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Gene Information
Gene symbol: APOA1
Gene name: apolipoprotein A-I
HGNC ID: 600
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 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. |
| 2 | 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. |
| 3 | 1345532 | The levels of lipoprotein A-I (LP A-I) containing apolipoprotein A-I (apo A-I) and devoid of apolipoprotein A-II (apo A-II) have been determined in a group of 86 children and adolescents with insulin-dependent diabetes of age between 1.3 and 22 years. |
| 4 | 1358344 | Apolipoprotein levels in normolipidemic non-insulin-dependent diabetes mellitus. |
| 5 | 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). |
| 6 | 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. |
| 7 | 1390605 | Glycosylated haemoglobin, plasma insulin, C-peptide and apolipoprotein A1 and B levels remained unchanged, and no improvement was seen in serum total cholesterol (6.2 (SE 0.3) v. 6.4 (SE 0.3) mmol/l for the Cr group, 6.2 (SE 0.4) v. 6.5 (SE 0.3) mmol/l for the placebo group), high-density-lipoprotein-cholesterol (1.1 (SE 0.1) v. 1.2 (SE 0.1) mmol/l for the Cr group, 1.0 (SE 0.1) v. 1.1 (SE 0.1) mmol/l for the placebo group) or triacylglycerols (2.5 (SE 0.4) v. 2.0 (SE 0.4) mmol/l for the Cr group, 2.4 (SE 0.2) v. 2.5 (SE 0.2) mmol/l for the placebo group). |
| 8 | 1516763 | Metabolism of HDL apolipoprotein A-I and A-II in type 1 (insulin-dependent) diabetes mellitus. |
| 9 | 1516763 | Concentrations of HDL cholesterol and apolipoprotein A-I are commonly increased in Type 1 (insulin-dependent) diabetes mellitus but the mechanisms whereby diabetes influences HDL metabolism have not been studied. |
| 10 | 1516763 | Input rates and fractional catabolic rates for apolipoproteins A-I and II were determined following injection of 125I-apolipoprotein A-I and 131I-apolipoprotein A-II tracers. |
| 11 | 1516763 | Additional multicompartmental analysis was performed using a model to describe the kinetics of HDL particles containing only apolipoprotein A-I (Lp A-I) and apolipoprotein A-I and apolipoprotein A-II (Lp A-I/A-II). |
| 12 | 1516763 | Firstly, the rate of apolipoprotein A-II synthesis was 22% lower than in control subjects (p less than 0.05). |
| 13 | 1516763 | Metabolism of HDL apolipoprotein A-I and A-II in type 1 (insulin-dependent) diabetes mellitus. |
| 14 | 1516763 | Concentrations of HDL cholesterol and apolipoprotein A-I are commonly increased in Type 1 (insulin-dependent) diabetes mellitus but the mechanisms whereby diabetes influences HDL metabolism have not been studied. |
| 15 | 1516763 | Input rates and fractional catabolic rates for apolipoproteins A-I and II were determined following injection of 125I-apolipoprotein A-I and 131I-apolipoprotein A-II tracers. |
| 16 | 1516763 | Additional multicompartmental analysis was performed using a model to describe the kinetics of HDL particles containing only apolipoprotein A-I (Lp A-I) and apolipoprotein A-I and apolipoprotein A-II (Lp A-I/A-II). |
| 17 | 1516763 | Firstly, the rate of apolipoprotein A-II synthesis was 22% lower than in control subjects (p less than 0.05). |
| 18 | 1516763 | Metabolism of HDL apolipoprotein A-I and A-II in type 1 (insulin-dependent) diabetes mellitus. |
| 19 | 1516763 | Concentrations of HDL cholesterol and apolipoprotein A-I are commonly increased in Type 1 (insulin-dependent) diabetes mellitus but the mechanisms whereby diabetes influences HDL metabolism have not been studied. |
| 20 | 1516763 | Input rates and fractional catabolic rates for apolipoproteins A-I and II were determined following injection of 125I-apolipoprotein A-I and 131I-apolipoprotein A-II tracers. |
| 21 | 1516763 | Additional multicompartmental analysis was performed using a model to describe the kinetics of HDL particles containing only apolipoprotein A-I (Lp A-I) and apolipoprotein A-I and apolipoprotein A-II (Lp A-I/A-II). |
| 22 | 1516763 | Firstly, the rate of apolipoprotein A-II synthesis was 22% lower than in control subjects (p less than 0.05). |
| 23 | 1516763 | Metabolism of HDL apolipoprotein A-I and A-II in type 1 (insulin-dependent) diabetes mellitus. |
| 24 | 1516763 | Concentrations of HDL cholesterol and apolipoprotein A-I are commonly increased in Type 1 (insulin-dependent) diabetes mellitus but the mechanisms whereby diabetes influences HDL metabolism have not been studied. |
| 25 | 1516763 | Input rates and fractional catabolic rates for apolipoproteins A-I and II were determined following injection of 125I-apolipoprotein A-I and 131I-apolipoprotein A-II tracers. |
| 26 | 1516763 | Additional multicompartmental analysis was performed using a model to describe the kinetics of HDL particles containing only apolipoprotein A-I (Lp A-I) and apolipoprotein A-I and apolipoprotein A-II (Lp A-I/A-II). |
| 27 | 1516763 | Firstly, the rate of apolipoprotein A-II synthesis was 22% lower than in control subjects (p less than 0.05). |
| 28 | 1521727 | HDL-cholesterol, and apolipoprotein A-I remained unchanged. |
| 29 | 1521727 | Total cholesterol, LDL-cholesterol, HDL-cholesterol, apolipoprotein A-I, apolipoprotein B remained unchanged during placebo treatment. |
| 30 | 1521727 | HDL-cholesterol, and apolipoprotein A-I remained unchanged. |
| 31 | 1521727 | Total cholesterol, LDL-cholesterol, HDL-cholesterol, apolipoprotein A-I, apolipoprotein B remained unchanged during placebo treatment. |
| 32 | 1526342 | Apolipoprotein A-I-containing particles and reverse cholesterol transport in IDDM. |
| 33 | 1531990 | Lipoprotein cholesterol, apolipoprotein A-I and B and lipoprotein (a) abnormalities in men with premature coronary artery disease. |
| 34 | 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). |
| 35 | 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. |
| 36 | 1531990 | Lipoprotein cholesterol, apolipoprotein A-I and B and lipoprotein (a) abnormalities in men with premature coronary artery disease. |
| 37 | 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). |
| 38 | 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. |
| 39 | 1531990 | Lipoprotein cholesterol, apolipoprotein A-I and B and lipoprotein (a) abnormalities in men with premature coronary artery disease. |
| 40 | 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). |
| 41 | 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. |
| 42 | 1532112 | Total cholesterol, triglycerides, high- and low-density lipoprotein cholesterol, apolipoprotein A-I, apolipoprotein B and Lp(a) were compared. |
| 43 | 1545765 | Apolipoprotein A-I was reduced by 9%. |
| 44 | 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. |
| 45 | 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. |
| 46 | 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. |
| 47 | 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. |
| 48 | 1576237 | Association in vivo of glycated apolipoprotein A-I with high density lipoproteins. |
| 49 | 1576237 | In diabetic patients, hyperglycaemia results in the non-enzymatic glycation of apolipoprotein A-I, the major protein of human high density lipoproteins. |
| 50 | 1576237 | The effect of the non-enzymatic glycation on the association of apolipoprotein A-I with high density lipoprotein in vivo has been studied in the rat. |
| 51 | 1576237 | The distribution volume obtained after injection of glycated apolipoprotein A-I was 2- to 3-fold higher in kidneys and approximately 30% lower in adrenals and ovaries than that obtained with apolipoprotein A-I. |
| 52 | 1576237 | Analysis by gel chromatography of serum from donor rats shows that glycation diminishes the interaction between apolipoprotein A-I and high density lipoprotein. |
| 53 | 1576237 | The findings in this study suggest that non-enzymatic glycation of apolipoprotein A-I may contribute to the development of atherosclerosis in patients with diabetes mellitus. |
| 54 | 1576237 | Association in vivo of glycated apolipoprotein A-I with high density lipoproteins. |
| 55 | 1576237 | In diabetic patients, hyperglycaemia results in the non-enzymatic glycation of apolipoprotein A-I, the major protein of human high density lipoproteins. |
| 56 | 1576237 | The effect of the non-enzymatic glycation on the association of apolipoprotein A-I with high density lipoprotein in vivo has been studied in the rat. |
| 57 | 1576237 | The distribution volume obtained after injection of glycated apolipoprotein A-I was 2- to 3-fold higher in kidneys and approximately 30% lower in adrenals and ovaries than that obtained with apolipoprotein A-I. |
| 58 | 1576237 | Analysis by gel chromatography of serum from donor rats shows that glycation diminishes the interaction between apolipoprotein A-I and high density lipoprotein. |
| 59 | 1576237 | The findings in this study suggest that non-enzymatic glycation of apolipoprotein A-I may contribute to the development of atherosclerosis in patients with diabetes mellitus. |
| 60 | 1576237 | Association in vivo of glycated apolipoprotein A-I with high density lipoproteins. |
| 61 | 1576237 | In diabetic patients, hyperglycaemia results in the non-enzymatic glycation of apolipoprotein A-I, the major protein of human high density lipoproteins. |
| 62 | 1576237 | The effect of the non-enzymatic glycation on the association of apolipoprotein A-I with high density lipoprotein in vivo has been studied in the rat. |
| 63 | 1576237 | The distribution volume obtained after injection of glycated apolipoprotein A-I was 2- to 3-fold higher in kidneys and approximately 30% lower in adrenals and ovaries than that obtained with apolipoprotein A-I. |
| 64 | 1576237 | Analysis by gel chromatography of serum from donor rats shows that glycation diminishes the interaction between apolipoprotein A-I and high density lipoprotein. |
| 65 | 1576237 | The findings in this study suggest that non-enzymatic glycation of apolipoprotein A-I may contribute to the development of atherosclerosis in patients with diabetes mellitus. |
| 66 | 1576237 | Association in vivo of glycated apolipoprotein A-I with high density lipoproteins. |
| 67 | 1576237 | In diabetic patients, hyperglycaemia results in the non-enzymatic glycation of apolipoprotein A-I, the major protein of human high density lipoproteins. |
| 68 | 1576237 | The effect of the non-enzymatic glycation on the association of apolipoprotein A-I with high density lipoprotein in vivo has been studied in the rat. |
| 69 | 1576237 | The distribution volume obtained after injection of glycated apolipoprotein A-I was 2- to 3-fold higher in kidneys and approximately 30% lower in adrenals and ovaries than that obtained with apolipoprotein A-I. |
| 70 | 1576237 | Analysis by gel chromatography of serum from donor rats shows that glycation diminishes the interaction between apolipoprotein A-I and high density lipoprotein. |
| 71 | 1576237 | The findings in this study suggest that non-enzymatic glycation of apolipoprotein A-I may contribute to the development of atherosclerosis in patients with diabetes mellitus. |
| 72 | 1576237 | Association in vivo of glycated apolipoprotein A-I with high density lipoproteins. |
| 73 | 1576237 | In diabetic patients, hyperglycaemia results in the non-enzymatic glycation of apolipoprotein A-I, the major protein of human high density lipoproteins. |
| 74 | 1576237 | The effect of the non-enzymatic glycation on the association of apolipoprotein A-I with high density lipoprotein in vivo has been studied in the rat. |
| 75 | 1576237 | The distribution volume obtained after injection of glycated apolipoprotein A-I was 2- to 3-fold higher in kidneys and approximately 30% lower in adrenals and ovaries than that obtained with apolipoprotein A-I. |
| 76 | 1576237 | Analysis by gel chromatography of serum from donor rats shows that glycation diminishes the interaction between apolipoprotein A-I and high density lipoprotein. |
