied by an increased activation of sterol regulatory element-binding protein. |
| 1134 | 16644688 | In summary, these data suggest that insulin insensitivity at the level of the intestine and aberrant insulin signaling are important underlying factors in intestinal overproduction of highly atherogenic apoB48-containing lipoproteins in the insulin-resistant state. |
| 1135 | 16644688 | Basal activation of the ERK pathway may be an important contributor to the aberrant insulin signaling and lipoprotein overproduction in this model. |
| 1136 | 16644688 | Intestinal insulin resistance and aberrant production of apolipoprotein B48 lipoproteins in an animal model of insulin resistance and metabolic dyslipidemia: evidence for activation of protein tyrosine phosphatase-1B, extracellular signal-related kinase, and sterol regulatory element-binding protein-1c in the fructose-fed hamster intestine. |
| 1137 | 16644688 | Intestinal lipoprotein production in chow-fed hamsters was responsive to the inhibitory effects of insulin, and a decrease in circulating levels of triglyceride-rich apolipoprotein (apo)B48-containing lipoproteins occurred 60 min after insulin administration. |
| 1138 | 16644688 | However, fructose-fed hamster intestine was not responsive to the insulin-induced downregulation of apoB48-lipoprotein production, suggesting insulin insensitivity at the level of the intestine. |
| 1139 | 16644688 | Enterocytes from the fructose-fed hamster exhibited normal activity of the insulin receptor but reduced levels of insulin receptor substrate-1 phosphorylation and mass and Akt protein mass. |
| 1140 | 16644688 | Conversely, the protein mass of the p110 subunit of phosphatidylinositol 3-kinase, protein tyrosine phosphatase-1B, and basal levels of phosphorylated extracellular signal-related kinase (ERK) were significantly increased in the fructose-fed hamster intestine. |
| 1141 | 16644688 | Modulating the ERK pathway through in vivo inhibition of mitogen-activated protein/ERK kinase 1/2, the upstream activator of ERK1/2, we observed a significant decrease in intestinal apoB48 synthesis and secretion. |
| 1142 | 16644688 | Interestingly, enhanced basal ERK activity in the fructose-fed hamster intestine was accompanied by an increased activation of sterol regulatory element-binding protein. |
| 1143 | 16644688 | In summary, these data suggest that insulin insensitivity at the level of the intestine and aberrant insulin signaling are important underlying factors in intestinal overproduction of highly atherogenic apoB48-containing lipoproteins in the insulin-resistant state. |
| 1144 | 16644688 | Basal activation of the ERK pathway may be an important contributor to the aberrant insulin signaling and lipoprotein overproduction in this model. |
| 1145 | 16712524 | The aim of the present study was to determine the relationship between the most accurate summary index of the lipoprotein-related risk of vascular disease, the apoB (apolipoprotein B-100)/apoA-I (apolipoprotein A-I) ratio, and body composition in established migrant South Asians and white Caucasians living in Canada. |
| 1146 | 16721486 | A common functional exon polymorphism in the microsomal triglyceride transfer protein gene is associated with type 2 diabetes, impaired glucose metabolism and insulin levels. |
| 1147 | 16721486 | The microsomal triglyceride transfer protein (MTP) is required for the assembly and secretion of apolipoprotein B-containing lipoproteins. |
| 1148 | 16721486 | Emerging evidence has indicated that the functional MTP exon polymorphism I128T is associated with dyslipidemia and other traits of the insulin-resistance syndrome, and the T128 variant seems to confer a reduced stability of MTP, resulting in reduced binding of LDL particles. |
| 1149 | 16721486 | In comparison to homozygote subjects of the wild allele, carriers of the less common allele of the MTP T128 genotype showed significantly lower postprandial insulin levels (P=0.017), lower diastolic blood pressure (P=0.049) and had a lower prevalence of impaired glucose metabolism and diabetes type 2 (P=0.03) in the MICK. |
| 1150 | 16734179 | Smoking (odds ratio 2.87 for current vs never, population attributable risk 35.7% for current and former smoker vs never), raised apolipoprotein B / apolipoprotein A1 ratio (3.25 for top vs lowest quintile, population attributable risk 49.2 for top four quintiles vs lowest quintile), history of hypertension (1.91, 17.9%), diabetes (2.37, 9.9%), abdominal obesity (1.12 for top vs lowest tertile and 1.62 for middle vs lowest tertile, 20.1% for top two tertiles vs lowest tertile), psychosocial factors (2.67, 32.5), daily consumption of fruits and vegetables (0.70, 13.7% for lack of daily consumption), regular alcohol consumption (0.91, 6.7%), and regular physical activity (0.86, 12.2%) were all significantly related to acute myocardial infarction (p < 0.0001 for all risk factors, and p = 0.03 for alcohol). |
| 1151 | 16784958 | Serum apolipoprotein B-48 and lipoprotein lipase levels were measured by the enzyme immunoassay method. |
| 1152 | 17046544 | Postprandial thrombin activatable fibrinolysis inhibitor and markers of endothelial dysfunction in type 2 diabetic patients. |
| 1153 | 17046544 | The aim of this study was to assess postprandial changes in thrombin activatable fibrinolysis inhibitor (TAFI) antigen, a thrombin-dependent fibrinolysis inhibitor with anti-inflammatory properties, and soluble markers of endothelial dysfunction in normotriglyceridemic type 2 diabetic patients. |
| 1154 | 17046544 | Fasting and postprandial TAFI antigen, thrombomodulin, tissue factor pathway inhibitor (TFPI), and plasminogen activator inhibitor 1 were assessed in 12 normotriglyceridemic type 2 diabetic patients treated with diet (hemoglobin A1c, 6.80% +/- 0.67%) and 14 controls. |
| 1155 | 17046544 | Fasting low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, free fatty acids and apolipoprotein B, and fasting and postprandial triglyceride, glucose, and insulin were also measured. |
| 1156 | 17046544 | This decrement was correlated with fasting TAFI, glucose and hemoglobin A1c, and the area under the curve of glucose. |
| 1157 | 17046544 | Thrombomodulin, TFPI, and plasminogen activator inhibitor 1 were similar in both groups, with thrombomodulin and TFPI showing a transient postprandial increase. |
| 1158 | 17137217 | Analyses of covariance adjusting for age, body mass index, hyperlipidemia, diabetes, smoking, drinking, and antihypertensive medication revealed that 17 polymorphisms in 16 genes (APOB, CAST, CLCNKB, CTNS, GHR, GYS1, HF1, IKBKAP, KCNJ11, LIPC, LPL, P2RY2, PON2, SLC4A1, TRH, VWF) were significantly associated with blood pressure variations. |
| 1159 | 17137217 | Multivariate logistic regression analysis with adjustment for the same factors revealed that 11 polymorphisms in 11 genes (CAST, CTLA4, F5, GC, GHR, LIPC, PLA2G7, SLC4A1, SLCI8A1, TRH, VWF) showed significant associations with hypertension. |
| 1160 | 17137217 | Five polymorphisms in five genes, CAST(calpastatin), LIPC (hepatic lipase), SLC4A1 (band 3 anion transporter), TRH (thyrotropin-releasing hormone), and VWF (von Willebrand factor), were significantly associated with both blood pressure variation and hypertension. |
| 1161 | 17227233 | Patients most suitable for use of MTP inhibitors include those with hepatic hypersecretion of apoB, including the metabolic syndrome, Type 2 diabetes mellitus and familial combined hyperlipidaemia, as well as homozygous and heterozygous familial hypercholesterolaemia. |
| 1162 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 1163 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 1164 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 1165 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 1166 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 1167 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 1168 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 1169 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 1170 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 1171 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 1172 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 1173 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 1174 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 1175 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 1176 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 1177 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 1178 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 1179 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 1180 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 1181 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 1182 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 1183 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 1184 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 1185 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 1186 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 1187 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 1188 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 1189 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 1190 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 1191 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 1192 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 1193 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 1194 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 1195 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 1196 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 1197 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 1198 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 1199 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 1200 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 1201 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 1202 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 1203 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 1204 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 1205 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 1206 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 1207 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 1208 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 1209 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 1210 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 1211 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 1212 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 1213 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 1214 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 1215 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 1216 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 1217 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 1218 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 1219 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 1220 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 1221 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 1222 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 1223 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 1224 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 1225 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 1226 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 1227 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 1228 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 1229 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 1230 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 1231 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 1232 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 1233 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 1234 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 1235 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 1236 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 1237 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 1238 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 1239 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 1240 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 1241 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 1242 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 1243 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 1244 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 1245 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 1246 | 17343371 | Chronic treatment of high fat fed ApoB100/CETP-Tgn mice with 7 corrected the plasma lipid parameters and improved insulin sensitivity. |
| 1247 | 17460328 | Apolipoprotein A-V association with intracellular lipid droplets. |
| 1248 | 17460328 | Apolipoprotein A-V (apoA-V) plays a key role in the regulation of triglyceride (TG) metabolism. |
| 1249 | 17460328 | Given the very low concentration of apoA-V in plasma, we hypothesized that apoA-V may influence plasma TG levels by affecting the assembly and/or secretion of apoB-containing lipoproteins. |
| 1250 | 17460328 | When apoA-V was overexpressed in cultured Hep3B cells, neither the amount of apoB secreted nor the density distribution of apoB-containing lipoproteins was affected. |
| 1251 | 17460328 | Fluorescence microscopy and cell lysate immunoprecipitation studies revealed that apoA-V is not associated with apoB intracellularly, yet immunoprecipitation of apoA-V from the cell culture medium resulted in coprecipitation of apoB. |
| 1252 | 17460328 | These data suggest that the apoA-V association with apoB-containing lipoproteins is a postsecretory event. |
| 1253 | 17460328 | Apolipoprotein A-V association with intracellular lipid droplets. |
| 1254 | 17460328 | Apolipoprotein A-V (apoA-V) plays a key role in the regulation of triglyceride (TG) metabolism. |
| 1255 | 17460328 | Given the very low concentration of apoA-V in plasma, we hypothesized that apoA-V may influence plasma TG levels by affecting the assembly and/or secretion of apoB-containing lipoproteins. |
| 1256 | 17460328 | When apoA-V was overexpressed in cultured Hep3B cells, neither the amount of apoB secreted nor the density distribution of apoB-containing lipoproteins was affected. |
| 1257 | 17460328 | Fluorescence microscopy and cell lysate immunoprecipitation studies revealed that apoA-V is not associated with apoB intracellularly, yet immunoprecipitation of apoA-V from the cell culture medium resulted in coprecipitation of apoB. |
| 1258 | 17460328 | These data suggest that the apoA-V association with apoB-containing lipoproteins is a postsecretory event. |
| 1259 | 17460328 | Apolipoprotein A-V association with intracellular lipid droplets. |
| 1260 | 17460328 | Apolipoprotein A-V (apoA-V) plays a key role in the regulation of triglyceride (TG) metabolism. |
| 1261 | 17460328 | Given the very low concentration of apoA-V in plasma, we hypothesized that apoA-V may influence plasma TG levels by affecting the assembly and/or secretion of apoB-containing lipoproteins. |
| 1262 | 17460328 | When apoA-V was overexpressed in cultured Hep3B cells, neither the amount of apoB secreted nor the density distribution of apoB-containing lipoproteins was affected. |
| 1263 | 17460328 | Fluorescence microscopy and cell lysate immunoprecipitation studies revealed that apoA-V is not associated with apoB intracellularly, yet immunoprecipitation of apoA-V from the cell culture medium resulted in coprecipitation of apoB. |
| 1264 | 17460328 | These data suggest that the apoA-V association with apoB-containing lipoproteins is a postsecretory event. |
| 1265 | 17460328 | Apolipoprotein A-V association with intracellular lipid droplets. |
| 1266 | 17460328 | Apolipoprotein A-V (apoA-V) plays a key role in the regulation of triglyceride (TG) metabolism. |
| 1267 | 17460328 | Given the very low concentration of apoA-V in plasma, we hypothesized that apoA-V may influence plasma TG levels by affecting the assembly and/or secretion of apoB-containing lipoproteins. |
| 1268 | 17460328 | When apoA-V was overexpressed in cultured Hep3B cells, neither the amount of apoB secreted nor the density distribution of apoB-containing lipoproteins was affected. |
| 1269 | 17460328 | Fluorescence microscopy and cell lysate immunoprecipitation studies revealed that apoA-V is not associated with apoB intracellularly, yet immunoprecipitation of apoA-V from the cell culture medium resulted in coprecipitation of apoB. |
| 1270 | 17460328 | These data suggest that the apoA-V association with apoB-containing lipoproteins is a postsecretory event. |
| 1271 | 17511634 | Clinical studies in adults indicate there is a positive and significant association between insulin resistance, dyslipidaemia, fasting intestinally derived lipoproteins [via apoB48 (apolipoprotein B48)] and visceral fat. |
| 1272 | 17511634 | Since little is known about postprandial dyslipidaemia in overweight children, we sought to compare fasting levels of apoB48 with the HOMA-IR (homoeostasis model assessment of insulin resistance) score, classic lipid profile and VAT (visceral adipose tissue). |