| 77 | 1576237 | The findings in this study suggest that non-enzymatic glycation of apolipoprotein A-I may contribute to the development of atherosclerosis in patients with diabetes mellitus. |
| 78 | 1576237 | Association in vivo of glycated apolipoprotein A-I with high density lipoproteins. |
| 79 | 1576237 | In diabetic patients, hyperglycaemia results in the non-enzymatic glycation of apolipoprotein A-I, the major protein of human high density lipoproteins. |
| 80 | 1576237 | The effect of the non-enzymatic glycation on the association of apolipoprotein A-I with high density lipoprotein in vivo has been studied in the rat. |
| 81 | 1576237 | The distribution volume obtained after injection of glycated apolipoprotein A-I was 2- to 3-fold higher in kidneys and approximately 30% lower in adrenals and ovaries than that obtained with apolipoprotein A-I. |
| 82 | 1576237 | Analysis by gel chromatography of serum from donor rats shows that glycation diminishes the interaction between apolipoprotein A-I and high density lipoprotein. |
| 83 | 1576237 | The findings in this study suggest that non-enzymatic glycation of apolipoprotein A-I may contribute to the development of atherosclerosis in patients with diabetes mellitus. |
| 84 | 1579407 | Apolipoprotein A-I, A-II, B, C-II, and C-III in children with insulin-dependent diabetes mellitus. |
| 85 | 1579407 | Plasma and lipoprotein lipids and apolipoprotein levels were measured in 123 insulin-dependent diabetic children (4- to 12-years-old), classified into good, fair, and poor diabetic control based on HbA1c and fructosamine levels, and in 62 comparable healthy controls. |
| 86 | 1579407 | We conclude that in children with insulin-dependent diabetes mellitus, abnormalities in plasma lipid, lipoprotein, and apolipoprotein levels occur, the extent of which depends on the degree (extent) of glycemic control (the poorer the control the more substantial the abnormality). |
| 87 | 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). |
| 88 | 1702705 | The thyroxine-binding site of human apolipoprotein-A-I: location in the N-terminal domain. |
| 89 | 1702705 | We tested the ability of nine monoclonal antibodies (MAb) against human apolipoprotein-A-I (apoA-I), the 28.3-kDa major apoprotein of high density lipoproteins (HDL), to inhibit its photoaffinity labeling with [125I]T4. |
| 90 | 1702705 | The thyroxine-binding site of human apolipoprotein-A-I: location in the N-terminal domain. |
| 91 | 1702705 | We tested the ability of nine monoclonal antibodies (MAb) against human apolipoprotein-A-I (apoA-I), the 28.3-kDa major apoprotein of high density lipoproteins (HDL), to inhibit its photoaffinity labeling with [125I]T4. |
| 92 | 1825896 | Hypertension, lipoprotein(a), and apolipoprotein A-I as risk factors for stroke in the Chinese. |
| 93 | 1825896 | We found the following protective factors: a serum high density lipoprotein-cholesterol concentration of greater than 1.59 mmol/l and a serum apolipoprotein A-I concentration of greater than or equal to 106 mg/dl. |
| 94 | 1825896 | When significant risk factors were entered into a multiple logistic regression model, we found a history of hypertension, a high serum lipoprotein(a) concentration, and a low apolipoprotein A-I concentration to be independent risk factors for all strokes. |
| 95 | 1825896 | Hypertension, lipoprotein(a), and apolipoprotein A-I as risk factors for stroke in the Chinese. |
| 96 | 1825896 | We found the following protective factors: a serum high density lipoprotein-cholesterol concentration of greater than 1.59 mmol/l and a serum apolipoprotein A-I concentration of greater than or equal to 106 mg/dl. |
| 97 | 1825896 | When significant risk factors were entered into a multiple logistic regression model, we found a history of hypertension, a high serum lipoprotein(a) concentration, and a low apolipoprotein A-I concentration to be independent risk factors for all strokes. |
| 98 | 1825896 | Hypertension, lipoprotein(a), and apolipoprotein A-I as risk factors for stroke in the Chinese. |
| 99 | 1825896 | We found the following protective factors: a serum high density lipoprotein-cholesterol concentration of greater than 1.59 mmol/l and a serum apolipoprotein A-I concentration of greater than or equal to 106 mg/dl. |
| 100 | 1825896 | When significant risk factors were entered into a multiple logistic regression model, we found a history of hypertension, a high serum lipoprotein(a) concentration, and a low apolipoprotein A-I concentration to be independent risk factors for all strokes. |
| 101 | 1827234 | Stepwise discriminant analysis revealed that Lp(a) was a risk factor for the presence of CAD in men, independent of smoking, hypertension, diabetes, LDL and HDL cholesterol, or apolipoprotein A-I and B levels. |
| 102 | 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. |
| 103 | 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). |
| 104 | 1832357 | Insulin insensitivity and hyperinsulinaemia were both associated with higher levels of hepatic lipase activity but did not influence lipoprotein lipase activity. |
| 105 | 1859294 | In patients for whom serum lipid values were available, lower levels of apolipoprotein A-I were associated with a higher risk of having ICAS. |
| 106 | 1859294 | However, the effect of apolipoprotein A-I as a predictor of the presence of ICAS was far outweighted by the effects of duration of smoking and hypertension. |
| 107 | 1859294 | In patients for whom serum lipid values were available, lower levels of apolipoprotein A-I were associated with a higher risk of having ICAS. |
| 108 | 1859294 | However, the effect of apolipoprotein A-I as a predictor of the presence of ICAS was far outweighted by the effects of duration of smoking and hypertension. |
| 109 | 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. |
| 110 | 1900041 | Coronary artery disease and apolipoprotein A-I/C-III gene polymorphism: a study of Saudi Arabians. |
| 111 | 1900041 | The infrequent band of 3.2-kb of the apolipoprotein A-I/C-III polymorphic region has previously been found to be associated with coronary artery disease and with hypertriglyceridaemia in Caucasians. |
| 112 | 1900041 | We studied the apolipoprotein A-I/C-III gene cluster polymorphism in 97 Saudi Arabians in relation to coronary artery disease. |
| 113 | 1900041 | Genomic blotting of Sac I-digested chromosomal DNA with the use of an apolipoprotein A-I gene probe revealed 4.2-kb and 3.2-kb hybridization bands. |
| 114 | 1900041 | Coronary artery disease and apolipoprotein A-I/C-III gene polymorphism: a study of Saudi Arabians. |
| 115 | 1900041 | The infrequent band of 3.2-kb of the apolipoprotein A-I/C-III polymorphic region has previously been found to be associated with coronary artery disease and with hypertriglyceridaemia in Caucasians. |
| 116 | 1900041 | We studied the apolipoprotein A-I/C-III gene cluster polymorphism in 97 Saudi Arabians in relation to coronary artery disease. |
| 117 | 1900041 | Genomic blotting of Sac I-digested chromosomal DNA with the use of an apolipoprotein A-I gene probe revealed 4.2-kb and 3.2-kb hybridization bands. |
| 118 | 1900041 | Coronary artery disease and apolipoprotein A-I/C-III gene polymorphism: a study of Saudi Arabians. |
| 119 | 1900041 | The infrequent band of 3.2-kb of the apolipoprotein A-I/C-III polymorphic region has previously been found to be associated with coronary artery disease and with hypertriglyceridaemia in Caucasians. |
| 120 | 1900041 | We studied the apolipoprotein A-I/C-III gene cluster polymorphism in 97 Saudi Arabians in relation to coronary artery disease. |
| 121 | 1900041 | Genomic blotting of Sac I-digested chromosomal DNA with the use of an apolipoprotein A-I gene probe revealed 4.2-kb and 3.2-kb hybridization bands. |
| 122 | 1900041 | Coronary artery disease and apolipoprotein A-I/C-III gene polymorphism: a study of Saudi Arabians. |
| 123 | 1900041 | The infrequent band of 3.2-kb of the apolipoprotein A-I/C-III polymorphic region has previously been found to be associated with coronary artery disease and with hypertriglyceridaemia in Caucasians. |
| 124 | 1900041 | We studied the apolipoprotein A-I/C-III gene cluster polymorphism in 97 Saudi Arabians in relation to coronary artery disease. |
| 125 | 1900041 | Genomic blotting of Sac I-digested chromosomal DNA with the use of an apolipoprotein A-I gene probe revealed 4.2-kb and 3.2-kb hybridization bands. |
| 126 | 1907527 | Meanwhile, heart rate, indices of glycemic control (serum glucose, hemoglobin A1c, fructosamine, and C-peptide levels), and serum lipids (cholesterol, high-density cholesterol, triglycerides, apolipoprotein A1 and B levels) did not change. |
| 127 | 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. |
| 128 | 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. |
| 129 | 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). |
| 130 | 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. |
| 131 | 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. |
| 132 | 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). |
| 133 | 2065046 | Cardiovascular disease is a frequent complication of insulin-dependent diabetes mellitus (IDDM), but the prevalence, interrelations, and risk factors of its principal components (coronary, cerebrovascular, and lower-extremity arterial disease) and of medial arterial wall calcification are not well understood. |
| 134 | 2065046 | Modeling of potential risk factors (e.g., diabetes duration and glycosylated hemoglobin) revealed that duration, female gender, fibrinogen, low density lipoprotein cholesterol, high density lipoprotein cholesterol, and high density lipoprotein cholesterol to apolipoprotein A-I ratio were independent predictors of LEAD, whereas for CHD only, diabetes duration and hypertension contributed to CHD. |
| 135 | 2065046 | Calcification revealed a mixed pattern, with duration, hypertension, and triglyceride to apolipoprotein A-I ratio being the statistically significant associated factors. |
| 136 | 2065046 | Cardiovascular disease is a frequent complication of insulin-dependent diabetes mellitus (IDDM), but the prevalence, interrelations, and risk factors of its principal components (coronary, cerebrovascular, and lower-extremity arterial disease) and of medial arterial wall calcification are not well understood. |
| 137 | 2065046 | Modeling of potential risk factors (e.g., diabetes duration and glycosylated hemoglobin) revealed that duration, female gender, fibrinogen, low density lipoprotein cholesterol, high density lipoprotein cholesterol, and high density lipoprotein cholesterol to apolipoprotein A-I ratio were independent predictors of LEAD, whereas for CHD only, diabetes duration and hypertension contributed to CHD. |
| 138 | 2065046 | Calcification revealed a mixed pattern, with duration, hypertension, and triglyceride to apolipoprotein A-I ratio being the statistically significant associated factors. |
| 139 | 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. |
| 140 | 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. |
| 141 | 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. |
| 142 | 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. |
| 143 | 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. |
| 144 | 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. |
| 145 | 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. |
| 146 | 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. |
| 147 | 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. |
| 148 | 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. |
| 149 | 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. |
| 150 | 2132196 | Apolipoprotein and lipid ratios in treated non-insulin dependent diabetics. |
| 151 | 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. |
| 152 | 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). |
| 153 | 2149688 | During treatment a decrease in plasma LDL-cholesterol (2.62 (2.17-3.11) (median (range] vs 2.00 (1.89-2.96) mmol l-1, p less than 0.05) and serum apolipoprotein A-I (1.47 (1.25-1.60) vs 1.23 (1.13-1.90) g l-1, p less than 0.05) was observed in the treated group. |
| 154 | 2182032 | Effect of different insulin regimens on plasma lipoprotein and apolipoprotein concentrations in patients with non-insulin-dependent diabetes mellitus. |
| 155 | 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. |
| 156 | 2201495 | The aim of this study was to examine the effect of Max EPA (a commercially available fish oil preparation) on serum cholesterol lipoproteins and apolipoproteins in insulin-dependent diabetic (IDDM) men with dosages that were likely to be acceptable to patients. |
| 157 | 2201495 | Changes in apolipoproteins were examined and showed that the level of apolipoprotein A-I increased after ingestion of fish oil and correlated significantly (P less than 0.05) with the rise in HDL cholesterol. |
| 158 | 2261842 | Restriction-fragment-length polymorphisms flanking the insulin and apolipoprotein A-I and C-III genes, although not associated with gestational diabetes mellitus, may be associated with hyperlipidemia and subsequent atherosclerosis. |
| 159 | 2318345 | Effects of omega-3 fish oils on plasma lipids, lipoprotein composition, and postheparin lipoprotein lipase in women with IDDM. |
| 160 | 2318345 | Because the apparent reduction in cardiovascular risk noted in nondiabetic populations that ingest diets rich in marine lipids containing omega-3 fatty acids is believed to result in part from their capacity to modify the composition and physicochemical behavior of lipoproteins, we sought to determine whether dietary supplementation with marine lipids might favorably affect lipoprotein composition in insulin-dependent diabetes mellitus (IDDM). |
| 161 | 2318345 | Weight, insulin requirements, and glycosylated hemoglobin remained stable. |
| 162 | 2318345 | High-density lipoprotein2 (HDL2) cholesterol (before, 10.98 +/- 5.45 mg/dl; after, 18.43 +/- 7.93; P less than 0.01), its major apolipoprotein A-I (apoAI), and the major phospholipids (sphingomyelin and lecithin) all rose significantly. |
| 163 | 2335181 | Results after 1 year of treatment in 30 type 1 diabetics (HCP-negative; age at onset of diabetes 16.5 +/- 1.7 years; duration of diabetes 18.5 +/- 1.6 years, on multiple insulin injections before catheter-pen application): 1. better quality of life (reduction of frequency of needle pricks, more flexibility, inconspicuous application of insulin in public); 2. daily insulin--increased number of "injections" (4.2 +/- 0.1 vs 5.8 +/- 0.1, p less than 0.01), reduction of units per kg BW (0.70 +/- 0.02 vs 0.60 +/- 0.01, p less than 0.01), reduction of intermediate-acting insulin (14.1 +/- 1.3 vs 9.2 +/- 1.2 U/d, p less than 0.05); 3. no change of HbA1 (10.8 +/- 0.8 vs 10.2 +/- 0.2%, normal range 7.7 to 8.4%), mean blood glucose (MBG) in stress situation (8.4 +/- 0.4 vs 7.7 +/- 0.3 mmol/l), serum cholesterol and body weight, both within normal range; 4. improvement (p less than 0.05) of serum triglycerides, serum HDL-cholesterol, ratio of apolipoprotein A1/B; 5. rare skin reactions at the needle site. |
| 164 | 2492924 | The 27-kilodalton thyroxine (T4)-binding protein is human apolipoprotein A-I: identification of a 68-kilodalton high density lipoprotein that binds T4. |
| 165 | 2492924 | We have identified a previously described 66K T4-binding protein as a lipoprotein composed of two molecules of apolipoprotein A-I, five of cholesteryl esters, nine of phosphatidylcholine, and two of sphingomyelin. |
| 166 | 2492924 | Since we have recently found that lipids inhibit the binding of T4 to apolipoprotein A-I, the very low lipid content (16 mol/mol) of this 68K HDL relative to that (greater than 100 mol/mol) of high mol wt HDL subfractions may account for the preferential binding of T4 to the low mol wt subfraction. |
| 167 | 2492924 | The 27-kilodalton thyroxine (T4)-binding protein is human apolipoprotein A-I: identification of a 68-kilodalton high density lipoprotein that binds T4. |
| 168 | 2492924 | We have identified a previously described 66K T4-binding protein as a lipoprotein composed of two molecules of apolipoprotein A-I, five of cholesteryl esters, nine of phosphatidylcholine, and two of sphingomyelin. |
| 169 | 2492924 | Since we have recently found that lipids inhibit the binding of T4 to apolipoprotein A-I, the very low lipid content (16 mol/mol) of this 68K HDL relative to that (greater than 100 mol/mol) of high mol wt HDL subfractions may account for the preferential binding of T4 to the low mol wt subfraction. |
| 170 | 2492924 | The 27-kilodalton thyroxine (T4)-binding protein is human apolipoprotein A-I: identification of a 68-kilodalton high density lipoprotein that binds T4. |
| 171 | 2492924 | We have identified a previously described 66K T4-binding protein as a lipoprotein composed of two molecules of apolipoprotein A-I, five of cholesteryl esters, nine of phosphatidylcholine, and two of sphingomyelin. |
| 172 | 2492924 | Since we have recently found that lipids inhibit the binding of T4 to apolipoprotein A-I, the very low lipid content (16 mol/mol) of this 68K HDL relative to that (greater than 100 mol/mol) of high mol wt HDL subfractions may account for the preferential binding of T4 to the low mol wt subfraction. |
| 173 | 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. |
| 174 | 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. |
| 175 | 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). |
| 176 | 2517634 | Discrepancy between the higher apolipoprotein A-I and the normal HDL-cholesterol in in NIDDM supports the theory of altered composition of HDL particles in diabetic patients. |
| 177 | 2517634 | The controversy between the higher apolipoprotein A-I and the higher incidence of atherosclerosis in patients with NIDDM makes the clinical usefulness of this laboratory measurement doubtful in these patients. |
| 178 | 2517634 | Discrepancy between the higher apolipoprotein A-I and the normal HDL-cholesterol in in NIDDM supports the theory of altered composition of HDL particles in diabetic patients. |
| 179 | 2517634 | The controversy between the higher apolipoprotein A-I and the higher incidence of atherosclerosis in patients with NIDDM makes the clinical usefulness of this laboratory measurement doubtful in these patients. |
| 180 | 2562831 | Insulin-receptor and apolipoprotein genes contribute to development of NIDDM in Chinese Americans. |
| 181 | 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. |
| 182 | 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). |
| 183 | 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. |
| 184 | 2562831 | Insulin-receptor and apolipoprotein genes contribute to development of NIDDM in Chinese Americans. |
| 185 | 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. |
| 186 | 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). |
| 187 | 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. |
| 188 | 2562831 | Insulin-receptor and apolipoprotein genes contribute to development of NIDDM in Chinese Americans. |
| 189 | 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. |
| 190 | 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). |
| 191 | 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. |
| 192 | 2576007 | Genetic outcross and backcross analysis of nonobese diabetic (NOD/Lt) mice with a related but diabetes-resistant strain, nonobese normal (NON/Lt), has demonstrated that susceptibility to insulin-dependent diabetes mellitus is controlled in a recessive fashion by multiple genetic loci, including one (Idd-1s) associated with H-2 on chromosome 17 and another (Idd-2s) associated with Thy-1b/Apoa-1b (formerly Alp-1) on chromosome 9. |
| 193 | 2576007 | Severe insulitis and concomitant high diabetes incidences occurred in all genotypic classes of congenic mice carrying Thy-1/Apoa-1 linkage markers for either NOD or NON alleles at Idd-2. |
| 194 | 2576007 | Restriction-fragment-length polymorphism analysis of two polymorphic markers proximal to Thy-1, low-density lipoprotein receptor Ldlr and Ets-1, a protooncogene, confirmed a recombinant chromosome 9, because homozygosity for NOD genomic fragments was found centromeric to an NON congenic segment of at least 20 centiMorgans spanning the Thy-1 and Mod-1 loci. |
| 195 | 2661890 | Apolipoprotein A-I (apo A-I) levels were higher in the VSA group than in the C and CAD groups, and the difference between the VSA and CAD groups was significant. |
| 196 | 2661890 | Apolipoprotein A-II (apo A-II) levels were significantly higher in the VSA group than in the C and CAD groups. |
| 197 | 2744159 | Apolipoprotein A-I and B had no significant effect, but if the lowest limit of normal apolipoprotein A-I level was considered as 1.27 g/l the difference was significant. |
| 198 | 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. |
| 199 | 2894928 | Serological and/or DNA markers for genes that confer susceptibility to the insulin-dependent form of the disorder (IDDM; type 1) have been identified in the HLA-D region of chromosome 6 and near the insulin gene on chromosome 11. |
| 200 | 2894928 | Patients with non-insulin-dependent diabetes mellitus (NIDDM; type 2) make up a more heterogeneous group than those with IDDM and it is likely that in these patients similar clinical phenotypes may be produced by different genetic defects. |
| 201 | 2894928 | The synthesis of either an abnormal insulin/proinsulin molecule or an abnormal insulin receptor can confer susceptibility to NIDDM. |
| 202 | 2894928 | In addition, studies of restriction fragment length polymorphism and disease associations suggest that two other genes may contribute to the development of NIDDM on chromosome 11, one near the insulin gene on the short arm of this chromosome and the other near the apolipoprotein A-I gene on the long arm. |
| 203 | 2898774 | [DNA restriction fragment length polymorphism (RFLP) of insulin and apolipoprotein A-I (apo A-I) genes in patients with diabetes mellitus coexistent with polyendocrinopathy]. |
| 204 | 2999561 | Comparative studies of the composition of LPDS obtained from normal donors and poorly controlled diabetic patients showed an increase in saturated and total unesterified fatty acids (UFA), lecithin, apolipoprotein A1, and immunoreactive insulin in the LPDS from diabetic patients. |
| 205 | 3072419 | Supine and upright heart rate, body weight, plasma sodium and potassium, serum creatinine, glucose, C-peptide, glycosylated haemoglobin, serum cholesterol and triglycerides, their lipoprotein fractions, apolipoprotein A1, A2 and B concentrations and the responses of serum glucose and insulin to a standard oral glucose loading test did not change. |
| 206 | 3089186 | We investigated associations of high-density-lipoprotein (HDL) cholesterol, apolipoprotein A-I, and triglyceride levels with hemoglobin A1 (HbA1) and insulin levels in nondiabetic subjects (137 women and 111 men). |
| 207 | 3089186 | In women, HDL cholesterol, apolipoprotein A-I, and log-triglyceride values were significantly correlated with those of HbA1 and log-fasting insulin. |
| 208 | 3089186 | Although there were weaker associations in men, apolipoprotein A-I and HbA1 values were inversely related. |
| 209 | 3089186 | These data suggest that HDL cholesterol and apolipoprotein A-I levels are closely linked to glucose metabolism in nondiabetic individuals. |
| 210 | 3089186 | We investigated associations of high-density-lipoprotein (HDL) cholesterol, apolipoprotein A-I, and triglyceride levels with hemoglobin A1 (HbA1) and insulin levels in nondiabetic subjects (137 women and 111 men). |
| 211 | 3089186 | In women, HDL cholesterol, apolipoprotein A-I, and log-triglyceride values were significantly correlated with those of HbA1 and log-fasting insulin. |
| 212 | 3089186 | Although there were weaker associations in men, apolipoprotein A-I and HbA1 values were inversely related. |