| 1273 | 17511634 | Fasting apoB48 was quantified in plasma using an adapted SDS/PAGE immunoblotting technique, and insulin, glucose, TC (total cholesterol), TAG (triacylglycerol), LDL (low-density lipoprotein) and HDL (high-density lipoprotein) were determined by calorimetric assay. |
| 1274 | 17511634 | Clinical studies in adults indicate there is a positive and significant association between insulin resistance, dyslipidaemia, fasting intestinally derived lipoproteins [via apoB48 (apolipoprotein B48)] and visceral fat. |
| 1275 | 17511634 | Since little is known about postprandial dyslipidaemia in overweight children, we sought to compare fasting levels of apoB48 with the HOMA-IR (homoeostasis model assessment of insulin resistance) score, classic lipid profile and VAT (visceral adipose tissue). |
| 1276 | 17511634 | Fasting apoB48 was quantified in plasma using an adapted SDS/PAGE immunoblotting technique, and insulin, glucose, TC (total cholesterol), TAG (triacylglycerol), LDL (low-density lipoprotein) and HDL (high-density lipoprotein) were determined by calorimetric assay. |
| 1277 | 17511634 | Clinical studies in adults indicate there is a positive and significant association between insulin resistance, dyslipidaemia, fasting intestinally derived lipoproteins [via apoB48 (apolipoprotein B48)] and visceral fat. |
| 1278 | 17511634 | Since little is known about postprandial dyslipidaemia in overweight children, we sought to compare fasting levels of apoB48 with the HOMA-IR (homoeostasis model assessment of insulin resistance) score, classic lipid profile and VAT (visceral adipose tissue). |
| 1279 | 17511634 | Fasting apoB48 was quantified in plasma using an adapted SDS/PAGE immunoblotting technique, and insulin, glucose, TC (total cholesterol), TAG (triacylglycerol), LDL (low-density lipoprotein) and HDL (high-density lipoprotein) were determined by calorimetric assay. |
| 1280 | 17525004 | PON1 activity is inversely related to LDL apoB carbonyl content in patients with coronary artery disease. |
| 1281 | 17525004 | The objective of this study was to investigate apolipoprotein B (apoB) carbonyl content as a parameter for studying low-density lipoprotein (LDL) oxidation in coronary artery disease (CAD) risk assessment and to explore the relationship between apoB carbonyl content (an index of protein oxidation) and paraoxonase 1 (PON1) activity in CAD patients and controls. |
| 1282 | 17525004 | All subjects were assayed for apoB carbonyl content, LDL-malondialdehyde (LDL-MDA), PON1 activity, and lipid and apolipoprotein levels. |
| 1283 | 17525004 | A significantly (p < 0.01) negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 1284 | 17525004 | CAD patients with associated risk factors had highly raised (p < 0.01) apoB carbonyl content and considerably depressed PON1 activity compared to those with no associated risk factors. |
| 1285 | 17525004 | CAD patients in group 1 also had significantly raised apoB levels and low HDL-cholesterol and apoA1 levels as compared to patients in group 2, while the other lipid variables did not show any significant difference. |
| 1286 | 17525004 | A significantly negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 1287 | 17525004 | PON1 activity is inversely related to LDL apoB carbonyl content in patients with coronary artery disease. |
| 1288 | 17525004 | The objective of this study was to investigate apolipoprotein B (apoB) carbonyl content as a parameter for studying low-density lipoprotein (LDL) oxidation in coronary artery disease (CAD) risk assessment and to explore the relationship between apoB carbonyl content (an index of protein oxidation) and paraoxonase 1 (PON1) activity in CAD patients and controls. |
| 1289 | 17525004 | All subjects were assayed for apoB carbonyl content, LDL-malondialdehyde (LDL-MDA), PON1 activity, and lipid and apolipoprotein levels. |
| 1290 | 17525004 | A significantly (p < 0.01) negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 1291 | 17525004 | CAD patients with associated risk factors had highly raised (p < 0.01) apoB carbonyl content and considerably depressed PON1 activity compared to those with no associated risk factors. |
| 1292 | 17525004 | CAD patients in group 1 also had significantly raised apoB levels and low HDL-cholesterol and apoA1 levels as compared to patients in group 2, while the other lipid variables did not show any significant difference. |
| 1293 | 17525004 | A significantly negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 1294 | 17525004 | PON1 activity is inversely related to LDL apoB carbonyl content in patients with coronary artery disease. |
| 1295 | 17525004 | The objective of this study was to investigate apolipoprotein B (apoB) carbonyl content as a parameter for studying low-density lipoprotein (LDL) oxidation in coronary artery disease (CAD) risk assessment and to explore the relationship between apoB carbonyl content (an index of protein oxidation) and paraoxonase 1 (PON1) activity in CAD patients and controls. |
| 1296 | 17525004 | All subjects were assayed for apoB carbonyl content, LDL-malondialdehyde (LDL-MDA), PON1 activity, and lipid and apolipoprotein levels. |
| 1297 | 17525004 | A significantly (p < 0.01) negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 1298 | 17525004 | CAD patients with associated risk factors had highly raised (p < 0.01) apoB carbonyl content and considerably depressed PON1 activity compared to those with no associated risk factors. |
| 1299 | 17525004 | CAD patients in group 1 also had significantly raised apoB levels and low HDL-cholesterol and apoA1 levels as compared to patients in group 2, while the other lipid variables did not show any significant difference. |
| 1300 | 17525004 | A significantly negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 1301 | 17525004 | PON1 activity is inversely related to LDL apoB carbonyl content in patients with coronary artery disease. |
| 1302 | 17525004 | The objective of this study was to investigate apolipoprotein B (apoB) carbonyl content as a parameter for studying low-density lipoprotein (LDL) oxidation in coronary artery disease (CAD) risk assessment and to explore the relationship between apoB carbonyl content (an index of protein oxidation) and paraoxonase 1 (PON1) activity in CAD patients and controls. |
| 1303 | 17525004 | All subjects were assayed for apoB carbonyl content, LDL-malondialdehyde (LDL-MDA), PON1 activity, and lipid and apolipoprotein levels. |
| 1304 | 17525004 | A significantly (p < 0.01) negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 1305 | 17525004 | CAD patients with associated risk factors had highly raised (p < 0.01) apoB carbonyl content and considerably depressed PON1 activity compared to those with no associated risk factors. |
| 1306 | 17525004 | CAD patients in group 1 also had significantly raised apoB levels and low HDL-cholesterol and apoA1 levels as compared to patients in group 2, while the other lipid variables did not show any significant difference. |
| 1307 | 17525004 | A significantly negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 1308 | 17525004 | PON1 activity is inversely related to LDL apoB carbonyl content in patients with coronary artery disease. |
| 1309 | 17525004 | The objective of this study was to investigate apolipoprotein B (apoB) carbonyl content as a parameter for studying low-density lipoprotein (LDL) oxidation in coronary artery disease (CAD) risk assessment and to explore the relationship between apoB carbonyl content (an index of protein oxidation) and paraoxonase 1 (PON1) activity in CAD patients and controls. |
| 1310 | 17525004 | All subjects were assayed for apoB carbonyl content, LDL-malondialdehyde (LDL-MDA), PON1 activity, and lipid and apolipoprotein levels. |
| 1311 | 17525004 | A significantly (p < 0.01) negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 1312 | 17525004 | CAD patients with associated risk factors had highly raised (p < 0.01) apoB carbonyl content and considerably depressed PON1 activity compared to those with no associated risk factors. |
| 1313 | 17525004 | CAD patients in group 1 also had significantly raised apoB levels and low HDL-cholesterol and apoA1 levels as compared to patients in group 2, while the other lipid variables did not show any significant difference. |
| 1314 | 17525004 | A significantly negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 1315 | 17525004 | PON1 activity is inversely related to LDL apoB carbonyl content in patients with coronary artery disease. |
| 1316 | 17525004 | The objective of this study was to investigate apolipoprotein B (apoB) carbonyl content as a parameter for studying low-density lipoprotein (LDL) oxidation in coronary artery disease (CAD) risk assessment and to explore the relationship between apoB carbonyl content (an index of protein oxidation) and paraoxonase 1 (PON1) activity in CAD patients and controls. |
| 1317 | 17525004 | All subjects were assayed for apoB carbonyl content, LDL-malondialdehyde (LDL-MDA), PON1 activity, and lipid and apolipoprotein levels. |
| 1318 | 17525004 | A significantly (p < 0.01) negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 1319 | 17525004 | CAD patients with associated risk factors had highly raised (p < 0.01) apoB carbonyl content and considerably depressed PON1 activity compared to those with no associated risk factors. |
| 1320 | 17525004 | CAD patients in group 1 also had significantly raised apoB levels and low HDL-cholesterol and apoA1 levels as compared to patients in group 2, while the other lipid variables did not show any significant difference. |
| 1321 | 17525004 | A significantly negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 1322 | 17525004 | PON1 activity is inversely related to LDL apoB carbonyl content in patients with coronary artery disease. |
| 1323 | 17525004 | The objective of this study was to investigate apolipoprotein B (apoB) carbonyl content as a parameter for studying low-density lipoprotein (LDL) oxidation in coronary artery disease (CAD) risk assessment and to explore the relationship between apoB carbonyl content (an index of protein oxidation) and paraoxonase 1 (PON1) activity in CAD patients and controls. |
| 1324 | 17525004 | All subjects were assayed for apoB carbonyl content, LDL-malondialdehyde (LDL-MDA), PON1 activity, and lipid and apolipoprotein levels. |
| 1325 | 17525004 | A significantly (p < 0.01) negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 1326 | 17525004 | CAD patients with associated risk factors had highly raised (p < 0.01) apoB carbonyl content and considerably depressed PON1 activity compared to those with no associated risk factors. |
| 1327 | 17525004 | CAD patients in group 1 also had significantly raised apoB levels and low HDL-cholesterol and apoA1 levels as compared to patients in group 2, while the other lipid variables did not show any significant difference. |
| 1328 | 17525004 | A significantly negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 1329 | 17647275 | Secretion of atherogenic risk factor apolipoprotein B-100 is increased by a potential mechanism of JNK/PKC-mediated insulin resistance in liver cells. |
| 1330 | 17647275 | Induction of insulin resistance was accompanied by a considerable rise in the production of hepatic very low density lipoprotein (VLDL) containing ApoB and triglyceride. |
| 1331 | 17647275 | Increased plasma levels of ApoB and triglyceride in VLDL are common characteristics of the dyslipidemia associated with insulin resistance and type 2 diabetes mellitus. |
| 1332 | 17647275 | Thus, we investigate whether phorbol 12-myristate-13-acetate (PMA)-induced insulin resistance affects the increase of ApoB secretion. |
| 1333 | 17647275 | PMA increased ApoB secretion and transcriptional level of microsomal triglyceride transfer protein (MTP). |
| 1334 | 17647275 | Additionally, PMA induced activation of c-jun N-terminal kinase (JNK) and protein kinase C (PKC) isoforms (alpha, betaI, delta, zeta, theta), and reduced AKT8 virus oncogene cellular homolog (AKT) activation in a time dependent manner. |
| 1335 | 17647275 | PMA-induced ApoB secretion, MTP promoter activities, and IRS1 degradation was significantly decreased by treatment of JNK and PKCs inhibitors. |
| 1336 | 17647275 | Orthovanadate, a potent tyrosine phosphatase inhibitor, increased tyrosine phosphorylation of IRS1 and decreased ApoB secretion of Chang liver cells although PMA was co-treated. |
| 1337 | 17647275 | From the results, it was concluded that PMA-induced insulin resistance, through induction of serine phosphorylation of IRS1 mediated by activated JNK and PKCs, increases ApoB secretion in Chang liver cells. |
| 1338 | 17647275 | Secretion of atherogenic risk factor apolipoprotein B-100 is increased by a potential mechanism of JNK/PKC-mediated insulin resistance in liver cells. |
| 1339 | 17647275 | Induction of insulin resistance was accompanied by a considerable rise in the production of hepatic very low density lipoprotein (VLDL) containing ApoB and triglyceride. |
| 1340 | 17647275 | Increased plasma levels of ApoB and triglyceride in VLDL are common characteristics of the dyslipidemia associated with insulin resistance and type 2 diabetes mellitus. |
| 1341 | 17647275 | Thus, we investigate whether phorbol 12-myristate-13-acetate (PMA)-induced insulin resistance affects the increase of ApoB secretion. |
| 1342 | 17647275 | PMA increased ApoB secretion and transcriptional level of microsomal triglyceride transfer protein (MTP). |
| 1343 | 17647275 | Additionally, PMA induced activation of c-jun N-terminal kinase (JNK) and protein kinase C (PKC) isoforms (alpha, betaI, delta, zeta, theta), and reduced AKT8 virus oncogene cellular homolog (AKT) activation in a time dependent manner. |
| 1344 | 17647275 | PMA-induced ApoB secretion, MTP promoter activities, and IRS1 degradation was significantly decreased by treatment of JNK and PKCs inhibitors. |
| 1345 | 17647275 | Orthovanadate, a potent tyrosine phosphatase inhibitor, increased tyrosine phosphorylation of IRS1 and decreased ApoB secretion of Chang liver cells although PMA was co-treated. |
| 1346 | 17647275 | From the results, it was concluded that PMA-induced insulin resistance, through induction of serine phosphorylation of IRS1 mediated by activated JNK and PKCs, increases ApoB secretion in Chang liver cells. |
| 1347 | 17647275 | Secretion of atherogenic risk factor apolipoprotein B-100 is increased by a potential mechanism of JNK/PKC-mediated insulin resistance in liver cells. |
| 1348 | 17647275 | Induction of insulin resistance was accompanied by a considerable rise in the production of hepatic very low density lipoprotein (VLDL) containing ApoB and triglyceride. |
| 1349 | 17647275 | Increased plasma levels of ApoB and triglyceride in VLDL are common characteristics of the dyslipidemia associated with insulin resistance and type 2 diabetes mellitus. |
| 1350 | 17647275 | Thus, we investigate whether phorbol 12-myristate-13-acetate (PMA)-induced insulin resistance affects the increase of ApoB secretion. |
| 1351 | 17647275 | PMA increased ApoB secretion and transcriptional level of microsomal triglyceride transfer protein (MTP). |
| 1352 | 17647275 | Additionally, PMA induced activation of c-jun N-terminal kinase (JNK) and protein kinase C (PKC) isoforms (alpha, betaI, delta, zeta, theta), and reduced AKT8 virus oncogene cellular homolog (AKT) activation in a time dependent manner. |
| 1353 | 17647275 | PMA-induced ApoB secretion, MTP promoter activities, and IRS1 degradation was significantly decreased by treatment of JNK and PKCs inhibitors. |
| 1354 | 17647275 | Orthovanadate, a potent tyrosine phosphatase inhibitor, increased tyrosine phosphorylation of IRS1 and decreased ApoB secretion of Chang liver cells although PMA was co-treated. |
| 1355 | 17647275 | From the results, it was concluded that PMA-induced insulin resistance, through induction of serine phosphorylation of IRS1 mediated by activated JNK and PKCs, increases ApoB secretion in Chang liver cells. |
| 1356 | 17647275 | Secretion of atherogenic risk factor apolipoprotein B-100 is increased by a potential mechanism of JNK/PKC-mediated insulin resistance in liver cells. |
| 1357 | 17647275 | Induction of insulin resistance was accompanied by a considerable rise in the production of hepatic very low density lipoprotein (VLDL) containing ApoB and triglyceride. |
| 1358 | 17647275 | Increased plasma levels of ApoB and triglyceride in VLDL are common characteristics of the dyslipidemia associated with insulin resistance and type 2 diabetes mellitus. |
| 1359 | 17647275 | Thus, we investigate whether phorbol 12-myristate-13-acetate (PMA)-induced insulin resistance affects the increase of ApoB secretion. |
| 1360 | 17647275 | PMA increased ApoB secretion and transcriptional level of microsomal triglyceride transfer protein (MTP). |