| 213 | 3089186 | These data suggest that HDL cholesterol and apolipoprotein A-I levels are closely linked to glucose metabolism in nondiabetic individuals. |
| 214 | 3089186 | We investigated associations of high-density-lipoprotein (HDL) cholesterol, apolipoprotein A-I, and triglyceride levels with hemoglobin A1 (HbA1) and insulin levels in nondiabetic subjects (137 women and 111 men). |
| 215 | 3089186 | In women, HDL cholesterol, apolipoprotein A-I, and log-triglyceride values were significantly correlated with those of HbA1 and log-fasting insulin. |
| 216 | 3089186 | Although there were weaker associations in men, apolipoprotein A-I and HbA1 values were inversely related. |
| 217 | 3089186 | These data suggest that HDL cholesterol and apolipoprotein A-I levels are closely linked to glucose metabolism in nondiabetic individuals. |
| 218 | 3089186 | We investigated associations of high-density-lipoprotein (HDL) cholesterol, apolipoprotein A-I, and triglyceride levels with hemoglobin A1 (HbA1) and insulin levels in nondiabetic subjects (137 women and 111 men). |
| 219 | 3089186 | In women, HDL cholesterol, apolipoprotein A-I, and log-triglyceride values were significantly correlated with those of HbA1 and log-fasting insulin. |
| 220 | 3089186 | Although there were weaker associations in men, apolipoprotein A-I and HbA1 values were inversely related. |
| 221 | 3089186 | These data suggest that HDL cholesterol and apolipoprotein A-I levels are closely linked to glucose metabolism in nondiabetic individuals. |
| 222 | 3106055 | Conversely, Type 1 diabetics had elevated serum apolipoprotein A-I values vs. controls and Type 2 diabetics (1.70 +/- 0.33 vs. 1.49 +/- 0.22 and 1.43 +/- 0.21 g 1-1, P less than 0.01). |
| 223 | 3111177 | In a group of normocholesterolemic, non-diabetic middle-aged males surviving an acute myocardial infarction for 4 +/- 2 years (mean +/- SD), we have previously described a low apolipoprotein A-I and a deficient fibrinolytic activity as two major characteristics. |
| 224 | 3111177 | Furthermore, patients with a poor prognosis in the normotensive group had lower high density lipoprotein (HDL) cholesterol and lower apolipoprotein A-I concentration in plasma than patients with a good prognosis. |
| 225 | 3111177 | In a group of normocholesterolemic, non-diabetic middle-aged males surviving an acute myocardial infarction for 4 +/- 2 years (mean +/- SD), we have previously described a low apolipoprotein A-I and a deficient fibrinolytic activity as two major characteristics. |
| 226 | 3111177 | Furthermore, patients with a poor prognosis in the normotensive group had lower high density lipoprotein (HDL) cholesterol and lower apolipoprotein A-I concentration in plasma than patients with a good prognosis. |
| 227 | 3112449 | [Clinical evaluation of serum apolipoprotein A-I, A-II and B levels in patients with diabetes mellitus]. |
| 228 | 3134018 | Non enzymatic glycation of apolipoprotein A-I. |
| 229 | 3134018 | In diabetic patients, hyperglycaemia results in the non enzymatic glycation of many proteins including apolipoprotein A-I. |
| 230 | 3134018 | Non enzymatic glycation of apolipoprotein A-I. |
| 231 | 3134018 | In diabetic patients, hyperglycaemia results in the non enzymatic glycation of many proteins including apolipoprotein A-I. |
| 232 | 3152618 | Effects of glyburide treatment on serum lipoprotein and apolipoprotein concentrations and ratios in non-insulin-dependent diabetes mellitus. |
| 233 | 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. |
| 234 | 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. |
| 235 | 3152618 | Effects of glyburide treatment on serum lipoprotein and apolipoprotein concentrations and ratios in non-insulin-dependent diabetes mellitus. |
| 236 | 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. |
| 237 | 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. |
| 238 | 3172677 | In males (n = 27) significantly (p less than 0.01) higher levels of HDL cholesterol and apolipoprotein A-I as well as lower concentrations of triglycerides and a lower total cholesterol/HDL cholesterol risk ratio than in nondiabetic control subjects could be found. |
| 239 | 3172677 | In long-term diabetic females (n = 20), apolipoprotein A-I levels were also increased (p less than 0.02). |
| 240 | 3172677 | In males (n = 27) significantly (p less than 0.01) higher levels of HDL cholesterol and apolipoprotein A-I as well as lower concentrations of triglycerides and a lower total cholesterol/HDL cholesterol risk ratio than in nondiabetic control subjects could be found. |
| 241 | 3172677 | In long-term diabetic females (n = 20), apolipoprotein A-I levels were also increased (p less than 0.02). |
| 242 | 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. |
| 243 | 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. |
| 244 | 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. |
| 245 | 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. |
| 246 | 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. |
| 247 | 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. |
| 248 | 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. |
| 249 | 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. |
| 250 | 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. |
| 251 | 3379125 | In 22 diabetic patients without overt hyperlipidemia, serum triglyceride, total cholesterol, high density lipoprotein (HDL)-cholesterol, HDL2-cholesterol, HDL3-cholesterol, and apolipoprotein A-I (apo A-I) levels did not change during omega-3 FO supplementation for 8 weeks. |
| 252 | 3384218 | The concentrations of the serum apolipoproteins A-I, A-II and B were higher at onset of diabetes than in the control children (p less than 0.001, p less than 0.01, p less than 0.05 respectively), with a significantly increased ratio of apolipoprotein A-I to A-II in the diabetic children (p less than 0.001). |
| 253 | 3384218 | The ratio of apolipoprotein A-I to B did not differ from that in control children. |
| 254 | 3384218 | The concentrations of the serum apolipoproteins A-I, A-II and B were higher at onset of diabetes than in the control children (p less than 0.001, p less than 0.01, p less than 0.05 respectively), with a significantly increased ratio of apolipoprotein A-I to A-II in the diabetic children (p less than 0.001). |
| 255 | 3384218 | The ratio of apolipoprotein A-I to B did not differ from that in control children. |
| 256 | 3426654 | Compared to a control series of normal individuals of the same age (50.0 +/- 5.8 years for males and 61.6 +/- 3.0 years for females), they showed a significant reduction of high-density lipoprotein (HDL)-cholesterol and of apolipoprotein A-I (respectively -18.2 and -9.5%). |
| 257 | 3452804 | [Polymorphism of the apolipoprotein A-I gene and susceptibility to non-insulin-dependent diabetes mellitus]. |
| 258 | 3923627 | Increased levels of HDL-cholesterol and apolipoprotein A-I after intensified insulin therapy for diabetes. |
| 259 | 3923627 | Levels of HDL-cholesterol and apolipoprotein A-I increased without significant changes in hemoglobin A1 (HbA1), triglyceride, or cholesterol. |
| 260 | 3923627 | These findings suggest that increases in HDL-cholesterol and apolipoprotein A-I were a result of the intensified insulin delivery. |
| 261 | 3923627 | Increased levels of HDL-cholesterol and apolipoprotein A-I after intensified insulin therapy for diabetes. |
| 262 | 3923627 | Levels of HDL-cholesterol and apolipoprotein A-I increased without significant changes in hemoglobin A1 (HbA1), triglyceride, or cholesterol. |
| 263 | 3923627 | These findings suggest that increases in HDL-cholesterol and apolipoprotein A-I were a result of the intensified insulin delivery. |
| 264 | 3923627 | Increased levels of HDL-cholesterol and apolipoprotein A-I after intensified insulin therapy for diabetes. |
| 265 | 3923627 | Levels of HDL-cholesterol and apolipoprotein A-I increased without significant changes in hemoglobin A1 (HbA1), triglyceride, or cholesterol. |
| 266 | 3923627 | These findings suggest that increases in HDL-cholesterol and apolipoprotein A-I were a result of the intensified insulin delivery. |
| 267 | 3936351 | Apolipoprotein A-I gene polymorphism and susceptibility of non-insulin-dependent diabetes mellitus. |
| 268 | 3936351 | A polymorphic DNA sequence of the apolipoprotein (apo) A-I gene region was studied in relation to non-insulin-dependent diabetes mellitus (NIDDM). |
| 269 | 3986978 | No relationships were found between score for severity of atherosclerosis and high-density lipoprotein cholesterol or plasma apolipoprotein A-I concentrations in either group. |
| 270 | 6225845 | Diabetic animals had higher HDL-apoA-I (apolipoprotein A-I) levels than did CO- and LF- but not BT-fed rats. |
| 271 | 6225845 | In LDL, apoB levels were lower and apoE levels were higher in LF-fed rats than in animals fed high fat diets. |
| 272 | 6229255 | Concentrations of HDL cholesterol, apolipoprotein (apo) A-I and apo A-II were found to be significantly decreased in patients with insulin-dependent diabetes (IDD) and non-insulin-dependent diabetes (NIDD) compared with carefully selected controls matched for sex, age and body weight. |
| 273 | 6229255 | No correlation between HbA1 and either HDL cholesterol or A-I and A-II was found in IDD and NIDD. |
| 274 | 6229255 | A positive correlation between HbA1 and either triglyceride or VLDL triglyceride was noted in IDD and NIDD. |
| 275 | 6229255 | There was also a positive correlation between insulin dosage in IDD and HDL cholesterol, apolipoprotein A-I and A-II. |
| 276 | 6406724 | [Radioimmunoassay of apolipoprotein A - I and A - II of human plasma high density lipoprotein and its clinical use]. |
| 277 | 6427534 | The glucose load did not significantly alter total plasma cholesterol, high-density lipoprotein cholesterol, and apolipoprotein A-I and A-II concentrations in normal and diabetic subjects. |
| 278 | 6432541 | Also the serum concentration of apolipoprotein A-I, the major protein constituent of the high density lipoprotein fraction, was higher in the diabetic children (P = 0.05). |
| 279 | 6432541 | There were no significant differences between the groups with regard to the serum triglyceride concentrations or the apolipoprotein C-II and C-III concentrations. |
| 280 | 6512413 | Apolipoprotein A-I of the control rat HDL showed four isoforms that focused at pI 5.8 (17.3%), 5.75 (30.6%), 5.65 (31.8%), and 5.55 (20.5%); however, the spontaneously diabetic BB and nondiabetic littermate rat HDL apoA-I was mainly represented by two isoforms that focused at pI 5.8 and 5.75. |
| 281 | 6653942 | In 28 diabetic children the platelet shape change after ADP stimulation was positively correlated with the serum concentration of apolipoprotein A-I and negatively correlated with serum triglyceride concentration. |
| 282 | 6781957 | HDL composition differed markedly in diabetics and controls: the apolipoprotein A-I/A-II ratio was significantly higher (P less than 0.001) in both diabetic men and women (diabetic men--4.1 +/- 0.5, mean +/- SD, controls 3.6 +/- 0.4; diabetic women--4.6 +/- 0.4, controls 3.9 +/- 0.5). |
| 283 | 6781957 | Subsequent analysis of plasma from four patients by analytic ultracentrifugation demonstrated a high correlation (r = 0.993, P less than 0.01) between the apolipoprotein A-I/A-II ratio and HDL2, the cholesterol-rich lighter subclass of HDL thought to be the group of particles involved in reduced risk of ASCVD. |
| 284 | 6781957 | Thus, whether a genetic or acquired abnormality, the high apolipoprotein A-I/A-II ratio in insulin-dependent diabetics does not appear to counteract their increased risk of developing ASCVD. |
| 285 | 6781957 | HDL composition differed markedly in diabetics and controls: the apolipoprotein A-I/A-II ratio was significantly higher (P less than 0.001) in both diabetic men and women (diabetic men--4.1 +/- 0.5, mean +/- SD, controls 3.6 +/- 0.4; diabetic women--4.6 +/- 0.4, controls 3.9 +/- 0.5). |
| 286 | 6781957 | Subsequent analysis of plasma from four patients by analytic ultracentrifugation demonstrated a high correlation (r = 0.993, P less than 0.01) between the apolipoprotein A-I/A-II ratio and HDL2, the cholesterol-rich lighter subclass of HDL thought to be the group of particles involved in reduced risk of ASCVD. |
| 287 | 6781957 | Thus, whether a genetic or acquired abnormality, the high apolipoprotein A-I/A-II ratio in insulin-dependent diabetics does not appear to counteract their increased risk of developing ASCVD. |
| 288 | 6781957 | HDL composition differed markedly in diabetics and controls: the apolipoprotein A-I/A-II ratio was significantly higher (P less than 0.001) in both diabetic men and women (diabetic men--4.1 +/- 0.5, mean +/- SD, controls 3.6 +/- 0.4; diabetic women--4.6 +/- 0.4, controls 3.9 +/- 0.5). |
| 289 | 6781957 | Subsequent analysis of plasma from four patients by analytic ultracentrifugation demonstrated a high correlation (r = 0.993, P less than 0.01) between the apolipoprotein A-I/A-II ratio and HDL2, the cholesterol-rich lighter subclass of HDL thought to be the group of particles involved in reduced risk of ASCVD. |
| 290 | 6781957 | Thus, whether a genetic or acquired abnormality, the high apolipoprotein A-I/A-II ratio in insulin-dependent diabetics does not appear to counteract their increased risk of developing ASCVD. |
| 291 | 6793437 | High-density lipoprotein cholesterol and apolipoprotein A-I levels at diagnosis in patients with non-insulin dependent diabetes. |
| 292 | 6793437 | Serum apolipoprotein A-I levels were not decreased in diabetics with normal serum triglyceride levels, so that the ratio of HDL-cholesterol to apolipoprotein A-I was significantly decreased in diabetics (p Less Than 0.005). |
| 293 | 6793437 | High-density lipoprotein cholesterol and apolipoprotein A-I levels at diagnosis in patients with non-insulin dependent diabetes. |
| 294 | 6793437 | Serum apolipoprotein A-I levels were not decreased in diabetics with normal serum triglyceride levels, so that the ratio of HDL-cholesterol to apolipoprotein A-I was significantly decreased in diabetics (p Less Than 0.005). |
| 295 | 6814965 | High density lipoprotein cholesterol and apolipoprotein a-1 concentrations in non-insulin dependent diabetics treated by diet and chlorpropamide. |
| 296 | 6814965 | Fasting serum concentrations of high density lipoprotein cholesterol (HDLC) and apolipoprotein A-I (apo A-I) were determined in non-insulin dependent diabetes at diagnosis, diabetics treated by diet alone, diabetics treated by diet plus chlorpropamide, and normal controls matched for sex, age and body weight. |
| 297 | 6818080 | There was a significant increase in serum apolipoprotein A-I in obese females treated with calorie restriction and metformin and in non-obese females treated with carbohydrate restriction and glibenclamide. |
| 298 | 7430134 | These particles are unusual in that they contain apolipoprotein A-I in addition to their usual complement of apolipoproteins. |
| 299 | 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). |
| 300 | 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. |
| 301 | 7604809 | Apolipoprotein A-I levels increased (p = 0.054) despite no significant change in the levels of high density lipoprotein cholesterol. |
| 302 | 7621978 | Non-enzymatic glycosylation of apolipoprotein A-I and its functional consequences. |
| 303 | 7621978 | Apolipoprotein (apo) A-I, the major HDL apolipoprotein, and the HDL-associated enzyme lecithin-cholesterol acyltransferase (LCAT), which uses apo A-I as a cofactor, play a crucial role in reverse cholesterol transport. |
| 304 | 7646575 | Atherogenic index and apolipoprotein B/apolipoprotein A-I ratio were also significantly decreased after 4 weeks. |
| 305 | 7648790 | Analysis of serum apolipoprotein A-I in elderly non-insulin-dependent diabetic patients. |
| 306 | 7648790 | Furthermore, serum lipids and apolipoprotein A-I and B levels were determined. |
| 307 | 7648790 | Analysis of serum apolipoprotein A-I in elderly non-insulin-dependent diabetic patients. |
| 308 | 7648790 | Furthermore, serum lipids and apolipoprotein A-I and B levels were determined. |
| 309 | 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). |
| 310 | 7729606 | Decreased interstitial apolipoprotein A-I levels in IDDM patients with diabetic nephropathy. |
| 311 | 7729606 | We studied healthy control subjects (n = 9), normoalbuminuric insulin-dependent diabetes mellitus (IDDM) patients (n = 16), and IDDM patients with diabetic nephropathy (n = 11) matched for age, body mass index, smoking habits, duration of diabetes, and metabolic control. |
| 312 | 7729606 | Interstitial apolipoprotein A-I (apoA-I) levels were significantly lower in patients with nephropathy (0.18 +/- 0.10 milligram [mean +/- SD]) compared with normoalbuminuric diabetic patients (0.29 +/- 0.08 milligram) and healthy control subjects (0.30 +/- 0.09 milligram). |
| 313 | 7729606 | Decreased interstitial apolipoprotein A-I levels in IDDM patients with diabetic nephropathy. |
| 314 | 7729606 | We studied healthy control subjects (n = 9), normoalbuminuric insulin-dependent diabetes mellitus (IDDM) patients (n = 16), and IDDM patients with diabetic nephropathy (n = 11) matched for age, body mass index, smoking habits, duration of diabetes, and metabolic control. |
| 315 | 7729606 | Interstitial apolipoprotein A-I (apoA-I) levels were significantly lower in patients with nephropathy (0.18 +/- 0.10 milligram [mean +/- SD]) compared with normoalbuminuric diabetic patients (0.29 +/- 0.08 milligram) and healthy control subjects (0.30 +/- 0.09 milligram). |
| 316 | 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. |
| 317 | 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. |
| 318 | 7758222 | It could, however, be explained by glycation of lysine residues in apolipoprotein A-I, which is the most potent activator of LCAT. |
| 319 | 7758885 | Insulin resistance and abnormal albumin excretion in non-diabetic first-degree relatives of patients with NIDDM. |
| 320 | 7758885 | To establish whether microalbuminuria in non-diabetic subjects as well is associated with insulin resistance and associated abnormalities in glucose and lipid metabolism, oral glucose tolerance tests were performed with measurement of urinary albumin excretion rate, lipids and lipoproteins in 582 male non-diabetic first-degree relatives of patients with NIDDM. |
| 321 | 7758885 | Abnormal albumin excretion rate (AER), defined as AER 15-200 micrograms/min, was associated with higher systolic blood pressure (p < 0.05), higher fasting glucose values (p < 0.05), lower HDL-cholesterol (p < 0.05) and lower apolipoprotein A-I (p < 0.05) concentrations than observed in subjects with normal AER. |
| 322 | 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. |
| 323 | 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. |
| 324 | 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. |
| 325 | 8062608 | Plasma cholesteryl ester transfer protein and its relationship to plasma lipoproteins and apolipoprotein A-I-containing lipoproteins in IDDM patients with microalbuminuria and clinical nephropathy. |
| 326 | 8111077 | We measured the activities of plasma lecithin:cholesterol acyltransferase (LCAT), post-heparin lipoprotein lipase, and the composition of the HDL subfractions HDL2 and HDL3, in ten poorly controlled type 1 diabetic patients admitted to a metabolic ward (six women and four men, aged 18-37 years). |
| 327 | 8111077 | LCAT activity increased significantly (P < 0.05) with improved metabolic control in the diabetic patients, and showed positive within-person correlation with HDL2 cholesterol ester (r = 0.67; P < 0.01), HDL2 free cholesterol (r = 0.67; P < 0.01), phosphatidylcholine (r = 0.49; P < 0.05), total phospholipids (r = 0.50; P < 0.01) and apolipoprotein A-I (apo A-I: r = 0.72; P < 0.01). |
| 328 | 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. |
| 329 | 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). |
| 330 | 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. |
| 331 | 8139126 | The serum concentrations of apolipoprotein C-II, C-III and E were significantly higher in the treated groups (p < 0.05). |
| 332 | 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. |
| 333 | 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. |
| 334 | 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). |
| 335 | 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. |
| 336 | 8139126 | The serum concentrations of apolipoprotein C-II, C-III and E were significantly higher in the treated groups (p < 0.05). |
| 337 | 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. |
| 338 | 8171526 | ApoA1, ApoB, and ApoA1/ApoB before and after combined pancreas-kidney transplantation. |
| 339 | 8261628 | The preferential site of non-enzymatic glycation of human apolipoprotein A-I in vivo. |
| 340 | 8269788 | After adjusting multiple factors of age, body mass index (BMI), estradiol (E2), fasting plasma insulin (FINS), fasting blood glucose (FBS) by the stepwise procedure analysis, the levels of HDL-C and Apo-A1 have significantly negative association with the level of testosterone (T) (P = 0.0012 and 0.0040), however, have no association with E2. |
| 341 | 8282362 | Serum lipid levels did not change significantly in either group of patients except for significant decreases in high-density lipoprotein cholesterol and apolipoprotein A-I in the group with normal glucose tolerance tests, but those changes remained within the normal range. |
| 342 | 8309265 | Immunomagnetic separation of subpopulations of apolipoprotein A-I. |
| 343 | 8314155 | Preliminary research on apolipoprotein A-I and A-II in patients with non-insulin-dependent diabetes mellitus (NIDDM). |
| 344 | 8314449 | Apolipoprotein(a) and cardiovascular disease in type 2 (non-insulin-dependent) diabetic patients with and without diabetic nephropathy. |
| 345 | 8314449 | Apolipoprotein A-I was lower (p < 0.05) in all diabetic groups as compared to healthy subjects (nephropathy vs healthy subjects): 1.50 +/- 0.25 vs 1.69 +/- 0.32 g/l (mean +/- SD). |
| 346 | 8316757 | Apolipoprotein-A1, Apolipoprotein-B (Apo-B), Lipoprotein(a) (Lp[a]) HDL-Cholesterol, Cholesterol (Chol) and Triglycerides (TG). were estimated in serum. |
| 347 | 8318568 | Decreased activation of lecithin:cholesterol acyltransferase by glycated apolipoprotein A-I. |
| 348 | 8318568 | Glycated apolipoprotein A-I isolated from diabetic subjects was tested in vitro for its ability to activate lecithin:cholesterol acyltransferase, the principal cholesterol-esterifying enzyme in plasma. |
| 349 | 8318568 | Activation by glycated apolipoprotein A-I was significantly lower at all concentrations than the activation by normal apolipoprotein A-I. |
| 350 | 8318568 | Linear regression analysis of the kinetic data shows that the ratio app Vmax/app Km was significantly lower (p < 0.01) for glycated apolipoprotein A-I (0.29 nmol.l/h.mumol) than for normal apolipoprotein A-I (0.78 nmol.l/h.mumol). |
| 351 | 8318568 | Decreased activation of lecithin:cholesterol acyltransferase by glycated apolipoprotein A-I. |
| 352 | 8318568 | Glycated apolipoprotein A-I isolated from diabetic subjects was tested in vitro for its ability to activate lecithin:cholesterol acyltransferase, the principal cholesterol-esterifying enzyme in plasma. |
| 353 | 8318568 | Activation by glycated apolipoprotein A-I was significantly lower at all concentrations than the activation by normal apolipoprotein A-I. |
| 354 | 8318568 | Linear regression analysis of the kinetic data shows that the ratio app Vmax/app Km was significantly lower (p < 0.01) for glycated apolipoprotein A-I (0.29 nmol.l/h.mumol) than for normal apolipoprotein A-I (0.78 nmol.l/h.mumol). |
| 355 | 8318568 | Decreased activation of lecithin:cholesterol acyltransferase by glycated apolipoprotein A-I. |