| 1361 | 17647275 | Additionally, PMA induced activation of c-jun N-terminal kinase (JNK) and protein kinase C (PKC) isoforms (alpha, betaI, delta, zeta, theta), and reduced AKT8 virus oncogene cellular homolog (AKT) activation in a time dependent manner. |
| 1362 | 17647275 | PMA-induced ApoB secretion, MTP promoter activities, and IRS1 degradation was significantly decreased by treatment of JNK and PKCs inhibitors. |
| 1363 | 17647275 | Orthovanadate, a potent tyrosine phosphatase inhibitor, increased tyrosine phosphorylation of IRS1 and decreased ApoB secretion of Chang liver cells although PMA was co-treated. |
| 1364 | 17647275 | From the results, it was concluded that PMA-induced insulin resistance, through induction of serine phosphorylation of IRS1 mediated by activated JNK and PKCs, increases ApoB secretion in Chang liver cells. |
| 1365 | 17647275 | Secretion of atherogenic risk factor apolipoprotein B-100 is increased by a potential mechanism of JNK/PKC-mediated insulin resistance in liver cells. |
| 1366 | 17647275 | Induction of insulin resistance was accompanied by a considerable rise in the production of hepatic very low density lipoprotein (VLDL) containing ApoB and triglyceride. |
| 1367 | 17647275 | Increased plasma levels of ApoB and triglyceride in VLDL are common characteristics of the dyslipidemia associated with insulin resistance and type 2 diabetes mellitus. |
| 1368 | 17647275 | Thus, we investigate whether phorbol 12-myristate-13-acetate (PMA)-induced insulin resistance affects the increase of ApoB secretion. |
| 1369 | 17647275 | PMA increased ApoB secretion and transcriptional level of microsomal triglyceride transfer protein (MTP). |
| 1370 | 17647275 | Additionally, PMA induced activation of c-jun N-terminal kinase (JNK) and protein kinase C (PKC) isoforms (alpha, betaI, delta, zeta, theta), and reduced AKT8 virus oncogene cellular homolog (AKT) activation in a time dependent manner. |
| 1371 | 17647275 | PMA-induced ApoB secretion, MTP promoter activities, and IRS1 degradation was significantly decreased by treatment of JNK and PKCs inhibitors. |
| 1372 | 17647275 | Orthovanadate, a potent tyrosine phosphatase inhibitor, increased tyrosine phosphorylation of IRS1 and decreased ApoB secretion of Chang liver cells although PMA was co-treated. |
| 1373 | 17647275 | From the results, it was concluded that PMA-induced insulin resistance, through induction of serine phosphorylation of IRS1 mediated by activated JNK and PKCs, increases ApoB secretion in Chang liver cells. |
| 1374 | 17647275 | Secretion of atherogenic risk factor apolipoprotein B-100 is increased by a potential mechanism of JNK/PKC-mediated insulin resistance in liver cells. |
| 1375 | 17647275 | Induction of insulin resistance was accompanied by a considerable rise in the production of hepatic very low density lipoprotein (VLDL) containing ApoB and triglyceride. |
| 1376 | 17647275 | Increased plasma levels of ApoB and triglyceride in VLDL are common characteristics of the dyslipidemia associated with insulin resistance and type 2 diabetes mellitus. |
| 1377 | 17647275 | Thus, we investigate whether phorbol 12-myristate-13-acetate (PMA)-induced insulin resistance affects the increase of ApoB secretion. |
| 1378 | 17647275 | PMA increased ApoB secretion and transcriptional level of microsomal triglyceride transfer protein (MTP). |
| 1379 | 17647275 | Additionally, PMA induced activation of c-jun N-terminal kinase (JNK) and protein kinase C (PKC) isoforms (alpha, betaI, delta, zeta, theta), and reduced AKT8 virus oncogene cellular homolog (AKT) activation in a time dependent manner. |
| 1380 | 17647275 | PMA-induced ApoB secretion, MTP promoter activities, and IRS1 degradation was significantly decreased by treatment of JNK and PKCs inhibitors. |
| 1381 | 17647275 | Orthovanadate, a potent tyrosine phosphatase inhibitor, increased tyrosine phosphorylation of IRS1 and decreased ApoB secretion of Chang liver cells although PMA was co-treated. |
| 1382 | 17647275 | From the results, it was concluded that PMA-induced insulin resistance, through induction of serine phosphorylation of IRS1 mediated by activated JNK and PKCs, increases ApoB secretion in Chang liver cells. |
| 1383 | 17647275 | Secretion of atherogenic risk factor apolipoprotein B-100 is increased by a potential mechanism of JNK/PKC-mediated insulin resistance in liver cells. |
| 1384 | 17647275 | Induction of insulin resistance was accompanied by a considerable rise in the production of hepatic very low density lipoprotein (VLDL) containing ApoB and triglyceride. |
| 1385 | 17647275 | Increased plasma levels of ApoB and triglyceride in VLDL are common characteristics of the dyslipidemia associated with insulin resistance and type 2 diabetes mellitus. |
| 1386 | 17647275 | Thus, we investigate whether phorbol 12-myristate-13-acetate (PMA)-induced insulin resistance affects the increase of ApoB secretion. |
| 1387 | 17647275 | PMA increased ApoB secretion and transcriptional level of microsomal triglyceride transfer protein (MTP). |
| 1388 | 17647275 | Additionally, PMA induced activation of c-jun N-terminal kinase (JNK) and protein kinase C (PKC) isoforms (alpha, betaI, delta, zeta, theta), and reduced AKT8 virus oncogene cellular homolog (AKT) activation in a time dependent manner. |
| 1389 | 17647275 | PMA-induced ApoB secretion, MTP promoter activities, and IRS1 degradation was significantly decreased by treatment of JNK and PKCs inhibitors. |
| 1390 | 17647275 | Orthovanadate, a potent tyrosine phosphatase inhibitor, increased tyrosine phosphorylation of IRS1 and decreased ApoB secretion of Chang liver cells although PMA was co-treated. |
| 1391 | 17647275 | From the results, it was concluded that PMA-induced insulin resistance, through induction of serine phosphorylation of IRS1 mediated by activated JNK and PKCs, increases ApoB secretion in Chang liver cells. |
| 1392 | 17647275 | Secretion of atherogenic risk factor apolipoprotein B-100 is increased by a potential mechanism of JNK/PKC-mediated insulin resistance in liver cells. |
| 1393 | 17647275 | Induction of insulin resistance was accompanied by a considerable rise in the production of hepatic very low density lipoprotein (VLDL) containing ApoB and triglyceride. |
| 1394 | 17647275 | Increased plasma levels of ApoB and triglyceride in VLDL are common characteristics of the dyslipidemia associated with insulin resistance and type 2 diabetes mellitus. |
| 1395 | 17647275 | Thus, we investigate whether phorbol 12-myristate-13-acetate (PMA)-induced insulin resistance affects the increase of ApoB secretion. |
| 1396 | 17647275 | PMA increased ApoB secretion and transcriptional level of microsomal triglyceride transfer protein (MTP). |
| 1397 | 17647275 | Additionally, PMA induced activation of c-jun N-terminal kinase (JNK) and protein kinase C (PKC) isoforms (alpha, betaI, delta, zeta, theta), and reduced AKT8 virus oncogene cellular homolog (AKT) activation in a time dependent manner. |
| 1398 | 17647275 | PMA-induced ApoB secretion, MTP promoter activities, and IRS1 degradation was significantly decreased by treatment of JNK and PKCs inhibitors. |
| 1399 | 17647275 | Orthovanadate, a potent tyrosine phosphatase inhibitor, increased tyrosine phosphorylation of IRS1 and decreased ApoB secretion of Chang liver cells although PMA was co-treated. |
| 1400 | 17647275 | From the results, it was concluded that PMA-induced insulin resistance, through induction of serine phosphorylation of IRS1 mediated by activated JNK and PKCs, increases ApoB secretion in Chang liver cells. |
| 1401 | 17652266 | Because arterial extracellular matrix contains several molecules, including biglycan, versican, hyaluronan, and elastin, that may affect plaque lipid retention and stability, we determined whether diabetes affects plaque content of these molecules in a porcine model of hyperlipidemia and diabetes. |
| 1402 | 17652266 | Hyaluronan, biglycan, versican, and apolipoprotein B (apoB) were detected with monospecific peptides or antisera, and elastin with Movat's pentachrome stain, and contents of each were quantified by computer-assisted morphometry. |
| 1403 | 17652266 | In the hyperlipidemic groups, diabetes was associated with a 4-fold increase in intimal area, with strong correlations between intimal area and immunostained areas for hyaluronan (R(2) = 0.83, p<0.0001), biglycan (R(2) = 0.72, p<0.0001), and apoB (R(2) = 0.23, p=0.0069). |
| 1404 | 17652266 | Because arterial extracellular matrix contains several molecules, including biglycan, versican, hyaluronan, and elastin, that may affect plaque lipid retention and stability, we determined whether diabetes affects plaque content of these molecules in a porcine model of hyperlipidemia and diabetes. |
| 1405 | 17652266 | Hyaluronan, biglycan, versican, and apolipoprotein B (apoB) were detected with monospecific peptides or antisera, and elastin with Movat's pentachrome stain, and contents of each were quantified by computer-assisted morphometry. |
| 1406 | 17652266 | In the hyperlipidemic groups, diabetes was associated with a 4-fold increase in intimal area, with strong correlations between intimal area and immunostained areas for hyaluronan (R(2) = 0.83, p<0.0001), biglycan (R(2) = 0.72, p<0.0001), and apoB (R(2) = 0.23, p=0.0069). |
| 1407 | 17712727 | The relationship of serum lipoprotein lipase mass with fasting serum apolipoprotein B-48 and remnant-like particle triglycerides in type 2 diabetic patients. |
| 1408 | 17848837 | Apolipoprotein E and lipoprotein lipase gene polymorphisms interaction on the atherogenic combined expression of hypertriglyceridemia and hyperapobetalipoproteinemia phenotypes. |
| 1409 | 17848837 | Apolipoprotein (apo) E and lipoprotein lipase (LPL) genes are involved in the catabolism of triglycerides (TG)-rich apoB-containing lipoproteins (VLDL). |
| 1410 | 17848837 | Several apoE and LPL gene variants affecting CAD risk, plasma TG or apoB concentrations have an allelic frequency of >5% in the general population. |
| 1411 | 17848837 | This study examined the combined effect of frequent apoE and LPL gene polymorphisms on the expression of hyperTG and hyperapoB. |
| 1412 | 17848837 | ApoE (E2, E3, and E4) and LPL (D9N, N291S, G188E, and P207L) were genotyped and fasting lipid profiles were assessed among 1,441 French-Canadian subjects. |
| 1413 | 17848837 | Multivariate analyses were performed to estimate the relationship between apoE and LPL gene variants and the risk of hyperTG (TG>1.7 mmol/l) and hyperapoB (apoB>0.9 g/l). |
| 1414 | 17848837 | Apolipoprotein E and lipoprotein lipase gene polymorphisms interaction on the atherogenic combined expression of hypertriglyceridemia and hyperapobetalipoproteinemia phenotypes. |
| 1415 | 17848837 | Apolipoprotein (apo) E and lipoprotein lipase (LPL) genes are involved in the catabolism of triglycerides (TG)-rich apoB-containing lipoproteins (VLDL). |
| 1416 | 17848837 | Several apoE and LPL gene variants affecting CAD risk, plasma TG or apoB concentrations have an allelic frequency of >5% in the general population. |
| 1417 | 17848837 | This study examined the combined effect of frequent apoE and LPL gene polymorphisms on the expression of hyperTG and hyperapoB. |
| 1418 | 17848837 | ApoE (E2, E3, and E4) and LPL (D9N, N291S, G188E, and P207L) were genotyped and fasting lipid profiles were assessed among 1,441 French-Canadian subjects. |
| 1419 | 17848837 | Multivariate analyses were performed to estimate the relationship between apoE and LPL gene variants and the risk of hyperTG (TG>1.7 mmol/l) and hyperapoB (apoB>0.9 g/l). |
| 1420 | 17872464 | For atherosclerotic background we used low-density lipoprotein receptor-deficient mice synthetizing only apolipoprotein B100 (LDLR(-/-) ApoB(100/100)). |
| 1421 | 17872464 | Diabetic background was obtained from transgenic mice overexpressing insulin-like growth factor-II (IGF-II) in pancreatic beta cells. |
| 1422 | 17872464 | Results indicated that IGF-II transgenic LDLR(-/-)ApoB(100/100) mice demonstrated insulin resistance, hyperglycemia, and mild hyperinsulinemia compared with hypercholesterolemic LDLR(-/-)ApoB(100/100) controls. |
| 1423 | 17872464 | In addition, old IGF-II/LDLR(-/-)ApoB(100/100) mice displayed significantly increased lesion calcification, which was more related to insulin resistance than glucose levels, and significantly higher baseline expression in aorta of several genes related to calcification and inflammation. |
| 1424 | 17872464 | Lipid levels of IGF-II/LDLR(-/-)ApoB(100/100) mice did not differ from LDLR(-/-)ApoB(100/100) controls at any time. |
| 1425 | 17872464 | For atherosclerotic background we used low-density lipoprotein receptor-deficient mice synthetizing only apolipoprotein B100 (LDLR(-/-) ApoB(100/100)). |
| 1426 | 17872464 | Diabetic background was obtained from transgenic mice overexpressing insulin-like growth factor-II (IGF-II) in pancreatic beta cells. |
| 1427 | 17872464 | Results indicated that IGF-II transgenic LDLR(-/-)ApoB(100/100) mice demonstrated insulin resistance, hyperglycemia, and mild hyperinsulinemia compared with hypercholesterolemic LDLR(-/-)ApoB(100/100) controls. |
| 1428 | 17872464 | In addition, old IGF-II/LDLR(-/-)ApoB(100/100) mice displayed significantly increased lesion calcification, which was more related to insulin resistance than glucose levels, and significantly higher baseline expression in aorta of several genes related to calcification and inflammation. |
| 1429 | 17872464 | Lipid levels of IGF-II/LDLR(-/-)ApoB(100/100) mice did not differ from LDLR(-/-)ApoB(100/100) controls at any time. |
| 1430 | 17872464 | For atherosclerotic background we used low-density lipoprotein receptor-deficient mice synthetizing only apolipoprotein B100 (LDLR(-/-) ApoB(100/100)). |
| 1431 | 17872464 | Diabetic background was obtained from transgenic mice overexpressing insulin-like growth factor-II (IGF-II) in pancreatic beta cells. |
| 1432 | 17872464 | Results indicated that IGF-II transgenic LDLR(-/-)ApoB(100/100) mice demonstrated insulin resistance, hyperglycemia, and mild hyperinsulinemia compared with hypercholesterolemic LDLR(-/-)ApoB(100/100) controls. |
| 1433 | 17872464 | In addition, old IGF-II/LDLR(-/-)ApoB(100/100) mice displayed significantly increased lesion calcification, which was more related to insulin resistance than glucose levels, and significantly higher baseline expression in aorta of several genes related to calcification and inflammation. |
| 1434 | 17872464 | Lipid levels of IGF-II/LDLR(-/-)ApoB(100/100) mice did not differ from LDLR(-/-)ApoB(100/100) controls at any time. |
| 1435 | 17872464 | For atherosclerotic background we used low-density lipoprotein receptor-deficient mice synthetizing only apolipoprotein B100 (LDLR(-/-) ApoB(100/100)). |
| 1436 | 17872464 | Diabetic background was obtained from transgenic mice overexpressing insulin-like growth factor-II (IGF-II) in pancreatic beta cells. |
| 1437 | 17872464 | Results indicated that IGF-II transgenic LDLR(-/-)ApoB(100/100) mice demonstrated insulin resistance, hyperglycemia, and mild hyperinsulinemia compared with hypercholesterolemic LDLR(-/-)ApoB(100/100) controls. |
| 1438 | 17872464 | In addition, old IGF-II/LDLR(-/-)ApoB(100/100) mice displayed significantly increased lesion calcification, which was more related to insulin resistance than glucose levels, and significantly higher baseline expression in aorta of several genes related to calcification and inflammation. |
| 1439 | 17872464 | Lipid levels of IGF-II/LDLR(-/-)ApoB(100/100) mice did not differ from LDLR(-/-)ApoB(100/100) controls at any time. |
| 1440 | 17884441 | A novel peroxisome proliferator--activated receptor alpha/gamma dual agonist ameliorates dyslipidemia and insulin resistance in prediabetic rhesus monkeys. |
| 1441 | 17884441 | Plasma triglyceride and apolipoprotein B-100 levels decreased, whereas apolipoprotein A-I increased during TAK-559 treatment. |
| 1442 | 17884445 | Serum sex hormone-binding globulin, a determinant of cardiometabolic disorders independent of abdominal obesity and insulin resistance in elderly men and women. |
| 1443 | 17884445 | The odds of low SHBG concentrations (<45 nmol/L in men, <55 nmol/L in women) for the likelihood of 2 types of dyslipidemias, MS, and diabetes were examined by regression analyses in standard models including age, smoking status, presence of abdominal obesity, and insulin resistance (homeostasis model assessment of insulin resistance). |
| 1444 | 17884445 | In both sexes, low SHBG was associated independently with high triglyceride/low high-density lipoprotein dyslipidemia and with MS, at significant 2.2- to 4.5-fold odds ratios, independent of waist circumference or homeostasis model assessment of insulin resistance index. |
| 1445 | 17884445 | Low SHBG among women was additionally associated with the likelihood of hypertriglyceridemia with elevated apolipoprotein B and-at borderline significance-with that of diabetes, again when adjusted for the same confounders. |
| 1446 | 17884445 | In an elderly population with prevalent MS, low SHBG levels significantly associate with high triglyceride/low high-density lipoprotein dyslipidemia, MS, and, in women alone, diabetes and a dyslipidemia marking small dense low-density lipoprotein particles, all independent of abdominal obesity and insulin resistance. |
| 1447 | 17907111 | This randomised, double-blind, parallel-group study assessed the effects of addition of the dual peroxisome proliferator-activated receptor (PPAR) alpha/gamma agonist, tesaglitazar, for 24 weeks to the therapeutic regimen of 392 poorly controlled (glycosylated haemoglobin [HbA1C] 7.5-10%) insulin-treated, type 2 diabetes patients. |
| 1448 | 17907111 | After 24 weeks, tesaglitazar caused greater improvements from baseline in triglycerides (p<0.0001), high-density lipoprotein cholesterol (HDL-C) (p<0.001), non-HDL-C (p<0.05), apolipoprotein (apo)A-I (p<0.05) and apoB levels (p<0.01) than placebo. |
| 1449 | 17917406 | Phospholipid transfer protein (PLTP) transfers phospholipids between apolipoprotein-B-containing lipoproteins (i.e., chylomicrons and very low-density lipoproteins) and HDL. |
| 1450 | 18056685 | Effect of apolipoprotein A-V on plasma triglyceride, lipoprotein size, and composition in genetically engineered mice. |
| 1451 | 18056685 | Transgenic (Tg) mice that overexpress the human apolipoprotein A-V gene (APOA5) yet lack an endogenous mouse apoa5 gene (APOA5 Tg mice) were generated. |
| 1452 | 18056685 | Subsequently, the effect of human apoA-V expression on plasma triglyceride (TG) concentration and lipoprotein and apolipoprotein distribution was determined and compared with that in mice deficient in apoA-V (apoa5(-/-) mice). |
| 1453 | 18056685 | SDS-PAGE analysis of the d < 1.063 g/ml plasma fraction revealed that the apoB-100/apoB-48 ratio was 14-fold higher in APOA5 Tg versus apoa5(-/-) mice and that the apoE/total apoB ratio was 7-fold greater in APOA5 Tg versus apoa5(-/-) mice. |
| 1454 | 18056685 | It is anticipated that a reduction in apoB-100/apoB-48 ratio as well as that for apoE/apoB would impair the uptake of VLDL and remnants in apoa5(-/-) mice, thereby contributing to increased plasma TG levels. |
| 1455 | 18056685 | Effect of apolipoprotein A-V on plasma triglyceride, lipoprotein size, and composition in genetically engineered mice. |
| 1456 | 18056685 | Transgenic (Tg) mice that overexpress the human apolipoprotein A-V gene (APOA5) yet lack an endogenous mouse apoa5 gene (APOA5 Tg mice) were generated. |
| 1457 | 18056685 | Subsequently, the effect of human apoA-V expression on plasma triglyceride (TG) concentration and lipoprotein and apolipoprotein distribution was determined and compared with that in mice deficient in apoA-V (apoa5(-/-) mice). |
| 1458 | 18056685 | SDS-PAGE analysis of the d < 1.063 g/ml plasma fraction revealed that the apoB-100/apoB-48 ratio was 14-fold higher in APOA5 Tg versus apoa5(-/-) mice and that the apoE/total apoB ratio was 7-fold greater in APOA5 Tg versus apoa5(-/-) mice. |
| 1459 | 18056685 | It is anticipated that a reduction in apoB-100/apoB-48 ratio as well as that for apoE/apoB would impair the uptake of VLDL and remnants in apoa5(-/-) mice, thereby contributing to increased plasma TG levels. |
| 1460 | 18160070 | The relation of leptin and insulin with obesity-related cardiovascular risk factors in US adults. |
| 1461 | 18160070 | This cross-sectional study, designed to examine whether leptin or insulin may mediate the endogenous relation of obesity with metabolic, inflammatory, and thrombogenic cardiovascular risk factors, included 522 men and 514 women aged >or=40 years who completed a physical examination during the third National Health and Nutrition Examination Survey. |
| 1462 | 18160070 | In multivariable analyses adjusted for race/ethnicity and lifestyle factors, waist circumference (WC) was positively associated with blood pressure, triglyceride, LDL cholesterol, total cholesterol:HDL ratio, apolipoprotein B, C-reactive protein (CRP), and fibrinogen concentrations, and negatively associated with HDL cholesterol and apolipoprotein A1 levels. |
| 1463 | 18160070 | The associations of WC with the metabolic CVD risk factors were largely attenuated after adjustment for insulin levels, while the associations of WC with the inflammatory and thrombogenic factors (CRP and fibrinogen, respectively) were largely explained by adjustment for leptin concentrations. |
| 1464 | 18160070 | However, leptin levels were not independently associated with CRP and fibrinogen in men and CRP in women when adjusted for WC. |
| 1465 | 18160070 | Positive associations of leptin and insulin with fibrinogen in women, independent of WC, were noted. |
| 1466 | 18160070 | These results suggest that insulin may be an important mediator of the association of obesity with metabolic but not inflammatory or thrombogenic CVD risk factors, while leptin does not appear to influence cardiovascular risk through a shared association with these risk factors. |
| 1467 | 18160070 | However, we cannot rule out the possibility that leptin and insulin influence cardiovascular risk in women through independent effects on fibrinogen concentrations. |
| 1468 | 18220807 | There are few epidemiological studies that show that glycated hemoglobin, fructosamine, an index of total non enzymatic glycated proteins in the blood, and glycated apolipoprotein B and other non enzymatic glycated proteins in the blood in non diabetic subjects are associated with cardiovascular diseases. |
| 1469 | 18220807 | In this paper we review: 1) the overall mechanisms of non enzymatic glycation of proteins; 2) the measurement of glycated hemoglobin, fructosamine, and glycated apolipoprotein B and their relationship with blood glucose levels in non diabetic subjects; 3) the association of glycated hemoglobin, fructosamine and glycated apolipoprotein B with cardiovascular disease. |
| 1470 | 18220807 | There are few epidemiological studies that show that glycated hemoglobin, fructosamine, an index of total non enzymatic glycated proteins in the blood, and glycated apolipoprotein B and other non enzymatic glycated proteins in the blood in non diabetic subjects are associated with cardiovascular diseases. |
| 1471 | 18220807 | In this paper we review: 1) the overall mechanisms of non enzymatic glycation of proteins; 2) the measurement of glycated hemoglobin, fructosamine, and glycated apolipoprotein B and their relationship with blood glucose levels in non diabetic subjects; 3) the association of glycated hemoglobin, fructosamine and glycated apolipoprotein B with cardiovascular disease. |
| 1472 | 18220942 | Dysregulation of lipoprotein metabolism in these circumstances may be caused by a combination of overproduction of VLDL apolipoprotein (apoB) B-100 and VLDL-apoC-III, decreased catabolism of apoB-containing particles, and increased catabolism of HDL apoA-I particles. |
| 1473 | 18220942 | Newer agents, including insulin sensitizers, cholesterol absorption inhibitors, CETP inhibitors, peroxisome proliferator-activated receptor-delta agonists and endocannabinoid-1 receptor blockers, have also been shown to improve plasma lipid and lipoprotein abnormalities in insulin resistant states; their mechanisms of action are at present being investigated. |
| 1474 | 18249172 | This is due to increased secretion and decreased clearance of apolipoprotein B-containing lipoproteins, coupled with decreased triglyceride secretion secondary to increased expression of Pgc-1 beta (Ppargc-1b), which promotes VLDL secretion, but decreased expression of Srebp-1c (Srebf1), Srebp-2 (Srebf2), and their targets, the lipogenic enzymes and the LDL receptor. |
| 1475 | 18277343 | ApoB/ApoA1 ratio and subclinical atherosclerosis. |
| 1476 | 18321395 | Momordica charantia (bitter melon) reduces plasma apolipoprotein B-100 and increases hepatic insulin receptor substrate and phosphoinositide-3 kinase interactions. |
| 1477 | 18321395 | Insulin resistance is characterized by significant down-regulation of hepatic insulin signalling as documented by attenuated phosphorylation of insulin receptor (IR), IR substrates 1 and 2, phosphoinositide-3 kinase, protein kinase B, and over-expression of phosphotyrosine phosphatase 1B. |
| 1478 | 18321395 | The aim of this study was to evaluate the effects of BMJ on plasma apoB levels and hepatic insulin signalling cascade in mice fed high-fat diet (HFD). |
| 1479 | 18321395 | The data indicate that BMJ not only improves glucose and insulin tolerance but also lowers plasma apoB-100 and apoB-48 in HFD-fed mice as well as modulates the phosphorylation status of IR and its downstream signalling molecules. |
| 1480 | 18321395 | Momordica charantia (bitter melon) reduces plasma apolipoprotein B-100 and increases hepatic insulin receptor substrate and phosphoinositide-3 kinase interactions. |
| 1481 | 18321395 | Insulin resistance is characterized by significant down-regulation of hepatic insulin signalling as documented by attenuated phosphorylation of insulin receptor (IR), IR substrates 1 and 2, phosphoinositide-3 kinase, protein kinase B, and over-expression of phosphotyrosine phosphatase 1B. |
| 1482 | 18321395 | The aim of this study was to evaluate the effects of BMJ on plasma apoB levels and hepatic insulin signalling cascade in mice fed high-fat diet (HFD). |
| 1483 | 18321395 | The data indicate that BMJ not only improves glucose and insulin tolerance but also lowers plasma apoB-100 and apoB-48 in HFD-fed mice as well as modulates the phosphorylation status of IR and its downstream signalling molecules. |
| 1484 | 18321395 | Momordica charantia (bitter melon) reduces plasma apolipoprotein B-100 and increases hepatic insulin receptor substrate and phosphoinositide-3 kinase interactions. |
| 1485 | 18321395 | Insulin resistance is characterized by significant down-regulation of hepatic insulin signalling as documented by attenuated phosphorylation of insulin receptor (IR), IR substrates 1 and 2, phosphoinositide-3 kinase, protein kinase B, and over-expression of phosphotyrosine phosphatase 1B. |
| 1486 | 18321395 | The aim of this study was to evaluate the effects of BMJ on plasma apoB levels and hepatic insulin signalling cascade in mice fed high-fat diet (HFD). |
| 1487 | 18321395 | The data indicate that BMJ not only improves glucose and insulin tolerance but also lowers plasma apoB-100 and apoB-48 in HFD-fed mice as well as modulates the phosphorylation status of IR and its downstream signalling molecules. |
| 1488 | 18418429 | In all subjects, basal glucose, cholesterol (total, HDL, and LDL), oxidized LDL (OxLDL), triglycerides, apolipoprotein (apo)A1, apoB, and apoE, nonesterified fatty acids, insulin, testosterone, sex hormone-binding globulin, homeostasis model assessment (HOMA) index, and free androgen index were determined in the follicular phase of the cycle. |
| 1489 | 18418429 | Elevated OxLDL and the relation of apoE and nonesterified fatty acids with insulin resistance suggest that women with PCOS are at increased risk for premature atherosclerosis. |
| 1490 | 18421072 | The aim of this study was to evaluate the impact of adipocyte fatty acid binding protein 4 (FABP4) on the lipid profile in type 2 diabetic subjects. |
| 1491 | 18421072 | Plasma levels of FABP4 and adiponectin and an extensive lipid profile were analyzed in 169 type 2 diabetic subjects and 105 controls. |
| 1492 | 18421072 | In type 2 diabetic subjects, FABP4 was positively correlated with plasma triglycerides (P = 0.007), apolipoprotein C-III (apoC-III) (P = 0.009), and all the components of triglyceride-rich lipoproteins, including VLDL triglycerides (P = 0.002), VLDL-cholesterol (P = 0.001), and VLDL apoB (P = 0.001). |
| 1493 | 18421072 | These correlations are not significantly affected by age, gender, body mass index, adiponectin, insulin, or any pharmacological treatment. |
| 1494 | 18421072 | The associations are even stronger when the FABP4/adiponectin ratio is considered. |
| 1495 | 18421072 | High FABP4 and low adiponectin levels are independent predictors of atherogenic dyslipidemia. |
| 1496 | 18421072 | In conclusion, FABP4 plasma concentrations hold strong potential for development as a clinical biomarker for atherogenic dyslipidemia, independent of obesity and insulin resistance, in type 2 diabetic subjects. |
| 1497 | 18457010 | Triglycerides, HDL-cholesterol, apolipoprotein B, apolipoprotein A1, glucose and HOMA index, were measured too. |
| 1498 | 18501722 | Further, a moderate improvement of dyslipidemia by metformin was reported, and therefore, the effect of metformin on the release of apolipoprotein B (ApoB) and ApoE in primary human hepatocytes was determined. |
| 1499 | 18501722 | Metformin at 0.5 and 1 mM reduced hepatic ApoB secretion but ApoE was not altered. |
| 1500 | 18501722 | Metformin is well known to stimulate the AMP kinase that subsequently reduces hepatic nuclear factor 4-alpha (HNF4-alpha) and HNF4-alpha regulated genes like ApoB. |
| 1501 | 18501722 | However, HNF4-alpha was only diminished by 1 mM metformin and ApoB mRNA was not suppressed indicating that this pathway may not explain reduced ApoB release. |
| 1502 | 18501722 | Further, a moderate improvement of dyslipidemia by metformin was reported, and therefore, the effect of metformin on the release of apolipoprotein B (ApoB) and ApoE in primary human hepatocytes was determined. |
| 1503 | 18501722 | Metformin at 0.5 and 1 mM reduced hepatic ApoB secretion but ApoE was not altered. |
| 1504 | 18501722 | Metformin is well known to stimulate the AMP kinase that subsequently reduces hepatic nuclear factor 4-alpha (HNF4-alpha) and HNF4-alpha regulated genes like ApoB. |
| 1505 | 18501722 | However, HNF4-alpha was only diminished by 1 mM metformin and ApoB mRNA was not suppressed indicating that this pathway may not explain reduced ApoB release. |
| 1506 | 18501722 | Further, a moderate improvement of dyslipidemia by metformin was reported, and therefore, the effect of metformin on the release of apolipoprotein B (ApoB) and ApoE in primary human hepatocytes was determined. |
| 1507 | 18501722 | Metformin at 0.5 and 1 mM reduced hepatic ApoB secretion but ApoE was not altered. |
| 1508 | 18501722 | Metformin is well known to stimulate the AMP kinase that subsequently reduces hepatic nuclear factor 4-alpha (HNF4-alpha) and HNF4-alpha regulated genes like ApoB. |
| 1509 | 18501722 | However, HNF4-alpha was only diminished by 1 mM metformin and ApoB mRNA was not suppressed indicating that this pathway may not explain reduced ApoB release. |
| 1510 | 18501722 | Further, a moderate improvement of dyslipidemia by metformin was reported, and therefore, the effect of metformin on the release of apolipoprotein B (ApoB) and ApoE in primary human hepatocytes was determined. |
| 1511 | 18501722 | Metformin at 0.5 and 1 mM reduced hepatic ApoB secretion but ApoE was not altered. |
| 1512 | 18501722 | Metformin is well known to stimulate the AMP kinase that subsequently reduces hepatic nuclear factor 4-alpha (HNF4-alpha) and HNF4-alpha regulated genes like ApoB. |
| 1513 | 18501722 | However, HNF4-alpha was only diminished by 1 mM metformin and ApoB mRNA was not suppressed indicating that this pathway may not explain reduced ApoB release. |
| 1514 | 18520050 | The blood glucose, hemoglobin A1c, lipid metabolic parameters and hepatic glycogen and triglyceride were measured, and histopathology and peroxisome proliferator-activated receptors (PPARs) alpha/delta/gamma expression of liver were determined by hematoxylin eosin and immunohistochemical staining. |
| 1515 | 18520050 | Berberine restored the increased blood glucose, hemoglobin A1c, total cholesterol, triglyceride, low density lipoprotein-cholesterol, apolipoprotein B and the decreased high density lipoprotein-cholesterol, apolipoprotein AI levels in diabetic rats to near the control ones. |
| 1516 | 18520050 | Berberine increased PPARalpha/delta expression and reduced PPARgamma expression in liver of diabetic rat to near the control ones. |
| 1517 | 18521458 | Apolipoprotein B/apolipoprotein A-I ratio in relation to various definitions of metabolic syndrome among Saudi patients with type 2 diabetes mellitus. |
| 1518 | 18549334 | Mipomersen (ISIS 301012) inhibits human apolipoprotein (apo)B-100 synthesis and lowers circulating apoB and low-density lipoprotein cholesterol levels. |
| 1519 | 18676970 | Concentration of apolipoprotein B is comparable with the apolipoprotein B/apolipoprotein A-I ratio and better than routine clinical lipid measurements in predicting coronary heart disease mortality: findings from a multi-ethnic US population. |
| 1520 | 18693145 | In particular, increase in apolipoprotein B48 synthesis has been demonstrated in animal models of diabetes and insulin resistance. |
| 1521 | 18702965 | Statin therapy alters the relationship between apolipoprotein B and low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol targets in high-risk patients: the MERCURY II (Measuring Effective Reductions in Cholesterol Using Rosuvastatin) trial. |