| 356 | 8318568 | Glycated apolipoprotein A-I isolated from diabetic subjects was tested in vitro for its ability to activate lecithin:cholesterol acyltransferase, the principal cholesterol-esterifying enzyme in plasma. |
| 357 | 8318568 | Activation by glycated apolipoprotein A-I was significantly lower at all concentrations than the activation by normal apolipoprotein A-I. |
| 358 | 8318568 | Linear regression analysis of the kinetic data shows that the ratio app Vmax/app Km was significantly lower (p < 0.01) for glycated apolipoprotein A-I (0.29 nmol.l/h.mumol) than for normal apolipoprotein A-I (0.78 nmol.l/h.mumol). |
| 359 | 8318568 | Decreased activation of lecithin:cholesterol acyltransferase by glycated apolipoprotein A-I. |
| 360 | 8318568 | Glycated apolipoprotein A-I isolated from diabetic subjects was tested in vitro for its ability to activate lecithin:cholesterol acyltransferase, the principal cholesterol-esterifying enzyme in plasma. |
| 361 | 8318568 | Activation by glycated apolipoprotein A-I was significantly lower at all concentrations than the activation by normal apolipoprotein A-I. |
| 362 | 8318568 | Linear regression analysis of the kinetic data shows that the ratio app Vmax/app Km was significantly lower (p < 0.01) for glycated apolipoprotein A-I (0.29 nmol.l/h.mumol) than for normal apolipoprotein A-I (0.78 nmol.l/h.mumol). |
| 363 | 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%. |
| 364 | 8349039 | Regulation of apolipoprotein A-I-containing lipoproteins in IDDM. |
| 365 | 8354314 | Patients with insulin dependent diabetes (IDDM) have been reported to have increased incidence of E2/2 homozygosity. |
| 366 | 8354314 | Apolipoprotein A1 (apoA1) and B (apoB) were measured by turbidometry. |
| 367 | 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. |
| 368 | 8354314 | Ratios of HDL-C/LDL-C and apoA1/apoB showed on opposite trend. |
| 369 | 8354314 | Patients with insulin dependent diabetes (IDDM) have been reported to have increased incidence of E2/2 homozygosity. |
| 370 | 8354314 | Apolipoprotein A1 (apoA1) and B (apoB) were measured by turbidometry. |
| 371 | 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. |
| 372 | 8354314 | Ratios of HDL-C/LDL-C and apoA1/apoB showed on opposite trend. |
| 373 | 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. |
| 374 | 8366982 | High-density lipoprotein cholesterol and serum apolipoprotein A I and E concentration was significantly reduced in uremic patients with respect to normal subjects and to the other groups considered. |
| 375 | 8366982 | Serum apolipoprotein A II and B levels were also decreased in uremics. |
| 376 | 8485116 | For apolipoprotein B predictive significance was observed in the middle-aged populations, whereas apolipoprotein A-I had a protective effect in elderly women. |
| 377 | 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. |
| 378 | 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. |
| 379 | 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. |
| 380 | 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. |
| 381 | 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. |
| 382 | 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. |
| 383 | 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. |
| 384 | 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. |
| 385 | 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. |
| 386 | 8542741 | In regression analyses the major determinants of plasma TBARS were fasting plasma glucose, insulin, and apolipoprotein A1 (inversely) levels. |
| 387 | 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. |
| 388 | 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. |
| 389 | 8759066 | Apolipoprotein A-I and B levels and the risk of ischemic heart disease during a five-year follow-up of men in the Québec cardiovascular study. |
| 390 | 8763631 | Recent data suggest the existence of a relationship between ischemic heart diseases and apolipoprotein A-I containing lipoproteins. |
| 391 | 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). |
| 392 | 8763631 | In contrast, their lipoprotein particles containing only apolipoprotein AI without apolipoprotein AII and apoAI/apoB ratio were lowered (p < 0.001). |
| 393 | 8763631 | Also, the distribution of particles containing apolipoprotein A-I without apolipoprotein A-II in non-insulin-dependent diabetics was found abnormal. |
| 394 | 8763631 | Recent data suggest the existence of a relationship between ischemic heart diseases and apolipoprotein A-I containing lipoproteins. |
| 395 | 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). |
| 396 | 8763631 | In contrast, their lipoprotein particles containing only apolipoprotein AI without apolipoprotein AII and apoAI/apoB ratio were lowered (p < 0.001). |
| 397 | 8763631 | Also, the distribution of particles containing apolipoprotein A-I without apolipoprotein A-II in non-insulin-dependent diabetics was found abnormal. |
| 398 | 8770324 | Genetic control of apolipoprotein A-I distribution among HDL subclasses. |
| 399 | 8817108 | The offspring (male and female) of NIDDM mothers had slightly lower serum apolipoprotein A-I levels than the offspring of NIDDM fathers. |
| 400 | 8831914 | Qualitative changes in HDL are characterised by an increased triglyceride content, changes in the free cholesterol-phospholipid ratio, and an increase in the number of glycosylated apolipoprotein A-I molecules, giving rise to major variations in the viscosity of HDL particles. |
| 401 | 8864962 | HDL cholesterol and apolipoprotein A-I kinetics were unchanged. |
| 402 | 8902158 | Apolipoprotein A-II level was lower in CAD+ than in CAD- subjects (27.1 +/- 0.7 versus 30.9 +/- 0.7 mg/dl, P < 0.05), HDL cholesterol and apolipoprotein A-I kinetics were similar in the two groups. |
| 403 | 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). |
| 404 | 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. |
| 405 | 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. |
| 406 | 8971074 | To determine the physiological response to an increase in hepatic glucokinase expression, transgenic mice expressing the human hepatic glucokinase gene under the control of a liver-specific human apolipoprotein A-I gene enhancer were generated. |
| 407 | 9026529 | Lack of association of the apolipoprotein A-I-C-III-A-IV gene XmnI and SstI polymorphisms and of the lipoprotein lipase gene mutations in familial combined hyperlipoproteinemia in French Canadian subjects. |
| 408 | 9115542 | The mean ApoB and Apo-A1 values were 112 mg/dl and 167 mg/dl for males and females. |
| 409 | 9137945 | Expression of mRNA for ovarian steroid-stimulating factor (apolipoprotein A-I and apolipoprotein A-I-like protein) in human granulosa cells. |
| 410 | 9137945 | The N-terminal sequence of the 3 bands corresponded completely with that of apolipoprotein A-I. |
| 411 | 9137945 | Expression of mRNA for ovarian steroid-stimulating factor (apolipoprotein A-I and apolipoprotein A-I-like protein) in human granulosa cells. |
| 412 | 9137945 | The N-terminal sequence of the 3 bands corresponded completely with that of apolipoprotein A-I. |
| 413 | 9180247 | Furthermore, elastin peptides were significantly and positively correlated to HDL-cholesterol and apolipoprotein A1 in both sexes. |
| 414 | 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. |
| 415 | 9229197 | Borderline statistically significant (P < 0.1) relationships were found with hypolipidaemic therapy, insulin dose, non-HDL-cholesterol, apolipoprotein A1 and lipoprotein (a). |
| 416 | 9323590 | The acceptors used were assumed to participate in only passive efflux by lipid-dependent mechanisms (phospholipid vesicles and trypsin-modified high density lipoproteins) or to stimulate efflux by apolipoprotein-dependent pathways (purified apolipoprotein A-I and high density lipoproteins). |
| 417 | 9324678 | Cholesterol, triglicerides, HDL and LDH1 cholesterole, apolipoprotein A1 and B, endogenous creatinine urinary protein and albumin excretion, beta-2-microglobulin were measured. |
| 418 | 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. |
| 419 | 9439928 | Anomalies of lipoprotein pattern and fibrinolysis in acromegalic patients: relation to growth hormone levels and insulin-like growth factor I. |
| 420 | 9439928 | We found elevated apolipoprotein A-I and Apo E-concentrations in acromegalic patients compared to controls (apo A-I: 1.79 +/- 0.06 vs. 1.46 +/- 0.04 g/l; p < 0.01; apo E: 98.35 +/- 6.4 vs. 72.53 +/- 3.38 mg/l; p < 0.05). 30% of the acromegalics showed increased plasminogen activator inhibitor activity (PAI) while 66% had increased tissue-type plasminogen activator (t-PA) concentrations. |
| 421 | 9439928 | There was a correlation between hGH and Lp(a) (r = 0.414; p = 0.05), between hGH and PAI (r = -0.59; p < 0.005) and IGF-I and t-PA activity (r = -0.44; p < 0.05). |
| 422 | 9450113 | Turnover of pro- and mature apolipoprotein A-I in diabetic patients and normolipidaemic controls. |
| 423 | 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. |
| 424 | 9611161 | The KKAy-CETP mice retained the principal characteristics of KKAy mice except that their plasma HDL levels were reduced (from 159 +/- 25 to 25 +/- 6 mg/dl) and their free apolipoprotein A-I concentrations increased (from 7 +/- 3 to 22 +/- 6 mg/dl). |
| 425 | 9611161 | These data support the premise that CETP-mediated remodeling of the HDL is responsible for the low levels of that lipoprotein that accompany hypertriglyceridemic non-insulin-dependent diabetes mellitus. |
| 426 | 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. |
| 427 | 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). |
| 428 | 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. |
| 429 | 9699898 | We conclude that atherogenic apolipoprotein abnormalities occur in normoglycaemic relatives of non-insulin dependent diabetic patients. |
| 430 | 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. |
| 431 | 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). |
| 432 | 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. |
| 433 | 9699898 | We conclude that atherogenic apolipoprotein abnormalities occur in normoglycaemic relatives of non-insulin dependent diabetic patients. |
| 434 | 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. |
| 435 | 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). |
| 436 | 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. |
| 437 | 9699898 | We conclude that atherogenic apolipoprotein abnormalities occur in normoglycaemic relatives of non-insulin dependent diabetic patients. |
| 438 | 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). |
| 439 | 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). |
| 440 | 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. |
| 441 | 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). |
| 442 | 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). |
| 443 | 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. |
| 444 | 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). |
| 445 | 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). |
| 446 | 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. |
| 447 | 9836526 | In vivo evidence for increased apolipoprotein A-I catabolism in subjects with impaired glucose tolerance. |
| 448 | 9868130 | [Relationship between urinary albumin excretion and blood vessel lesion in non-insulin-dependent diabetics]. |
| 449 | 9868130 | To search the relationships between urinary albumin excretion and blood vessel lesion in non-insulin-dependent diabetics, we compared the differences of blood-lipid, blood pressure, coronary heart disease and retina disease between 58 patients. |
| 450 | 9868130 | The group with microalbuminuria had significantly lower concentration of apolipoprotein A, and apolipoprotein A1/apolipoprotein B100 than that of the group with normal albuminuria, but there was no significant change in concentrations of trigly cerides, total cholesterol, high density lipoprotein, and apolipoprotein B100. |
| 451 | 9868130 | There was negative correlation with apolipoprotein A1 and value of apolipoprotein A1/apolipoprotein B100, but positive correlation with systolic blood pressure by linear regression analysis for urinary albumin excretion. |
| 452 | 9868130 | [Relationship between urinary albumin excretion and blood vessel lesion in non-insulin-dependent diabetics]. |
| 453 | 9868130 | To search the relationships between urinary albumin excretion and blood vessel lesion in non-insulin-dependent diabetics, we compared the differences of blood-lipid, blood pressure, coronary heart disease and retina disease between 58 patients. |
| 454 | 9868130 | The group with microalbuminuria had significantly lower concentration of apolipoprotein A, and apolipoprotein A1/apolipoprotein B100 than that of the group with normal albuminuria, but there was no significant change in concentrations of trigly cerides, total cholesterol, high density lipoprotein, and apolipoprotein B100. |
| 455 | 9868130 | There was negative correlation with apolipoprotein A1 and value of apolipoprotein A1/apolipoprotein B100, but positive correlation with systolic blood pressure by linear regression analysis for urinary albumin excretion. |
| 456 | 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. |
| 457 | 9878681 | High density lipoprotein cholesterol levels are genetically influenced and are related to apoA1 and hepatic lipase (LIPC) gene functions. |
| 458 | 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. |
| 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 | 9915662 | Niaspan, an extended-release niacin formulation, is as potent as immediate-release niacin in increasing levels of HDL cholesterol; subfractions HDL2 and HDL3; apolipoprotein A-I, the major protein of HDL, and its cardioprotective subfraction lipoprotein A-I. |
| 463 | 9920153 | In a sample of 221 nondiabetic African American men (n = 105) and women (n = 116) with a mean age of 31 years, we examined the relationship of the plasma insulin concentration with the body mass index (BMI), blood pressure, plasma lipids, and sex hormones, including free testosterone, estradiol, and SHBG. |
| 464 | 9920153 | There was a significant inverse correlation of insulin with SHBG in both men (r = .28, P = .007) and women (r = .27, P = .02). |
| 465 | 9920153 | Stepwise multiple regression analyses with insulin as the dependent variable detected the BMI, triglyceride, and apolipoprotein A1 as significant contributors to the plasma insulin concentration in men. |
| 466 | 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. |
| 467 | 10381292 | Besides this, low high density lipoprotein-cholesterol (HDL-C) and apolipoprotein A-I (ApoA-I) levels could be found in the majority of the sample. |
| 468 | 10479666 | In addition, HDL(2) from diabetics did not protect against apolipoprotein B-100 fragmentation in LDL. |
| 469 | 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. |
| 470 | 10485310 | Compared to controls, at birth, macrosomic newborns had higher serum lipids, apolipoprotein A-I and B-100, and lipoprotein (very low density lipoprotein, low density lipoprotein, high density lipoprotein-2 and high density lipoprotein-3) levels. |
| 471 | 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. |
| 472 | 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. |
| 473 | 10591679 | There was little change in apolipoprotein A-I distribution. |
| 474 | 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. |
| 475 | 10781652 | Body composition measures, apolipoprotein (apo) B and apo A-I, Lp(a), cholesterol, HDL, LDL, triglycerides, thyroxine (TT4), free thyroxine (FT4), triiodothyronine (TT3), free triiodothyronine (FT3), TSH, and leptin were determined. |
| 476 | 10781652 | In conclusion more women with Turner's syndrome than controls have high levels of apolipoprotein A-I and Lp(a), but only after dichomitization, while other markers of lipid metabolism are normal. |
| 477 | 10781652 | Replacement therapy with female sex hormones lowered Lp(a), HDL cholesterol and apolipoprotein A-I. |
| 478 | 10781652 | Body composition measures, apolipoprotein (apo) B and apo A-I, Lp(a), cholesterol, HDL, LDL, triglycerides, thyroxine (TT4), free thyroxine (FT4), triiodothyronine (TT3), free triiodothyronine (FT3), TSH, and leptin were determined. |
| 479 | 10781652 | In conclusion more women with Turner's syndrome than controls have high levels of apolipoprotein A-I and Lp(a), but only after dichomitization, while other markers of lipid metabolism are normal. |
| 480 | 10781652 | Replacement therapy with female sex hormones lowered Lp(a), HDL cholesterol and apolipoprotein A-I. |
| 481 | 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. |
| 482 | 10902867 | Glycated apolipoprotein A-I assay by combination of affinity chromatography and latex immunoagglutination. |
| 483 | 10902867 | The degree of glycation of plasma apolipoprotein A-I was measured by a combination of gel filtration, boronate affinity chromatography and latex immunoagglutination. |
| 484 | 10902867 | The plasma concentrations of apolipoprotein A-I determined by this combination method (y) correlated well with those determined by turbidimetric immunoassay (x) (y=1.12x + 1.9, r=0.964). |
| 485 | 10902867 | The inter- and intra-assay coefficients of variation in the glycated apolipoprotein A-I assay were 4.1-5.0% and 4.0-4.4%, respectively. |
| 486 | 10902867 | Labile glycated apolipoprotein A-I did not interfere with the measurement of glycated apolipoprotein A-I. |
| 487 | 10902867 | Reference values for glycated apolipoprotein A-I were determined to be 2.4-4.0% (n=140), with no significant difference between men and women. |
| 488 | 10902867 | The mean concentration of plasma glycated apolipoprotein A-I in patients with uncontrolled diabetes mellitus (5.11%) was significantly higher than in normal subjects (3.12%, P<0.001). |
| 489 | 10902867 | The method is simple, rapid and highly sensitive for determination of the glycation level of plasma apolipoprotein A-I. |
| 490 | 10902867 | Glycated apolipoprotein A-I assay by combination of affinity chromatography and latex immunoagglutination. |
| 491 | 10902867 | The degree of glycation of plasma apolipoprotein A-I was measured by a combination of gel filtration, boronate affinity chromatography and latex immunoagglutination. |
| 492 | 10902867 | The plasma concentrations of apolipoprotein A-I determined by this combination method (y) correlated well with those determined by turbidimetric immunoassay (x) (y=1.12x + 1.9, r=0.964). |
| 493 | 10902867 | The inter- and intra-assay coefficients of variation in the glycated apolipoprotein A-I assay were 4.1-5.0% and 4.0-4.4%, respectively. |
| 494 | 10902867 | Labile glycated apolipoprotein A-I did not interfere with the measurement of glycated apolipoprotein A-I. |
| 495 | 10902867 | Reference values for glycated apolipoprotein A-I were determined to be 2.4-4.0% (n=140), with no significant difference between men and women. |
| 496 | 10902867 | The mean concentration of plasma glycated apolipoprotein A-I in patients with uncontrolled diabetes mellitus (5.11%) was significantly higher than in normal subjects (3.12%, P<0.001). |
| 497 | 10902867 | The method is simple, rapid and highly sensitive for determination of the glycation level of plasma apolipoprotein A-I. |
| 498 | 10902867 | Glycated apolipoprotein A-I assay by combination of affinity chromatography and latex immunoagglutination. |
| 499 | 10902867 | The degree of glycation of plasma apolipoprotein A-I was measured by a combination of gel filtration, boronate affinity chromatography and latex immunoagglutination. |
| 500 | 10902867 | The plasma concentrations of apolipoprotein A-I determined by this combination method (y) correlated well with those determined by turbidimetric immunoassay (x) (y=1.12x + 1.9, r=0.964). |
| 501 | 10902867 | The inter- and intra-assay coefficients of variation in the glycated apolipoprotein A-I assay were 4.1-5.0% and 4.0-4.4%, respectively. |
| 502 | 10902867 | Labile glycated apolipoprotein A-I did not interfere with the measurement of glycated apolipoprotein A-I. |
| 503 | 10902867 | Reference values for glycated apolipoprotein A-I were determined to be 2.4-4.0% (n=140), with no significant difference between men and women. |
| 504 | 10902867 | The mean concentration of plasma glycated apolipoprotein A-I in patients with uncontrolled diabetes mellitus (5.11%) was significantly higher than in normal subjects (3.12%, P<0.001). |
| 505 | 10902867 | The method is simple, rapid and highly sensitive for determination of the glycation level of plasma apolipoprotein A-I. |
| 506 | 10902867 | Glycated apolipoprotein A-I assay by combination of affinity chromatography and latex immunoagglutination. |
| 507 | 10902867 | The degree of glycation of plasma apolipoprotein A-I was measured by a combination of gel filtration, boronate affinity chromatography and latex immunoagglutination. |
| 508 | 10902867 | The plasma concentrations of apolipoprotein A-I determined by this combination method (y) correlated well with those determined by turbidimetric immunoassay (x) (y=1.12x + 1.9, r=0.964). |
| 509 | 10902867 | The inter- and intra-assay coefficients of variation in the glycated apolipoprotein A-I assay were 4.1-5.0% and 4.0-4.4%, respectively. |
| 510 | 10902867 | Labile glycated apolipoprotein A-I did not interfere with the measurement of glycated apolipoprotein A-I. |
| 511 | 10902867 | Reference values for glycated apolipoprotein A-I were determined to be 2.4-4.0% (n=140), with no significant difference between men and women. |
| 512 | 10902867 | The mean concentration of plasma glycated apolipoprotein A-I in patients with uncontrolled diabetes mellitus (5.11%) was significantly higher than in normal subjects (3.12%, P<0.001). |
| 513 | 10902867 | The method is simple, rapid and highly sensitive for determination of the glycation level of plasma apolipoprotein A-I. |
| 514 | 10902867 | Glycated apolipoprotein A-I assay by combination of affinity chromatography and latex immunoagglutination. |
| 515 | 10902867 | The degree of glycation of plasma apolipoprotein A-I was measured by a combination of gel filtration, boronate affinity chromatography and latex immunoagglutination. |
| 516 | 10902867 | The plasma concentrations of apolipoprotein A-I determined by this combination method (y) correlated well with those determined by turbidimetric immunoassay (x) (y=1.12x + 1.9, r=0.964). |
| 517 | 10902867 | The inter- and intra-assay coefficients of variation in the glycated apolipoprotein A-I assay were 4.1-5.0% and 4.0-4.4%, respectively. |
| 518 | 10902867 | Labile glycated apolipoprotein A-I did not interfere with the measurement of glycated apolipoprotein A-I. |
| 519 | 10902867 | Reference values for glycated apolipoprotein A-I were determined to be 2.4-4.0% (n=140), with no significant difference between men and women. |
| 520 | 10902867 | The mean concentration of plasma glycated apolipoprotein A-I in patients with uncontrolled diabetes mellitus (5.11%) was significantly higher than in normal subjects (3.12%, P<0.001). |
| 521 | 10902867 | The method is simple, rapid and highly sensitive for determination of the glycation level of plasma apolipoprotein A-I. |
| 522 | 10902867 | Glycated apolipoprotein A-I assay by combination of affinity chromatography and latex immunoagglutination. |
| 523 | 10902867 | The degree of glycation of plasma apolipoprotein A-I was measured by a combination of gel filtration, boronate affinity chromatography and latex immunoagglutination. |
| 524 | 10902867 | The plasma concentrations of apolipoprotein A-I determined by this combination method (y) correlated well with those determined by turbidimetric immunoassay (x) (y=1.12x + 1.9, r=0.964). |