| 1522 | 18720163 | Evaluation of serum biomarkers in nutritional disorders: glycated apolipoprotein B, fasting serum glucose, fructosamine, stable and labile glycated hemoglobin in diabetic and non-diabetic subjects. |
| 1523 | 18720163 | Our aim is to evaluate, in diabetic and non diabetic subjects, the relationship of ApoB-G with serum fasting glucose, fructosamine, stable and labile fractions of glycated hemoglobin ((S)HbA(1c), (L)HbA(1c), respectively) and insulin. |
| 1524 | 18777156 | Our aim was to study, at the same glycemic control, how treatment with either the insulin secretagogue repaglinide or exogenous insulin aspart affects endogenous insulin secretion, plasma insulin and IAPP (islet amyloid polypeptide) levels, GH-IGF (growth hormone-insulin-like growth factor) axis and plasma lipoprotein concentrations in patients with type 2 diabetes. |
| 1525 | 18777156 | Blood glucose, C-peptide, free human insulin, free total (human and analogue) insulin, proinsulin, IAPP, IGF-I, IGFBP-1 (IGF binding protein-1), GHBP (growth hormone binding protein) and plasma lipoprotein concentrations were measured. |
| 1526 | 18777156 | Proinsulin, GHBP were higher and IAPP levels tended to be higher during repaglinide compared to insulin aspart. |
| 1527 | 18777156 | Postprandial plasma total cholesterol, triglycerides and apolipoprotein B concentrations were higher on repaglinide than on insulin aspart treatment. |
| 1528 | 18940384 | Plasma activity of MMP-2 and MMP-9, high-sensitivity C-reactive protein concentration, dense low-density lipoprotein, and insulin-resistance markers were measured in 38 nondiabetic women with (n = 19) and without (n = 19) MetS. |
| 1529 | 18940384 | MMP-2 activity positively correlated with waist, homeostasis model assessment, and high-sensitivity C-reactive protein (P < .02) as well as with apolipoprotein B, dense low-density lipoprotein, triglycerides/high-density lipoprotein cholesterol index (P < .001) and negatively with high-density lipoprotein cholesterol (P < .002). |
| 1530 | 18940393 | We assessed body mass index, hemoglobin A(1c) (HbA(1c)), fasting plasma glucose (FPG), postprandial plasma glucose (PPG), fasting plasma insulin (FPI), postprandial plasma insulin (PPI), lipid profile, lipoprotein parameters, and lipoprotein (a) at baseline and after 3 and 6 months. |
| 1531 | 18940393 | No high-density lipoprotein cholesterol, apolipoprotein A-I, apolipoprotein B, and lipoprotein (a) changes were present in both groups with respect to the baseline values. |
| 1532 | 18945448 | Relationship of apoE polymorphism with lipoprotein(a), apoA, apoB and lipid levels in atherosclerotic infarct. |
| 1533 | 18991244 | The effects of the different egg diets on apolipoprotein A1 and B (Apo A1 and B), lipoprotein (a), creatinine, cystatin C, C-reactive protein, serum amyloid protein A, interleukin 6, triglycerides, glucose, total-, high-density lipoprotein and low-density lipo-protein cholesterol concentrations were analyzed. |
| 1534 | 18991244 | Consumption of omega-3 enriched eggs resulted in higher levels of ApoA1, lower ApoB/ApoA1 ratio and lower plasma glucose. |
| 1535 | 19147732 | Targets of statin therapy: LDL cholesterol, non-HDL cholesterol, and apolipoprotein B in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS). |
| 1536 | 19264209 | The non fasting ApoB/ApoA1 ratio was superior to any of the cholesterol ratios for estimation of the risk of acute myocardial infection in all ethnic groups. |
| 1537 | 19264209 | Anti-IL-5 and anti-IL-6 antibodies were effective for the treatment of respectively hypereosinophilic syndrome and rheumatoid arthritis. |
| 1538 | 19273907 | To assess the hypothesis that both hepatic and peripheral insulin resistance contribute to atherogenesis, we crossed mice deficient for the LDL receptor (Ldlr-/- mice) with mice that express low levels of IR in the liver and lack IR in peripheral tissues (the L1B6 mouse strain). |
| 1539 | 19273907 | Unexpectedly, compared with Ldlr-/- controls, L1B6Ldlr-/- mice fed a Western diet showed reduced VLDL and LDL levels, reduced atherosclerosis, decreased hepatic AKT signaling, decreased expression of genes associated with lipogenesis, and diminished VLDL apoB and lipid secretion. |
| 1540 | 19273907 | These findings suggest a dual action of hepatic IR on lipoprotein levels, in which the ability to increase VLDL apoB and lipid secretion via AKT/GSK is offset by upregulation of Ldlr. |
| 1541 | 19273907 | To assess the hypothesis that both hepatic and peripheral insulin resistance contribute to atherogenesis, we crossed mice deficient for the LDL receptor (Ldlr-/- mice) with mice that express low levels of IR in the liver and lack IR in peripheral tissues (the L1B6 mouse strain). |
| 1542 | 19273907 | Unexpectedly, compared with Ldlr-/- controls, L1B6Ldlr-/- mice fed a Western diet showed reduced VLDL and LDL levels, reduced atherosclerosis, decreased hepatic AKT signaling, decreased expression of genes associated with lipogenesis, and diminished VLDL apoB and lipid secretion. |
| 1543 | 19273907 | These findings suggest a dual action of hepatic IR on lipoprotein levels, in which the ability to increase VLDL apoB and lipid secretion via AKT/GSK is offset by upregulation of Ldlr. |
| 1544 | 19344229 | By study end, HbA1c, fasting plasma glucose (FPG), LDL-C, total cholesterol (TC), non-high-density lipoprotein cholesterol (HDL-C), apolipoprotein B (ApoB), and high-sensitivity C-reactive protein (hsCRP) were significantly reduced with COL versus placebo. |
| 1545 | 19388968 | Carotid intima-media thickness and apolipoprotein B/apolipoprotein A-I ratio in middle-aged patients with Type 2 diabetes. |
| 1546 | 19413703 | However, this potentially anti-atherogenic role of PLTP has been challenged recently by another picture: PLTP arose as a pro-atherogenic factor through its ability to increase the production of apolipoprotein B-containing lipoproteins, to decrease their antioxidative protection and to trigger inflammation. |
| 1547 | 19413703 | Both PLTP and related cholesteryl ester transfer protein (CETP) are secreted proteins, and adipose tissue is an important contributor to the systemic pools of these two proteins. |
| 1548 | 19413703 | Coincidently, high levels of PLTP and CETP have been found in the plasma of obese patients. |
| 1549 | 19413703 | PLTP activity and mass have been reported to be abnormally elevated in type 2 diabetes mellitus (T2DM) and insulin-resistant states, and this elevation is frequently associated with hypertriglyceridemia and obesity. |
| 1550 | 19413703 | This review article presents the state of knowledge on the implication of PLTP in lipoprotein metabolism, on its atherogenic potential, and the complexity of its implication in obesity, insulin resistance and T2DM. |
| 1551 | 19481769 | The aim of the present study was to compare the ability of these 3 clinical approaches to identify individuals at increased cardiometabolic risk as suggested by the presence of deteriorated markers such as hyperinsulinemia, elevated apolipoprotein B levels, small low-density lipoprotein particles, high C-reactive protein concentrations, and low adiponectin levels. |
| 1552 | 19481769 | Men with the hypertriglyceridemic waist phenotype were characterized by alterations in their lipoprotein-lipid profile that included small low-density lipoprotein particles, increased apolipoprotein B and insulin levels, as well as reduced adiponectin concentrations, which were similar to individuals meeting the NCEP-ATP III or the IDF criteria. |
| 1553 | 19481769 | The aim of the present study was to compare the ability of these 3 clinical approaches to identify individuals at increased cardiometabolic risk as suggested by the presence of deteriorated markers such as hyperinsulinemia, elevated apolipoprotein B levels, small low-density lipoprotein particles, high C-reactive protein concentrations, and low adiponectin levels. |
| 1554 | 19481769 | Men with the hypertriglyceridemic waist phenotype were characterized by alterations in their lipoprotein-lipid profile that included small low-density lipoprotein particles, increased apolipoprotein B and insulin levels, as well as reduced adiponectin concentrations, which were similar to individuals meeting the NCEP-ATP III or the IDF criteria. |
| 1555 | 19498343 | Plasma concentrations of the acute-phase reactant serum amyloid A (SAA) are elevated in both obesity and cardiovascular disease. |
| 1556 | 19498343 | Moreover, SAA was localized with apoB-containing lipoproteins and biglycan in the vascular wall. |
| 1557 | 19498343 | Taken together, these data suggest male apoE-deficient mice are a model of metabolic syndrome and that chronic low level inflammation associated with increased SAA concentrations may mediate atherosclerotic lesion formation. |
| 1558 | 19505224 | Atorvastatin affects low density lipoprotein and non-high density lipoprotein cholesterol relations with apolipoprotein B in type 2 diabetes mellitus: modification by triglycerides and cholesteryl ester transfer protein. |
| 1559 | 19520708 | The joint effects of apolipoprotein B, apolipoprotein A1, LDL cholesterol, and HDL cholesterol on risk: 3510 cases of acute myocardial infarction and 9805 controls. |
| 1560 | 19582722 | PTMs, such as glycosylation and phosphorylation of apolipoprotein B100 (apoB), are known to be involved with modulating the metabolism of apoB-containing lipoproteins. |
| 1561 | 19592617 | Naringenin prevents dyslipidemia, apolipoprotein B overproduction, and hyperinsulinemia in LDL receptor-null mice with diet-induced insulin resistance. |
| 1562 | 19604523 | The following variables were assessed at baseline; after washout; and at 1, 2, and 3 months of treatment: body mass index, fasting plasma glucose, glycosylated hemoglobin, total cholesterol, LDL cholesterol, LDL subclasses, LDL size, high-density lipoprotein cholesterol, triglycerides, apolipoprotein A-1, and apolipoprotein B-100. |
| 1563 | 19605528 | Soy protein reduces serum LDL cholesterol and the LDL cholesterol:HDL cholesterol and apolipoprotein B:apolipoprotein A-I ratios in adults with type 2 diabetes. |
| 1564 | 19605528 | SPI consumption reduced serum LDL cholesterol (P = 0.04), LDL cholesterol:HDL cholesterol (P = 0.02), and apolipoprotein B:apolipoprotein A-I (P = 0.05) compared with MPI. |
| 1565 | 19605528 | SPI did not affect serum total cholesterol, HDL cholesterol, triacylglycerol, apolipoprotein B, or apolipoprotein A-I. |
| 1566 | 19605528 | Soy protein reduces serum LDL cholesterol and the LDL cholesterol:HDL cholesterol and apolipoprotein B:apolipoprotein A-I ratios in adults with type 2 diabetes. |
| 1567 | 19605528 | SPI consumption reduced serum LDL cholesterol (P = 0.04), LDL cholesterol:HDL cholesterol (P = 0.02), and apolipoprotein B:apolipoprotein A-I (P = 0.05) compared with MPI. |
| 1568 | 19605528 | SPI did not affect serum total cholesterol, HDL cholesterol, triacylglycerol, apolipoprotein B, or apolipoprotein A-I. |
| 1569 | 19605528 | Soy protein reduces serum LDL cholesterol and the LDL cholesterol:HDL cholesterol and apolipoprotein B:apolipoprotein A-I ratios in adults with type 2 diabetes. |
| 1570 | 19605528 | SPI consumption reduced serum LDL cholesterol (P = 0.04), LDL cholesterol:HDL cholesterol (P = 0.02), and apolipoprotein B:apolipoprotein A-I (P = 0.05) compared with MPI. |
| 1571 | 19605528 | SPI did not affect serum total cholesterol, HDL cholesterol, triacylglycerol, apolipoprotein B, or apolipoprotein A-I. |
| 1572 | 19657359 | The DASH-diet group complied with the diet as shown by significant reductions in systolic (P<0.001) and diastolic (P=0.005) BP, and in plasma C-reactive protein (P<0.01), LDL-cholesterol (P<0.01) and apolipoprotein B (P=0.001), a novel finding. |
| 1573 | 19680556 | We re-sequenced all exons, intron-exon boundaries and selected conserved non-coding sequences of candidate genes involved in aging-related processes, including dietary restriction (PPARG, PPARGC1A, SIRT1, SIRT3, UCP2, UCP3), metabolism (IGF1R, APOB, SCD), autophagy (BECN1, FRAP1), stem cell activation (NOTCH1, DLL1), tumor suppression (TP53, CDKN2A, ING1), DNA methylation (TRDMT1, DNMT3A, DNMT3B) Progeria syndromes (LMNA, ZMPSTE24, KL) and stress response (CRYAB, HSPB2). |
| 1574 | 19914667 | Adiponectin is independently associated with apolipoprotein B to A-1 ratio in Koreans. |
| 1575 | 19914667 | The aim of this study was to assess the association of serum apo B/A-1 ratio with insulin resistance and adiponectin in patients with different grades of glucose intolerance. |
| 1576 | 19914667 | There were significant differences in metabolic parameters among the groups, including waist circumference, insulin, HOMA-IR, and apo B/A-1 ratio, which increased sequentially with glucose intolerance, whereas adiponectin level decreased with increasing severity of glucose intolerance. |
| 1577 | 19914667 | The apo B/A-1 ratio was significantly correlated with TC, triglycerides, LDL-C, HDL-C, adiponectin, and HOMA-IR in normal glucose tolerance, impaired fasting glucose, and type 2 diabetes mellitus. |
| 1578 | 19914667 | In conclusion, apo B/A-1 ratio was significantly associated with insulin resistance according to glucose intolerance; and serum adiponectin was an important independent factor associated with apo B/A-1 ratio in Koreans. |
| 1579 | 19951850 | Although there were differences in the prevalences of hyperlipidemia and hypertension between the sexes, adjusted logistic regression analysis demonstrated little contribution of diet and exercise habits to the risks of diabetes, hyperlipidemia, or hypertension after adjusting for age, sex, waist-to-hip ratio, serum blood sugar levels, cholesterol, triglycerides, apolipoprotein A1, apolipoprotein B, glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, creatinine, uric acid, and blood pressure. |
| 1580 | 20005515 | The effect of PPAR-alpha agonism on apolipoprotein metabolism in humans. |
| 1581 | 20005515 | The potent and specific PPAR-alpha agonist LY518674, reduced VLDL apoB-100 levels through enhanced fractional catabolism similar to what is seen with fibrates. |
| 1582 | 20005515 | The changes in apoB metabolism in response to PPAR-alpha activation with fibrates and specific PPAR-alpha agonists would be expected to reduce the risk of cardiovascular disease. |
| 1583 | 20005515 | The effect of PPAR-alpha agonism on apolipoprotein metabolism in humans. |
| 1584 | 20005515 | The potent and specific PPAR-alpha agonist LY518674, reduced VLDL apoB-100 levels through enhanced fractional catabolism similar to what is seen with fibrates. |
| 1585 | 20005515 | The changes in apoB metabolism in response to PPAR-alpha activation with fibrates and specific PPAR-alpha agonists would be expected to reduce the risk of cardiovascular disease. |
| 1586 | 20019460 | The mentioned protective protein dysfunctions, firstly described in a general population to date, are high-density lipoprotein (HDL), apolipoprotein (apo) A-I, A-II, and apoC-III, apart from adiponectin. |
| 1587 | 20019460 | Based on published findings of the TARF study, this review discusses the role of inflammatory mediators such as elevated C-reactive protein (CRP), apoB, apoC-III, fibrinogen, and low adiponectin serum levels in cardiometabolic risk comprising MetS, type 2 diabetes, and CHD, the degree of independence of these mediators from the ATP-III-defined MetS, and the influence of sex. |
| 1588 | 20019460 | Moreover, it is emphasized that dysfunctions of adiponectin and protective proteins related to HDL particles increase not only cardiometabolic risk significantly but also CHD risk among half of Turkish adults in a magnitude similar to or greater than that associated with traditional risk factors. |
| 1589 | 20116212 | Apolipoprotein A-I positively associated with diabetes in women independently of apolipoprotein E genotype and apolipoprotein B levels. |
| 1590 | 20185740 | Effect of ezetimibe on hepatic fat, inflammatory markers, and apolipoprotein B-100 kinetics in insulin-resistant obese subjects on a weight loss diet. |
| 1591 | 20190014 | PPARgamma agonists improve insulin sensitivity and hyperglycemia and are effective in treating type 2 diabetes mellitus (T2DM), whereas PPARalpha agonists are used to treat dyslipidemia and atherosclerosis. |
| 1592 | 20190014 | The goal here was to examine the efficacy of a selective PPARalpha agonist {(S)-3-[3-(1-carboxy-1-methyl-ethoxy)-phenyl]-piperidine-1-carboxylic acid 4-trifluoromethyl-benzyl ester; CP-900691} on lipid, glycemic, and inflammation indices in 14 cynomolgus monkeys with spontaneous T2DM maintained on daily insulin therapy. |
| 1593 | 20190014 | CP-900691 treatment increased plasma high-density lipoprotein cholesterol (HDLC) (33 +/- 3 to 60 +/- 4 mg/dL, p < 0.001) and apolipoprotein A1 (96 +/- 5 to 157 +/- 5 mg/dL, p < 0.001), reduced plasma triglycerides (547 +/- 102 to 356 +/- 90 mg/dL, p < 0.01), and apolipoprotein B (62 +/- 3 to 45 +/- 3 mg/dL, p < 0.01), improved the lipoprotein index (HDL to non-HDLC ratio; 0.28 +/- 0.06 to 0.79 +/- 0.16, p < 0.001), decreased body weight (p < 0.01) and C-reactive protein (CRP) (1700 +/- 382 to 304 +/- 102 ng/ml, p < 0.01), and increased adiponectin (1697 +/- 542 to 4242 +/- 1070 ng/ml, p < 0.001) compared with baseline. |
| 1594 | 20213498 | The ApoB/ApoA1 ratio is associated with metabolic syndrome and its components in a Chinese population. |
| 1595 | 20213498 | In this study, we assessed whether the apolipoprotein B/apolipoprotein A1 ratio (ApoB/ApoA1) is related to metabolic syndrome (MS) and its components in an urban Chinese population. |
| 1596 | 20213498 | The high ApoB/ApoA1 group was defined as the gender-specific upper quartile of the ApoB/ApoA1 ratio. |
| 1597 | 20213498 | The ApoB/ApoA1 ratio was significantly higher in subjects with MS, compared to those without (p < 0.05). |
| 1598 | 20213498 | After adjusting for age and gender, subjects with MS (odds ratio [OR] = 3.5) or IR (OR = 2.3) were more likely to be in the high ApoB/ApoA1 group. |
| 1599 | 20213498 | The ApoB/ApoA1 ratio increased significantly as the number of MS components increased (p < 0.05). |
| 1600 | 20213498 | Taken together, these data demonstrate that the ApoB/ApoA1 ratio is strongly associated with MS and its components in an urban Chinese population. |
| 1601 | 20213498 | The ApoB/ApoA1 ratio is associated with metabolic syndrome and its components in a Chinese population. |
| 1602 | 20213498 | In this study, we assessed whether the apolipoprotein B/apolipoprotein A1 ratio (ApoB/ApoA1) is related to metabolic syndrome (MS) and its components in an urban Chinese population. |
| 1603 | 20213498 | The high ApoB/ApoA1 group was defined as the gender-specific upper quartile of the ApoB/ApoA1 ratio. |
| 1604 | 20213498 | The ApoB/ApoA1 ratio was significantly higher in subjects with MS, compared to those without (p < 0.05). |
| 1605 | 20213498 | After adjusting for age and gender, subjects with MS (odds ratio [OR] = 3.5) or IR (OR = 2.3) were more likely to be in the high ApoB/ApoA1 group. |
| 1606 | 20213498 | The ApoB/ApoA1 ratio increased significantly as the number of MS components increased (p < 0.05). |
| 1607 | 20213498 | Taken together, these data demonstrate that the ApoB/ApoA1 ratio is strongly associated with MS and its components in an urban Chinese population. |
| 1608 | 20213498 | The ApoB/ApoA1 ratio is associated with metabolic syndrome and its components in a Chinese population. |
| 1609 | 20213498 | In this study, we assessed whether the apolipoprotein B/apolipoprotein A1 ratio (ApoB/ApoA1) is related to metabolic syndrome (MS) and its components in an urban Chinese population. |
| 1610 | 20213498 | The high ApoB/ApoA1 group was defined as the gender-specific upper quartile of the ApoB/ApoA1 ratio. |
| 1611 | 20213498 | The ApoB/ApoA1 ratio was significantly higher in subjects with MS, compared to those without (p < 0.05). |
| 1612 | 20213498 | After adjusting for age and gender, subjects with MS (odds ratio [OR] = 3.5) or IR (OR = 2.3) were more likely to be in the high ApoB/ApoA1 group. |
| 1613 | 20213498 | The ApoB/ApoA1 ratio increased significantly as the number of MS components increased (p < 0.05). |
| 1614 | 20213498 | Taken together, these data demonstrate that the ApoB/ApoA1 ratio is strongly associated with MS and its components in an urban Chinese population. |
| 1615 | 20213498 | The ApoB/ApoA1 ratio is associated with metabolic syndrome and its components in a Chinese population. |
| 1616 | 20213498 | In this study, we assessed whether the apolipoprotein B/apolipoprotein A1 ratio (ApoB/ApoA1) is related to metabolic syndrome (MS) and its components in an urban Chinese population. |
| 1617 | 20213498 | The high ApoB/ApoA1 group was defined as the gender-specific upper quartile of the ApoB/ApoA1 ratio. |
| 1618 | 20213498 | The ApoB/ApoA1 ratio was significantly higher in subjects with MS, compared to those without (p < 0.05). |
| 1619 | 20213498 | After adjusting for age and gender, subjects with MS (odds ratio [OR] = 3.5) or IR (OR = 2.3) were more likely to be in the high ApoB/ApoA1 group. |
| 1620 | 20213498 | The ApoB/ApoA1 ratio increased significantly as the number of MS components increased (p < 0.05). |
| 1621 | 20213498 | Taken together, these data demonstrate that the ApoB/ApoA1 ratio is strongly associated with MS and its components in an urban Chinese population. |
| 1622 | 20213498 | The ApoB/ApoA1 ratio is associated with metabolic syndrome and its components in a Chinese population. |
| 1623 | 20213498 | In this study, we assessed whether the apolipoprotein B/apolipoprotein A1 ratio (ApoB/ApoA1) is related to metabolic syndrome (MS) and its components in an urban Chinese population. |
| 1624 | 20213498 | The high ApoB/ApoA1 group was defined as the gender-specific upper quartile of the ApoB/ApoA1 ratio. |
| 1625 | 20213498 | The ApoB/ApoA1 ratio was significantly higher in subjects with MS, compared to those without (p < 0.05). |
| 1626 | 20213498 | After adjusting for age and gender, subjects with MS (odds ratio [OR] = 3.5) or IR (OR = 2.3) were more likely to be in the high ApoB/ApoA1 group. |
| 1627 | 20213498 | The ApoB/ApoA1 ratio increased significantly as the number of MS components increased (p < 0.05). |
| 1628 | 20213498 | Taken together, these data demonstrate that the ApoB/ApoA1 ratio is strongly associated with MS and its components in an urban Chinese population. |
| 1629 | 20213498 | The ApoB/ApoA1 ratio is associated with metabolic syndrome and its components in a Chinese population. |
| 1630 | 20213498 | In this study, we assessed whether the apolipoprotein B/apolipoprotein A1 ratio (ApoB/ApoA1) is related to metabolic syndrome (MS) and its components in an urban Chinese population. |
| 1631 | 20213498 | The high ApoB/ApoA1 group was defined as the gender-specific upper quartile of the ApoB/ApoA1 ratio. |
| 1632 | 20213498 | The ApoB/ApoA1 ratio was significantly higher in subjects with MS, compared to those without (p < 0.05). |
| 1633 | 20213498 | After adjusting for age and gender, subjects with MS (odds ratio [OR] = 3.5) or IR (OR = 2.3) were more likely to be in the high ApoB/ApoA1 group. |
| 1634 | 20213498 | The ApoB/ApoA1 ratio increased significantly as the number of MS components increased (p < 0.05). |
| 1635 | 20213498 | Taken together, these data demonstrate that the ApoB/ApoA1 ratio is strongly associated with MS and its components in an urban Chinese population. |
| 1636 | 20213498 | The ApoB/ApoA1 ratio is associated with metabolic syndrome and its components in a Chinese population. |
| 1637 | 20213498 | In this study, we assessed whether the apolipoprotein B/apolipoprotein A1 ratio (ApoB/ApoA1) is related to metabolic syndrome (MS) and its components in an urban Chinese population. |
| 1638 | 20213498 | The high ApoB/ApoA1 group was defined as the gender-specific upper quartile of the ApoB/ApoA1 ratio. |
| 1639 | 20213498 | The ApoB/ApoA1 ratio was significantly higher in subjects with MS, compared to those without (p < 0.05). |
| 1640 | 20213498 | After adjusting for age and gender, subjects with MS (odds ratio [OR] = 3.5) or IR (OR = 2.3) were more likely to be in the high ApoB/ApoA1 group. |
| 1641 | 20213498 | The ApoB/ApoA1 ratio increased significantly as the number of MS components increased (p < 0.05). |
| 1642 | 20213498 | Taken together, these data demonstrate that the ApoB/ApoA1 ratio is strongly associated with MS and its components in an urban Chinese population. |
| 1643 | 20363402 | Open tubular capillary electrochromatography: a useful microreactor for collagen I glycation and interaction studies with low-density lipoprotein particles. |
| 1644 | 20363402 | One of the consequences of high level of glucose in the blood circulation is glycation of long-lived proteins, such as collagen I, the most abundant component of the extracellular matrix (ECM) in the arterial wall. |
| 1645 | 20363402 | AGEs, as reactive molecules, can provoke cross-linking of collagen I fibrils. |
| 1646 | 20363402 | Since binding of low-density lipoproteins (LDLs) to the ECM of the inner layer of the arterial wall, the intima, has been implicated to be involved in the onset of the development of an atherosclerotic plaque, collagen modifications, which can affect the affinity of native and oxidized LDL for collagen I, can promote the entrapment of LDLs in the intima and accelerate the progression of atherosclerosis. |
| 1647 | 20363402 | In this study, open tubular capillary electrochromatography is proposed as a new microreactor to study in situ glycation of collagen I. |
| 1648 | 20363402 | The kinetics of glycation was first investigated in a fused silica collagen I-coated capillary. |
| 1649 | 20363402 | Native and oxidized LDL, and selected peptide fragments from apolipoprotein B-100, the protein covering LDL particles, were injected as marker compounds to clarify the interactions between LDLs and the glycated collagen I coating. |
| 1650 | 20363402 | Atomic force microscopy images complemented our studies, highlighting the difference between unmodified and glycated collagen I surfaces. |
| 1651 | 20368963 | Single nucleotide polymorphism (SNP) in adiponectin gene has been associated with insulin resistance, diabetes, and cardiovascular disease (CVD). |
| 1652 | 20368963 | Male subjects with T/T genotype showed significantly lower level of adiponectin and HDL-cholesterol and significantly higher C-reactive protein (CRP) level compared to G/G and G/T genotypes. |
| 1653 | 20368963 | In G/G genotype, protein intake was negatively correlated to body weight, BMI, and waist circumference, and there were positive correlation between carbohydrate intake and BMI, waist-hip ratio, and ApoB/apoA-1 ratio in G/T genotype. |
| 1654 | 20494664 | At 3 months, the mean BMI had decreased (34.4 to 31.7 kg/m(2), p <0.001), BNP had increased (median 18 to 28 pg/ml, p <0.001), and low-density lipoprotein, C-reactive protein, apolipoprotein B (all p <0.002), and angina frequency (p = 0.017) and severity (p = 0.052) had decreased. |
| 1655 | 20494664 | The percentage of change in BNP was inversely associated with the percentage of change in insulin (r = -0.339, p = 0.005, n = 63 nondiabetics). |
| 1656 | 20538481 | Among traditional cardiovascular risk factors, apolipoprotein (apo)B/apoA1 ratio is considered to have the strongest predictive value for ischemic stroke. |
| 1657 | 20538481 | In this case-control study, we evaluated apoB/apoA1 ratio as a predictor of ischemic stroke in a cohort of elderly subjects. |
| 1658 | 20538481 | The association between apoB/apoA1 ratio and stroke was determined by multivariate logistic regression modeling after adjusting for potential confounding factors, including lipid parameters. |
| 1659 | 20538481 | Stroke patients exhibited a higher apoB/apoA1 ratio than controls (1.04±0.33 vs 0.86±0.22; P<.001). |
| 1660 | 20538481 | In univariate analysis, crude odds ratio (OR) for apoB/apoA1 ratio was 1.27 per 0.1 increase (95% confidence interval [CI]=1.15-1.39; P<.001). |
| 1661 | 20538481 | Compared with subjects with an apoB/apoA1 ratio in the lowest quartile, those within the highest quartile had a 6.3-fold increase in the odds of suffering an ischemic stroke (95% CI=3.17-12.48; P<.001). |
| 1662 | 20538481 | Our findings support elevated apoB/apoA1 ratio as an independent predictor of ischemic stroke in individuals over age 70. |
| 1663 | 20538481 | Among traditional cardiovascular risk factors, apolipoprotein (apo)B/apoA1 ratio is considered to have the strongest predictive value for ischemic stroke. |
| 1664 | 20538481 | In this case-control study, we evaluated apoB/apoA1 ratio as a predictor of ischemic stroke in a cohort of elderly subjects. |
| 1665 | 20538481 | The association between apoB/apoA1 ratio and stroke was determined by multivariate logistic regression modeling after adjusting for potential confounding factors, including lipid parameters. |
| 1666 | 20538481 | Stroke patients exhibited a higher apoB/apoA1 ratio than controls (1.04±0.33 vs 0.86±0.22; P<.001). |
| 1667 | 20538481 | In univariate analysis, crude odds ratio (OR) for apoB/apoA1 ratio was 1.27 per 0.1 increase (95% confidence interval [CI]=1.15-1.39; P<.001). |
| 1668 | 20538481 | Compared with subjects with an apoB/apoA1 ratio in the lowest quartile, those within the highest quartile had a 6.3-fold increase in the odds of suffering an ischemic stroke (95% CI=3.17-12.48; P<.001). |
| 1669 | 20538481 | Our findings support elevated apoB/apoA1 ratio as an independent predictor of ischemic stroke in individuals over age 70. |
| 1670 | 20538481 | Among traditional cardiovascular risk factors, apolipoprotein (apo)B/apoA1 ratio is considered to have the strongest predictive value for ischemic stroke. |
| 1671 | 20538481 | In this case-control study, we evaluated apoB/apoA1 ratio as a predictor of ischemic stroke in a cohort of elderly subjects. |
| 1672 | 20538481 | The association between apoB/apoA1 ratio and stroke was determined by multivariate logistic regression modeling after adjusting for potential confounding factors, including lipid parameters. |
| 1673 | 20538481 | Stroke patients exhibited a higher apoB/apoA1 ratio than controls (1.04±0.33 vs 0.86±0.22; P<.001). |
| 1674 | 20538481 | In univariate analysis, crude odds ratio (OR) for apoB/apoA1 ratio was 1.27 per 0.1 increase (95% confidence interval [CI]=1.15-1.39; P<.001). |
| 1675 | 20538481 | Compared with subjects with an apoB/apoA1 ratio in the lowest quartile, those within the highest quartile had a 6.3-fold increase in the odds of suffering an ischemic stroke (95% CI=3.17-12.48; P<.001). |
| 1676 | 20538481 | Our findings support elevated apoB/apoA1 ratio as an independent predictor of ischemic stroke in individuals over age 70. |
| 1677 | 20538481 | Among traditional cardiovascular risk factors, apolipoprotein (apo)B/apoA1 ratio is considered to have the strongest predictive value for ischemic stroke. |
| 1678 | 20538481 | In this case-control study, we evaluated apoB/apoA1 ratio as a predictor of ischemic stroke in a cohort of elderly subjects. |
| 1679 | 20538481 | The association between apoB/apoA1 ratio and stroke was determined by multivariate logistic regression modeling after adjusting for potential confounding factors, including lipid parameters. |
| 1680 | 20538481 | Stroke patients exhibited a higher apoB/apoA1 ratio than controls (1.04±0.33 vs 0.86±0.22; P<.001). |
| 1681 | 20538481 | In univariate analysis, crude odds ratio (OR) for apoB/apoA1 ratio was 1.27 per 0.1 increase (95% confidence interval [CI]=1.15-1.39; P<.001). |
| 1682 | 20538481 | Compared with subjects with an apoB/apoA1 ratio in the lowest quartile, those within the highest quartile had a 6.3-fold increase in the odds of suffering an ischemic stroke (95% CI=3.17-12.48; P<.001). |
| 1683 | 20538481 | Our findings support elevated apoB/apoA1 ratio as an independent predictor of ischemic stroke in individuals over age 70. |
| 1684 | 20538481 | Among traditional cardiovascular risk factors, apolipoprotein (apo)B/apoA1 ratio is considered to have the strongest predictive value for ischemic stroke. |
| 1685 | 20538481 | In this case-control study, we evaluated apoB/apoA1 ratio as a predictor of ischemic stroke in a cohort of elderly subjects. |
| 1686 | 20538481 | The association between apoB/apoA1 ratio and stroke was determined by multivariate logistic regression modeling after adjusting for potential confounding factors, including lipid parameters. |
| 1687 | 20538481 | Stroke patients exhibited a higher apoB/apoA1 ratio than controls (1.04±0.33 vs 0.86±0.22; P<.001). |
| 1688 | 20538481 | In univariate analysis, crude odds ratio (OR) for apoB/apoA1 ratio was 1.27 per 0.1 increase (95% confidence interval [CI]=1.15-1.39; P<.001). |
| 1689 | 20538481 | Compared with subjects with an apoB/apoA1 ratio in the lowest quartile, those within the highest quartile had a 6.3-fold increase in the odds of suffering an ischemic stroke (95% CI=3.17-12.48; P<.001). |
| 1690 | 20538481 | Our findings support elevated apoB/apoA1 ratio as an independent predictor of ischemic stroke in individuals over age 70. |
| 1691 | 20538481 | Among traditional cardiovascular risk factors, apolipoprotein (apo)B/apoA1 ratio is considered to have the strongest predictive value for ischemic stroke. |
| 1692 | 20538481 | In this case-control study, we evaluated apoB/apoA1 ratio as a predictor of ischemic stroke in a cohort of elderly subjects. |
| 1693 | 20538481 | The association between apoB/apoA1 ratio and stroke was determined by multivariate logistic regression modeling after adjusting for potential confounding factors, including lipid parameters. |
| 1694 | 20538481 | Stroke patients exhibited a higher apoB/apoA1 ratio than controls (1.04±0.33 vs 0.86±0.22; P<.001). |
| 1695 | 20538481 | In univariate analysis, crude odds ratio (OR) for apoB/apoA1 ratio was 1.27 per 0.1 increase (95% confidence interval [CI]=1.15-1.39; P<.001). |
| 1696 | 20538481 | Compared with subjects with an apoB/apoA1 ratio in the lowest quartile, those within the highest quartile had a 6.3-fold increase in the odds of suffering an ischemic stroke (95% CI=3.17-12.48; P<.001). |
| 1697 | 20538481 | Our findings support elevated apoB/apoA1 ratio as an independent predictor of ischemic stroke in individuals over age 70. |
| 1698 | 20683626 | Negative correlation between serum syndecan-1 and apolipoprotein A1 in patients with type 2 diabetes mellitus. |
| 1699 | 20683626 | In this study, serum syndecan-1 was detected by ELISA, and potential correlations between syndecan-1 and triglyceride, cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, lipoprotein a, apolipoprotein (apo) B, apoA1 and apoB/apoA1 were analyzed. |
| 1700 | 20683626 | Serum syndecan-1 level correlated negatively with apoA1 (r = -0.46, P = 0.003). |
| 1701 | 20683626 | Multiple regression analysis showed that apoA1 (b = -0.43, P = 0.003) was a predictor of serum syndecan-1 levels in subjects with type 2 diabetes. |
| 1702 | 20876207 | Plasma apoB and glyc-apoB were determined in different apoB-containing lipoproteins including buoyant and SD-LDL in MS (n=18) and type 2 diabetes (DM) [n=48; 12 statin-untreated (DM-S) and 36 statin-treated (DM+S)]. |
| 1703 | 20876207 | Statin-induced changes in its level may be important in decreasing apoB glycation in diabetes. |
| 1704 | 20876207 | Plasma apoB and glyc-apoB were determined in different apoB-containing lipoproteins including buoyant and SD-LDL in MS (n=18) and type 2 diabetes (DM) [n=48; 12 statin-untreated (DM-S) and 36 statin-treated (DM+S)]. |
| 1705 | 20876207 | Statin-induced changes in its level may be important in decreasing apoB glycation in diabetes. |
| 1706 | 21127475 | Apolipoprotein B (Apo B) (-0.0404 ± 0.02 g/l, -5.6%, P = 0.06) and insulin levels also decreased by 9.5% (-0.16 ± 0.08 pmol/l, P = 0.06) while blood glucose and leptin levels did not change. |
| 1707 | 21128827 | The ratio of apolipoprotein B and apolipoprotein A-1 concentrations (2.5) was significantly reduced in the CH group compared to the initial value (3.0). |
| 1708 | 21129046 | Apolipoprotein B/A-I and total cholesterol/high-density lipoprotein cholesterol ratios both predict cardiovascular events in the general population independently of nonlipid risk factors, albuminuria and C-reactive protein. |
| 1709 | 21257006 | However, the relative value of MS, apoB lipoproteins, and estimates of insulin resistance is unknown in predicting atherosclerosis in DM. |
| 1710 | 21257006 | Cross-sectional analyses of white subjects in 2 community-based studies were performed (n = 611 patients with DM, n = 803 subjects without DM) using multivariate analysis of traditional risk factors and then adding MS, apoB, and homeostasis model assessment of insulin resistance (HOMA-IR). |
| 1711 | 21257006 | In conclusion, insulin resistance estimates add value to MS and apoB in predicting coronary artery calcification scores in DM and warrant further evaluation in clinic for identification of patients with DM at higher risk for atherosclerotic cardiovascular disease. |
| 1712 | 21257006 | However, the relative value of MS, apoB lipoproteins, and estimates of insulin resistance is unknown in predicting atherosclerosis in DM. |
| 1713 | 21257006 | Cross-sectional analyses of white subjects in 2 community-based studies were performed (n = 611 patients with DM, n = 803 subjects without DM) using multivariate analysis of traditional risk factors and then adding MS, apoB, and homeostasis model assessment of insulin resistance (HOMA-IR). |
| 1714 | 21257006 | In conclusion, insulin resistance estimates add value to MS and apoB in predicting coronary artery calcification scores in DM and warrant further evaluation in clinic for identification of patients with DM at higher risk for atherosclerotic cardiovascular disease. |
| 1715 | 21257006 | However, the relative value of MS, apoB lipoproteins, and estimates of insulin resistance is unknown in predicting atherosclerosis in DM. |
| 1716 | 21257006 | Cross-sectional analyses of white subjects in 2 community-based studies were performed (n = 611 patients with DM, n = 803 subjects without DM) using multivariate analysis of traditional risk factors and then adding MS, apoB, and homeostasis model assessment of insulin resistance (HOMA-IR). |
| 1717 | 21257006 | In conclusion, insulin resistance estimates add value to MS and apoB in predicting coronary artery calcification scores in DM and warrant further evaluation in clinic for identification of patients with DM at higher risk for atherosclerotic cardiovascular disease. |
| 1718 | 21292266 | In addition to the oxidative profile, physical and biological characteristics of LDL(-) consist of nonenzymatic glycosylation, increased expression and activity of platelet-activating factor acetylhydrolase (PAF-AH) and phospholipase A(2) (PLA(2)), enriched NEFA content, hemoglobin and ApoB-100 cross-linking, and increase in ApoC-III and ApoE in LDL. |
| 1719 | 21419755 | Apolipoprotein A-I, apolipoprotein B, and apolipoprotein B/apolipoprotein A-I ratio: reference intervals compared with values in different pathophysiological conditions from the FINRISK 2007 study. |
| 1720 | 21472338 | Serum glucose, ApoAI, ApoB, ApoA1/ApoB, cholesterol and triglyceride levels were significantly higher in the T2D rats than in the controls, but there were no significant differences in serum insulin. |
| 1721 | 21505149 | Further studies investigating potential mechanisms responsible for the change in lipoprotein cholesterol profile revealed that adiponectin-producing macrophages altered expression of key genes in liver tissue, including apoA1, apoB, apoE, the LDL receptor, (P < 0.05), and ATP-binding cassette G1 (P < 0.01). |
| 1722 | 21505149 | In addition, Ad-TG mice also exhibited higher total and high-molecular-weight adipnection levels in plasma and increased expression of the anti-inflammatory cytokine IL-10 as well as a decrease in the proinflammatory cytokine IL-6 in adipose tissue. |
| 1723 | 21518411 | Cardiometabolic risk factors as apolipoprotein B, triglyceride/HDL-cholesterol ratio and C-reactive protein, in adolescents with and without obesity: cross-sectional study in middle class suburban children. |
| 1724 | 21562068 | Significantly more patients with and without diabetes achieved specified levels of LDL-C (< 2.59, < 1.99, < 1.81 mmol/L), non-HDL-C (< 3.37, < 2.59 mmol/L) and apoB (< 0.9, < 0.8 g/L) with ezetimibe/statin versus statin. |
| 1725 | 21562068 | A greater percentage of patients achieved both the LDL-C and apoB targets and all three LDL-C, apoB, and non-HDL-C targets with ezetimibe/statin versus statin in both subgroups. |
| 1726 | 21562068 | Significantly more patients with and without diabetes achieved specified levels of LDL-C (< 2.59, < 1.99, < 1.81 mmol/L), non-HDL-C (< 3.37, < 2.59 mmol/L) and apoB (< 0.9, < 0.8 g/L) with ezetimibe/statin versus statin. |
| 1727 | 21562068 | A greater percentage of patients achieved both the LDL-C and apoB targets and all three LDL-C, apoB, and non-HDL-C targets with ezetimibe/statin versus statin in both subgroups. |
| 1728 | 21723246 | The renal proteoglycans biglycan and decorin were detectable in glomeruli, with a significant increase in renal biglycan content in diabetic mice on the high-cholesterol diet. |
| 1729 | 21723246 | Renal biglycan and renal apolipoprotein B were colocalized, and regression analyses showed a significant relation between renal biglycan and renal apolipoprotein B content. |
| 1730 | 21789282 | Not only overt but also subclinical hypo- and hyperthyroidism, through different mechanisms, are associated with lipid alterations, mainly concerning total and LDL cholesterol and less often HDL cholesterol, triglycerides, lipoprotein (a), apolipoprotein A1, and apolipoprotein B. |
| 1731 | 21808658 | Microsomal triglyceride transfer protein (MTP) facilitates the transport of dietary and endogenous fat by the intestine and liver by assisting in the assembly and secretion of triglyceride-rich apolipoprotein B-containing lipoproteins. |
| 1732 | 21821825 | We evaluated whether AA and IC modify CAD risk associated with secretory phospholipase A(2) (sPLA(2)) type IIA mass and activity, lipoprotein-associated PLA(2) activity, lipoprotein (a) [Lp(a)], oxidized phospholipids on apoB-100 (OxPL/apoB), myeloperoxidase, and high sensitivity C-reactive protein. |
| 1733 | 21971522 | The review also highlights translational control of apolipoprotein B (apoB) mRNA by insulin as a clear example of endocrine modulation of mRNA translation to bring about changes in specific metabolic pathways. |
| 1734 | 21971522 | Recent findings made on the role of 5'-untranslated regions (5'-UTR), 3'-UTR, RNA binding proteins, and RNA granules in mediating insulin regulation of apoB mRNA translation, apoB protein synthesis, and hepatic lipoprotein production are discussed. |
| 1735 | 21971522 | The review also highlights translational control of apolipoprotein B (apoB) mRNA by insulin as a clear example of endocrine modulation of mRNA translation to bring about changes in specific metabolic pathways. |
| 1736 | 21971522 | Recent findings made on the role of 5'-untranslated regions (5'-UTR), 3'-UTR, RNA binding proteins, and RNA granules in mediating insulin regulation of apoB mRNA translation, apoB protein synthesis, and hepatic lipoprotein production are discussed. |
| 1737 | 22212222 | CETP inhibitor torcetrapib promotes reverse cholesterol transport in obese insulin-resistant CETP-ApoB100 transgenic mice. |
| 1738 | 22212222 | We therefore evaluated the effects of CETP inhibitor torcetrapib in CETP-apolipoprotein (apo)B100 mice made obese and insulin resistant with a 60% high-fat diet. |
| 1739 | 22212222 | In conclusion, CETP inhibition by torcetrapib improves RCT in CETP-apoB100 mice. |
| 1740 | 22212222 | CETP inhibitor torcetrapib promotes reverse cholesterol transport in obese insulin-resistant CETP-ApoB100 transgenic mice. |
| 1741 | 22212222 | We therefore evaluated the effects of CETP inhibitor torcetrapib in CETP-apolipoprotein (apo)B100 mice made obese and insulin resistant with a 60% high-fat diet. |
| 1742 | 22212222 | In conclusion, CETP inhibition by torcetrapib improves RCT in CETP-apoB100 mice. |
| 1743 | 22363922 | The Association between Apolipoprotein A-II and Metabolic Syndrome in Korean Adults: A Comparison Study of Apolipoprotein A-I and Apolipoprotein B. |
| 1744 | 22407494 | Clinical parameters, cardiorespiratory capacity, glycemic and lipid profile, apolipoprotein A-I (ApoA-I), apolipoprotein B (ApoB), Lipoprotein(a) [Lp(a)], insulin resistance (HOMA-IR), high-sensitivity CRP (hsCRP), fibrinogen were measured before and after 3 months. |
| 1745 | 22407494 | Long-term RT ameliorated glycemic control, insulin sensitivity and ApoB/ApoA-I ratio in individuals with T2DM. |
| 1746 | 22407494 | Clinical parameters, cardiorespiratory capacity, glycemic and lipid profile, apolipoprotein A-I (ApoA-I), apolipoprotein B (ApoB), Lipoprotein(a) [Lp(a)], insulin resistance (HOMA-IR), high-sensitivity CRP (hsCRP), fibrinogen were measured before and after 3 months. |
| 1747 | 22407494 | Long-term RT ameliorated glycemic control, insulin sensitivity and ApoB/ApoA-I ratio in individuals with T2DM. |
| 1748 | 22481012 | At 4 ± 2 months, glycosylated hemoglobin had decreased by a mean of 2.1%, but the only effect on the lipid profile were statistically significant decreases in nonesterified fatty acids and apolipoprotein B concentration. |
| 1749 | 22516441 | On-treatment non-high-density lipoprotein cholesterol, apolipoprotein B, triglycerides, and lipid ratios in relation to residual vascular risk after treatment with potent statin therapy: JUPITER (justification for the use of statins in prevention: an intervention trial evaluating rosuvastatin). |
| 1750 | 22517367 | Overproduction of apolipoprotein B (apoB)-containing lipoproteins by the liver and the intestine is 1 of the hallmarks of insulin resistance and type 2 diabetes and a well-established risk factor of cardiovascular disease. |
| 1751 | 22517367 | ApoB-synthesizing organs can deposit synthesized neutral lipids into at least 3 different types of LDs, each decorated with a subset of specific proteins: perilipin-decorated cytosolic LDs, and 2 types of LDs formed in the lumen of the endoplasmic reticulum, the secretion-destined LDs containing apoB, and resident lumenal LDs coated with microsomal triglyceride transfer protein and exchangeable apolipoproteins. |
| 1752 | 22517367 | Overproduction of apolipoprotein B (apoB)-containing lipoproteins by the liver and the intestine is 1 of the hallmarks of insulin resistance and type 2 diabetes and a well-established risk factor of cardiovascular disease. |
| 1753 | 22517367 | ApoB-synthesizing organs can deposit synthesized neutral lipids into at least 3 different types of LDs, each decorated with a subset of specific proteins: perilipin-decorated cytosolic LDs, and 2 types of LDs formed in the lumen of the endoplasmic reticulum, the secretion-destined LDs containing apoB, and resident lumenal LDs coated with microsomal triglyceride transfer protein and exchangeable apolipoproteins. |
| 1754 | 22752805 | We tested 140 with MI individuals for factor V (FV) Leiden, FV H1299R, Prothrombin G20210A, factor XIII (FXIII) V34L, β-fibrinogen b-455G/A, plasminogen activator inhibitor-1 (PAI-1)-675 4G/5G, human platelet antigens 1 (HPA-1) a/b, apolipoprotein B (ApoB) R3500Q, apolipoprotein E (ApoE), E2, E3, and E4, angiotensin-converting enzyme (ACE) D/I, 5,10 methylenetetrahydrofolate reductase (MTHFR) 677C/T, and MTHFR 1298A/C polymorphisms using a ViennaLab CVD strip assay. |
| 1755 | 22946216 | In groups with higher content of uric acid, the significant difference between median and quartiles was determined concerning the indicators of height, body mass, triglycerides concentration, beta-lipoprotein fractions content, pre beta-lipoprotein fractions content, apolipoprotein E in blood serum and apolipoprotein B=100 lipoproteins, but not both apolipoprotein C=III and apolipoprotein E in lipoproteins of high density. |
| 1756 | 22965469 | Association of the apolipoprotein B/apolipoprotein A-I ratio and low-density lipoprotein cholesterol with insulin resistance in a Chinese population with abdominal obesity. |
| 1757 | 22965469 | The aim of this study is to assess the relationships among the apolipoprotein B/apolipoprotein A-I ratio (apoB/apoA-I ratio), low-density lipoprotein cholesterol (LDL-C) and insulin resistance (IR) in a Chinese population with abdominal obesity. |
| 1758 | 22965469 | After adjustment for age, HOMA2-IR was positively correlated with the apoB/apoA-I ratio, LDL-C, TC and TG; and negatively correlated with HDL-C in men (all p < 0.0001). |
| 1759 | 22965469 | HOMA2-IR was also positively correlated with the apoB/apoA-I ratio, LDL-C, TC and TG; and negatively correlated with HDL-C in women (all p < 0.01). |
| 1760 | 22965469 | Both LDL-C and apoB/apoA-I were independent risk factors of MetS, and the apoB/apoA-I ratio was stronger in this regard than LDL-C for this obese population. |
| 1761 | 22965469 | Association of the apolipoprotein B/apolipoprotein A-I ratio and low-density lipoprotein cholesterol with insulin resistance in a Chinese population with abdominal obesity. |
| 1762 | 22965469 | The aim of this study is to assess the relationships among the apolipoprotein B/apolipoprotein A-I ratio (apoB/apoA-I ratio), low-density lipoprotein cholesterol (LDL-C) and insulin resistance (IR) in a Chinese population with abdominal obesity. |
| 1763 | 22965469 | After adjustment for age, HOMA2-IR was positively correlated with the apoB/apoA-I ratio, LDL-C, TC and TG; and negatively correlated with HDL-C in men (all p < 0.0001). |
| 1764 | 22965469 | HOMA2-IR was also positively correlated with the apoB/apoA-I ratio, LDL-C, TC and TG; and negatively correlated with HDL-C in women (all p < 0.01). |
| 1765 | 22965469 | Both LDL-C and apoB/apoA-I were independent risk factors of MetS, and the apoB/apoA-I ratio was stronger in this regard than LDL-C for this obese population. |
| 1766 | 22965469 | Association of the apolipoprotein B/apolipoprotein A-I ratio and low-density lipoprotein cholesterol with insulin resistance in a Chinese population with abdominal obesity. |
| 1767 | 22965469 | The aim of this study is to assess the relationships among the apolipoprotein B/apolipoprotein A-I ratio (apoB/apoA-I ratio), low-density lipoprotein cholesterol (LDL-C) and insulin resistance (IR) in a Chinese population with abdominal obesity. |
| 1768 | 22965469 | After adjustment for age, HOMA2-IR was positively correlated with the apoB/apoA-I ratio, LDL-C, TC and TG; and negatively correlated with HDL-C in men (all p < 0.0001). |
| 1769 | 22965469 | HOMA2-IR was also positively correlated with the apoB/apoA-I ratio, LDL-C, TC and TG; and negatively correlated with HDL-C in women (all p < 0.01). |
| 1770 | 22965469 | Both LDL-C and apoB/apoA-I were independent risk factors of MetS, and the apoB/apoA-I ratio was stronger in this regard than LDL-C for this obese population. |
| 1771 | 22965469 | Association of the apolipoprotein B/apolipoprotein A-I ratio and low-density lipoprotein cholesterol with insulin resistance in a Chinese population with abdominal obesity. |
| 1772 | 22965469 | The aim of this study is to assess the relationships among the apolipoprotein B/apolipoprotein A-I ratio (apoB/apoA-I ratio), low-density lipoprotein cholesterol (LDL-C) and insulin resistance (IR) in a Chinese population with abdominal obesity. |
| 1773 | 22965469 | After adjustment for age, HOMA2-IR was positively correlated with the apoB/apoA-I ratio, LDL-C, TC and TG; and negatively correlated with HDL-C in men (all p < 0.0001). |
| 1774 | 22965469 | HOMA2-IR was also positively correlated with the apoB/apoA-I ratio, LDL-C, TC and TG; and negatively correlated with HDL-C in women (all p < 0.01). |
| 1775 | 22965469 | Both LDL-C and apoB/apoA-I were independent risk factors of MetS, and the apoB/apoA-I ratio was stronger in this regard than LDL-C for this obese population. |
| 1776 | 22965469 | Association of the apolipoprotein B/apolipoprotein A-I ratio and low-density lipoprotein cholesterol with insulin resistance in a Chinese population with abdominal obesity. |
| 1777 | 22965469 | The aim of this study is to assess the relationships among the apolipoprotein B/apolipoprotein A-I ratio (apoB/apoA-I ratio), low-density lipoprotein cholesterol (LDL-C) and insulin resistance (IR) in a Chinese population with abdominal obesity. |
| 1778 | 22965469 | After adjustment for age, HOMA2-IR was positively correlated with the apoB/apoA-I ratio, LDL-C, TC and TG; and negatively correlated with HDL-C in men (all p < 0.0001). |
| 1779 | 22965469 | HOMA2-IR was also positively correlated with the apoB/apoA-I ratio, LDL-C, TC and TG; and negatively correlated with HDL-C in women (all p < 0.01). |
| 1780 | 22965469 | Both LDL-C and apoB/apoA-I were independent risk factors of MetS, and the apoB/apoA-I ratio was stronger in this regard than LDL-C for this obese population. |
| 1781 | 22966069 | In sham and OVX mice, HFD feeding induced fatty liver, and insulin reduced hepatic apoB100 and liver triglyceride export. |
| 1782 | 23028139 | GLP-1 and GLP-2 as yin and yang of intestinal lipoprotein production: evidence for predominance of GLP-2-stimulated postprandial lipemia in normal and insulin-resistant states. |
| 1783 | 23028139 | A short (30-min) intravenous infusion of GLP-2 resulted in a marked increase in postprandial apolipoprotein B48 (apoB48) and triglyceride (TG) levels in the TG-rich lipoprotein (TRL) fraction, whereas GLP-1 infusion decreased lipid absorption and levels of TRL-TG and apoB48. |
| 1784 | 23028139 | Interestingly, fructose-fed, insulin-resistant hamsters showed a more pronounced response, including possible hypersensitivity to GLP-2 or reduced sensitivity to GLP-1. |
| 1785 | 23059459 | We added further gene manipulations to increase hyperlipidemia by using mice with both ApoE and ApoB48 knockout on the ob/+ (leptin mutation) mice. |
| 1786 | 23059459 | We found that ApoE knockout combined with leptin receptor knockout produced a lipid profile most closely modeling human dyslipidemia that promotes neuropathy. |
| 1787 | 23059459 | ApoE knockout combined with additional ApoB48 and leptin knockout produced similar changes of smaller magnitude, but, notably, an increase in HDL-cholesterol. |
| 1788 | 23059459 | We added further gene manipulations to increase hyperlipidemia by using mice with both ApoE and ApoB48 knockout on the ob/+ (leptin mutation) mice. |
| 1789 | 23059459 | We found that ApoE knockout combined with leptin receptor knockout produced a lipid profile most closely modeling human dyslipidemia that promotes neuropathy. |
| 1790 | 23059459 | ApoE knockout combined with additional ApoB48 and leptin knockout produced similar changes of smaller magnitude, but, notably, an increase in HDL-cholesterol. |
| 1791 | 23060933 | The aim of this study was to explore the relationship between serum profiles of adiponectin, leptin, resistin and visfatin and traditional and non-traditional cardiovascular risk factors in patients with type 2 diabetes mellitus (T2DM). |
| 1792 | 23060933 | Levels of adipocytokines (adiponectin, leptin, resistin and visfatin), lipids (total cholesterol, triglycerides), lipoproteins [HDL-cholesterol, LDL-cholesterol, lipoprotein (a)], apolipoproteins (Apo-A1 and Apo-B), non-traditional cardiovascular risk markers [asymmetric dimethylarginine (ADMA), homocysteine] and the inflammatory marker hs-CRP were measured, and anthropometric variables were determined. |
| 1793 | 23060933 | Serum adiponectin levels were decreased and leptin, resistin and visfatin levels were increased in T2DM patients compared to controls. |
| 1794 | 23060933 | These results suggest that decreased serum adiponectin and increased leptin, resistin and visfatin levels in T2DM may be novel biochemical risk factors for cardiovascular complications. |
| 1795 | 23136583 | Lipoprotein(a) (Lp[a]) is a LDL-like particle consisting of an ApoA moiety linked to one molecule of ApoB(100). |
| 1796 | 23212539 | The strength of the association slightly decreased after further adjustment for apolipoprotein B, smoking, and albumin excretion rate. |
| 1797 | 23251757 | Such RvR may relate to lack of strict target attainment for all atherogenic variables [LDL-C, non-high-density lipoprotein cholesterol (HDL-C) and/or apolipoprotein B(100)]. |
| 1798 | 23466071 | Inhibition of sphingolipid synthesis improves dyslipidemia in the diet-induced hamster model of insulin resistance: evidence for the role of sphingosine and sphinganine in hepatic VLDL-apoB100 overproduction. |
| 1799 | 23466071 | Taken together, these data suggest that a) hepatic VLDL-apoB100 overproduction may be stimulated by ceramides and sphingosine and b) inhibition of sphingolipid synthesis can reduce circulating VLDL in hamsters and improve circulating lipids--an effect that is possibly due to improved insulin signaling and reduced lipogenesis but is independent of changes in inflammation. |
| 1800 | 23466071 | Inhibition of sphingolipid synthesis improves dyslipidemia in the diet-induced hamster model of insulin resistance: evidence for the role of sphingosine and sphinganine in hepatic VLDL-apoB100 overproduction. |
| 1801 | 23466071 | Taken together, these data suggest that a) hepatic VLDL-apoB100 overproduction may be stimulated by ceramides and sphingosine and b) inhibition of sphingolipid synthesis can reduce circulating VLDL in hamsters and improve circulating lipids--an effect that is possibly due to improved insulin signaling and reduced lipogenesis but is independent of changes in inflammation. |
| 1802 | 23555769 | Moreover, PLA2G7 methylation is associated with the levels of total cholesterols (TC, r = 0.462, P = 0.009), triglyceride (TG, r = 0.414, P = 0.02) and Apolipoprotein B (ApoB, r = 0.396, P = 0.028) in females but not in males (adjusted P>0.4). |
| 1803 | 23555769 | PLA2G7 methylation might exert its effects on the risk of CHD by regulating the levels of TC, TG, and ApoB in females. |
| 1804 | 23555769 | Moreover, PLA2G7 methylation is associated with the levels of total cholesterols (TC, r = 0.462, P = 0.009), triglyceride (TG, r = 0.414, P = 0.02) and Apolipoprotein B (ApoB, r = 0.396, P = 0.028) in females but not in males (adjusted P>0.4). |
| 1805 | 23555769 | PLA2G7 methylation might exert its effects on the risk of CHD by regulating the levels of TC, TG, and ApoB in females. |
| 1806 | 23659066 | The cells absorb LDLP via apoB-100 endocytosis and VLDLP through apoE/B-100 receptors. |
| 1807 | 23720882 | The fasting plasma glucose, glycated hemoglobin, serum total cholesterol, triglyceride, LDL-cholesterol, apolipoprotein B (ApoB) and high-sensitive C-reactive protein (hsCRP) levels were significantly increased, whereas HDL-cholesterol and serum nitrite levels were significantly decreased in T2D patients. |
| 1808 | 23721961 | Insulin plays a key role in the regulation of ApoB. |
| 1809 | 23721961 | Insulin decreases ApoB secretion by promoting ApoB degradation in the hepatocyte. |
| 1810 | 23721961 | In parallel, insulin promotes clearance of circulating ApoB particles by the liver via the low-density lipoprotein receptor (LDLR), LDLR-related protein 1 (LRP1), and heparan sulfate proteoglycans (HSPGs). |
| 1811 | 23721961 | Consequently, the insulin-resistant state of type 2 diabetes (T2D) is associated with increased secretion and decreased clearance of ApoB. |
| 1812 | 23721961 | Here, we review the mechanisms by which insulin controls the secretion and uptake of ApoB in normal and diabetic livers. |
| 1813 | 23721961 | Insulin plays a key role in the regulation of ApoB. |
| 1814 | 23721961 | Insulin decreases ApoB secretion by promoting ApoB degradation in the hepatocyte. |
| 1815 | 23721961 | In parallel, insulin promotes clearance of circulating ApoB particles by the liver via the low-density lipoprotein receptor (LDLR), LDLR-related protein 1 (LRP1), and heparan sulfate proteoglycans (HSPGs). |
| 1816 | 23721961 | Consequently, the insulin-resistant state of type 2 diabetes (T2D) is associated with increased secretion and decreased clearance of ApoB. |
| 1817 | 23721961 | Here, we review the mechanisms by which insulin controls the secretion and uptake of ApoB in normal and diabetic livers. |
| 1818 | 23721961 | Insulin plays a key role in the regulation of ApoB. |
| 1819 | 23721961 | Insulin decreases ApoB secretion by promoting ApoB degradation in the hepatocyte. |
| 1820 | 23721961 | In parallel, insulin promotes clearance of circulating ApoB particles by the liver via the low-density lipoprotein receptor (LDLR), LDLR-related protein 1 (LRP1), and heparan sulfate proteoglycans (HSPGs). |
| 1821 | 23721961 | Consequently, the insulin-resistant state of type 2 diabetes (T2D) is associated with increased secretion and decreased clearance of ApoB. |
| 1822 | 23721961 | Here, we review the mechanisms by which insulin controls the secretion and uptake of ApoB in normal and diabetic livers. |
| 1823 | 23721961 | Insulin plays a key role in the regulation of ApoB. |
| 1824 | 23721961 | Insulin decreases ApoB secretion by promoting ApoB degradation in the hepatocyte. |
| 1825 | 23721961 | In parallel, insulin promotes clearance of circulating ApoB particles by the liver via the low-density lipoprotein receptor (LDLR), LDLR-related protein 1 (LRP1), and heparan sulfate proteoglycans (HSPGs). |
| 1826 | 23721961 | Consequently, the insulin-resistant state of type 2 diabetes (T2D) is associated with increased secretion and decreased clearance of ApoB. |
| 1827 | 23721961 | Here, we review the mechanisms by which insulin controls the secretion and uptake of ApoB in normal and diabetic livers. |
| 1828 | 23721961 | Insulin plays a key role in the regulation of ApoB. |
| 1829 | 23721961 | Insulin decreases ApoB secretion by promoting ApoB degradation in the hepatocyte. |
| 1830 | 23721961 | In parallel, insulin promotes clearance of circulating ApoB particles by the liver via the low-density lipoprotein receptor (LDLR), LDLR-related protein 1 (LRP1), and heparan sulfate proteoglycans (HSPGs). |
| 1831 | 23721961 | Consequently, the insulin-resistant state of type 2 diabetes (T2D) is associated with increased secretion and decreased clearance of ApoB. |
| 1832 | 23721961 | Here, we review the mechanisms by which insulin controls the secretion and uptake of ApoB in normal and diabetic livers. |
| 1833 | 23728830 | Effects of ezetimibe/simvastatin 10/20 mg vs. atorvastatin 20 mg on apolipoprotein B/apolipoprotein A1 in Korean patients with type 2 diabetes mellitus: results of a randomized controlled trial. |
| 1834 | 23819752 | Compared with other statins, pitavastatin has distinct pharmacological features that translate into a broad range of actions on both apolipoprotein-B-containing and apolipoprotein-A-containing lipoproteins. |
| 1835 | 23820620 | C57BL6 wild-type (C57) mice were compared with atherosclerotic LDLr(-/-) ApoB(100/100) (LRKOB100) and atherosclerotic/diabetic IGF-II × LDLr(-/-) ApoB(100/100) (LRKOB100/IGF) mice. |
| 1836 | 23842942 | The anti obesity effect of water soluble fraction of Gymnema sylvestre extract (120 mg/kg, p.o. for 21 days) in HFD fed rats was evaluated by the measurement of body weight gain, food intake, hemodynamic changes (systolic, diastolic, mean blood pressure and heart rate), serum lipid profiles (triglycerides, total cholesterol, LDL-cholesterol, HDL-cholesterol), leptin, insulin, glucose, apolipoproteins A1 and B, lactate dehydrogenase (LDH) and antioxidant enzymes such as reduced glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S transferase (GST), superoxide dismutase (SOD) and catalase (CAT) levels in liver tissues. |
| 1837 | 23842942 | Water soluble fraction of G. sylvestre ethanolic extract and rimonabant significantly reduced serum lipids, leptin, insulin, glucose, apolipoprotein B and LDH levels while it significantly increased the HDL-cholesterol, apolipoprotein A1 and antioxidant enzymes levels in liver tissue as compared to the HFD fed rats. |
| 1838 | 23858765 | This study was aimed to observe if the lipid profiles, apoprotein B100 (ApoB100), ApoAI, high density lipoprotein (HDL) and its subclasses could be improved by controlling the blood glucose. |
| 1839 | 23858765 | Fasting blood glucose (FPG), glycated hemoglobin A1c (HbA1c), lipid profiles, ApoB100, ApoAI and HDL subclasses were measured at beginning and a month later. |
| 1840 | 23858765 | Meanwhile, therapy with insulin intensive therapy (MDI, CSII) group had the most powerful effect on decreasing ApoB100 concentration (P < 0.05). |
| 1841 | 23858765 | This study was aimed to observe if the lipid profiles, apoprotein B100 (ApoB100), ApoAI, high density lipoprotein (HDL) and its subclasses could be improved by controlling the blood glucose. |
| 1842 | 23858765 | Fasting blood glucose (FPG), glycated hemoglobin A1c (HbA1c), lipid profiles, ApoB100, ApoAI and HDL subclasses were measured at beginning and a month later. |
| 1843 | 23858765 | Meanwhile, therapy with insulin intensive therapy (MDI, CSII) group had the most powerful effect on decreasing ApoB100 concentration (P < 0.05). |
| 1844 | 23858765 | This study was aimed to observe if the lipid profiles, apoprotein B100 (ApoB100), ApoAI, high density lipoprotein (HDL) and its subclasses could be improved by controlling the blood glucose. |
| 1845 | 23858765 | Fasting blood glucose (FPG), glycated hemoglobin A1c (HbA1c), lipid profiles, ApoB100, ApoAI and HDL subclasses were measured at beginning and a month later. |
| 1846 | 23858765 | Meanwhile, therapy with insulin intensive therapy (MDI, CSII) group had the most powerful effect on decreasing ApoB100 concentration (P < 0.05). |
| 1847 | 23890516 | Age, abdominal obesity, and baseline high-sensitivity C-reactive protein are associated with low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B responses to ezetimibe/simvastatin and atorvastatin in patients with metabolic syndrome. |
| 1848 | 23904453 | Saturated fatty acids activate ERK signaling to downregulate hepatic sortilin 1 in obese and diabetic mice. |
| 1849 | 23904453 | Hepatic sortilin 1 (Sort1), a cellular trafficking receptor, is a novel regulator of plasma lipid metabolism and reduces plasma cholesterol and triglycerides by inhibiting hepatic apolipoprotein B production. |
| 1850 | 23904453 | Mechanistic studies showed that the saturated fatty acid palmitate activated extracellular signal-regulated kinase (ERK) and inhibited Sort1 protein by mechanisms involving Sort1 protein ubiquitination and degradation. |
| 1851 | 23904453 | Consistently, hepatic ERK signaling was activated in diabetic mice, whereas blocking ERK signaling by an ERK inhibitor increased hepatic Sort1 protein in mice. |
| 1852 | 15615695 | RSK4 and PAK5 are novel candidate genes in diabetic rat kidney and brain. |
| 1853 | 15615695 | In multiple ChIP assays, ribosomal S6 kinase 4 (RSK4) and p21-activated kinase 5 (PAK5) were confirmed, and in vitro binding of HNF4alpha was evidenced by electrophoretic mobility shift assays (EMSA) using oligonucleotides, which harbor novel binding sites. |
| 1854 | 15615695 | We also used EMSA to probe for binding sites in promoters of HNF1alpha, apolipoprotein B, alpha1-antitrypsin, and angiotensinogen. |
| 1855 | 15615695 | We further studied RSK4 and PAK5 kinase expression in streptozotocin-induced diabetic rat kidney and brain and observed significant repression of HNF4alpha, RSK4, and PAK5 as determined by quantitative real-time reverse transcriptase-polymerase chain reaction. |
| 1856 | 15615695 | RSK4 and PAK5 may provide a molecular rationale for late-stage complications in disease, and further studies are warranted to explore these targets for the treatment of diabetic nephro- and neuropathy, frequently seen in patients with HNF4alpha dysfunction. |