| 525 | 10902867 | The inter- and intra-assay coefficients of variation in the glycated apolipoprotein A-I assay were 4.1-5.0% and 4.0-4.4%, respectively. |
| 526 | 10902867 | Labile glycated apolipoprotein A-I did not interfere with the measurement of glycated apolipoprotein A-I. |
| 527 | 10902867 | Reference values for glycated apolipoprotein A-I were determined to be 2.4-4.0% (n=140), with no significant difference between men and women. |
| 528 | 10902867 | The mean concentration of plasma glycated apolipoprotein A-I in patients with uncontrolled diabetes mellitus (5.11%) was significantly higher than in normal subjects (3.12%, P<0.001). |
| 529 | 10902867 | The method is simple, rapid and highly sensitive for determination of the glycation level of plasma apolipoprotein A-I. |
| 530 | 10902867 | Glycated apolipoprotein A-I assay by combination of affinity chromatography and latex immunoagglutination. |
| 531 | 10902867 | The degree of glycation of plasma apolipoprotein A-I was measured by a combination of gel filtration, boronate affinity chromatography and latex immunoagglutination. |
| 532 | 10902867 | The plasma concentrations of apolipoprotein A-I determined by this combination method (y) correlated well with those determined by turbidimetric immunoassay (x) (y=1.12x + 1.9, r=0.964). |
| 533 | 10902867 | The inter- and intra-assay coefficients of variation in the glycated apolipoprotein A-I assay were 4.1-5.0% and 4.0-4.4%, respectively. |
| 534 | 10902867 | Labile glycated apolipoprotein A-I did not interfere with the measurement of glycated apolipoprotein A-I. |
| 535 | 10902867 | Reference values for glycated apolipoprotein A-I were determined to be 2.4-4.0% (n=140), with no significant difference between men and women. |
| 536 | 10902867 | The mean concentration of plasma glycated apolipoprotein A-I in patients with uncontrolled diabetes mellitus (5.11%) was significantly higher than in normal subjects (3.12%, P<0.001). |
| 537 | 10902867 | The method is simple, rapid and highly sensitive for determination of the glycation level of plasma apolipoprotein A-I. |
| 538 | 10902867 | Glycated apolipoprotein A-I assay by combination of affinity chromatography and latex immunoagglutination. |
| 539 | 10902867 | The degree of glycation of plasma apolipoprotein A-I was measured by a combination of gel filtration, boronate affinity chromatography and latex immunoagglutination. |
| 540 | 10902867 | The plasma concentrations of apolipoprotein A-I determined by this combination method (y) correlated well with those determined by turbidimetric immunoassay (x) (y=1.12x + 1.9, r=0.964). |
| 541 | 10902867 | The inter- and intra-assay coefficients of variation in the glycated apolipoprotein A-I assay were 4.1-5.0% and 4.0-4.4%, respectively. |
| 542 | 10902867 | Labile glycated apolipoprotein A-I did not interfere with the measurement of glycated apolipoprotein A-I. |
| 543 | 10902867 | Reference values for glycated apolipoprotein A-I were determined to be 2.4-4.0% (n=140), with no significant difference between men and women. |
| 544 | 10902867 | The mean concentration of plasma glycated apolipoprotein A-I in patients with uncontrolled diabetes mellitus (5.11%) was significantly higher than in normal subjects (3.12%, P<0.001). |
| 545 | 10902867 | The method is simple, rapid and highly sensitive for determination of the glycation level of plasma apolipoprotein A-I. |
| 546 | 10915225 | To determine if ketoacidosis contributes to reduced apolipoprotein A1 (apoA1) expression in insulin-deficient diabetic rats, we examined the regulation of apoA1 gene expression in response to changes in ambient pH or ketone body concentrations. |
| 547 | 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). |
| 548 | 10996359 | Inefficiency of insulin therapy to correct apolipoprotein A-I metabolic abnormalities in non-insulin-dependent diabetes mellitus. |
| 549 | 11092511 | Effect of weight reduction on the distribution of apolipoprotein A-I in high-density lipoprotein subfractions in obese non-insulin-dependent diabetic subjects. |
| 550 | 11092511 | Plasma apolipoprotein A-I (apo A-I) decreased substantially and significantly at 8 and 12 weeks with both diets, and was reflected in the reduction of apo A-I in HDL subclasses alpha1, alpha2, pre-beta1, and pre-beta2 + pre-beta3. |
| 551 | 11092511 | Effect of weight reduction on the distribution of apolipoprotein A-I in high-density lipoprotein subfractions in obese non-insulin-dependent diabetic subjects. |
| 552 | 11092511 | Plasma apolipoprotein A-I (apo A-I) decreased substantially and significantly at 8 and 12 weeks with both diets, and was reflected in the reduction of apo A-I in HDL subclasses alpha1, alpha2, pre-beta1, and pre-beta2 + pre-beta3. |
| 553 | 11123853 | PPAR alpha activated by fibric acids form heterodimers with the 9-cis retinoic acid receptor (RXR). |
| 554 | 11123853 | Furthermore, they decrease triglycerides by increasing lipoprotein lipase gene expression and by decreasing apolipoprotein C-III gene expression. |
| 555 | 11123853 | Fibric acids increase high-density lipoprotein (HDL) cholesterol partly by increasing apolipoprotein A-I and apolipoprotein A-II gene expression. |
| 556 | 11215482 | Previously, we developed an immunoturbidimetric assay method for lipoprotein A-I(LpA-I) on sera pre-absorbed with anti-apolipoprotein A-II. |
| 557 | 11215482 | The serum levels of LpA-I did not correlate with those of diabetic markers such as fasted blood glucose, glycohemoglobin(HbA1c) and fructosamine, but correlated well with the levels of total cholesterol and HDL cholesterol, phospholipids, apolipoprotein A-I and seemed to correlate inversely with arteriosclerosis index. |
| 558 | 11290824 | They formed complexes with lipoproteins in culture medium, notably binding to apolipoprotein A-I-containing particles. |
| 559 | 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. |
| 560 | 11379865 | Effect of erythropoietin therapy on serum apolipoprotein A1 levels in patients undergoing chronic peritoneal dialysis. |
| 561 | 11431575 | Decreased HDL cholesterol and apolipoprotein A-I levels are strong cardiovascular risk factors, which does not seem to be better assessed with the assay of various HDL sub-fractions (HDL(2) et HDL(3), LpA-I et LpA-I: A-II.). |
| 562 | 11463575 | Serum apolipoprotein A(1) (apoA(1)) concentration is inversely correlated with the risk of premature atherosclerosis. |
| 563 | 11463575 | Serum apoA(1) concentrations are regulated, in part, at the transcriptional level. |
| 564 | 11463575 | ApoA(1) mRNA is synthesized primarily in the liver and small intestine, under the direction of a number of signaling molecules and tissue-specific regulatory elements. |
| 565 | 11463575 | Previously, we demonstrated that extracellular acidosis suppresses apoA(1) mRNA levels at the level of transcription. |
| 566 | 11463575 | Here we demonstrate that intracellular acidosis, in the absence of extracellular pH changes, represses apoA(1) promoter activity. |
| 567 | 11463575 | Repression occurs through a pH responsive element (pH-RE) located within the apoA(1) gene promoter. |
| 568 | 11463575 | Acidosis increases the specific DNA binding activity of a putative repressor protein within the immediate 5'-flanking region of the apoA(1) gene. |
| 569 | 11463575 | The cis-element that binds the putative repressor protein contains a negative thyroid hormone response element (nTRE) located 3' and adjacent to the apoA(1) TATA box. |
| 570 | 11463575 | Inhibition of tyrosine kinase activity and diacylglycerol-stimulated protein kinase C (PKC) signaling pathways with tyrophostin A47 and phorbol myristate acetate, respectively, did not affect the repression of apoA(1) promoter activity with acidosis. |
| 571 | 11463575 | These results suggest that transcriptional repression of the apoA(1) gene by alterations in ambient pH is associated with enhanced DNA binding activity of a repressor protein, through a mechanism which appears to be independent of de novo mRNA and protein synthesis, tyrosine kinase activity, or PKC activation. |
| 572 | 11463575 | Serum apolipoprotein A(1) (apoA(1)) concentration is inversely correlated with the risk of premature atherosclerosis. |
| 573 | 11463575 | Serum apoA(1) concentrations are regulated, in part, at the transcriptional level. |
| 574 | 11463575 | ApoA(1) mRNA is synthesized primarily in the liver and small intestine, under the direction of a number of signaling molecules and tissue-specific regulatory elements. |
| 575 | 11463575 | Previously, we demonstrated that extracellular acidosis suppresses apoA(1) mRNA levels at the level of transcription. |
| 576 | 11463575 | Here we demonstrate that intracellular acidosis, in the absence of extracellular pH changes, represses apoA(1) promoter activity. |
| 577 | 11463575 | Repression occurs through a pH responsive element (pH-RE) located within the apoA(1) gene promoter. |
| 578 | 11463575 | Acidosis increases the specific DNA binding activity of a putative repressor protein within the immediate 5'-flanking region of the apoA(1) gene. |
| 579 | 11463575 | The cis-element that binds the putative repressor protein contains a negative thyroid hormone response element (nTRE) located 3' and adjacent to the apoA(1) TATA box. |
| 580 | 11463575 | Inhibition of tyrosine kinase activity and diacylglycerol-stimulated protein kinase C (PKC) signaling pathways with tyrophostin A47 and phorbol myristate acetate, respectively, did not affect the repression of apoA(1) promoter activity with acidosis. |
| 581 | 11463575 | These results suggest that transcriptional repression of the apoA(1) gene by alterations in ambient pH is associated with enhanced DNA binding activity of a repressor protein, through a mechanism which appears to be independent of de novo mRNA and protein synthesis, tyrosine kinase activity, or PKC activation. |
| 582 | 11463575 | Serum apolipoprotein A(1) (apoA(1)) concentration is inversely correlated with the risk of premature atherosclerosis. |
| 583 | 11463575 | Serum apoA(1) concentrations are regulated, in part, at the transcriptional level. |
| 584 | 11463575 | ApoA(1) mRNA is synthesized primarily in the liver and small intestine, under the direction of a number of signaling molecules and tissue-specific regulatory elements. |
| 585 | 11463575 | Previously, we demonstrated that extracellular acidosis suppresses apoA(1) mRNA levels at the level of transcription. |
| 586 | 11463575 | Here we demonstrate that intracellular acidosis, in the absence of extracellular pH changes, represses apoA(1) promoter activity. |
| 587 | 11463575 | Repression occurs through a pH responsive element (pH-RE) located within the apoA(1) gene promoter. |
| 588 | 11463575 | Acidosis increases the specific DNA binding activity of a putative repressor protein within the immediate 5'-flanking region of the apoA(1) gene. |
| 589 | 11463575 | The cis-element that binds the putative repressor protein contains a negative thyroid hormone response element (nTRE) located 3' and adjacent to the apoA(1) TATA box. |
| 590 | 11463575 | Inhibition of tyrosine kinase activity and diacylglycerol-stimulated protein kinase C (PKC) signaling pathways with tyrophostin A47 and phorbol myristate acetate, respectively, did not affect the repression of apoA(1) promoter activity with acidosis. |
| 591 | 11463575 | These results suggest that transcriptional repression of the apoA(1) gene by alterations in ambient pH is associated with enhanced DNA binding activity of a repressor protein, through a mechanism which appears to be independent of de novo mRNA and protein synthesis, tyrosine kinase activity, or PKC activation. |
| 592 | 11463575 | Serum apolipoprotein A(1) (apoA(1)) concentration is inversely correlated with the risk of premature atherosclerosis. |
| 593 | 11463575 | Serum apoA(1) concentrations are regulated, in part, at the transcriptional level. |
| 594 | 11463575 | ApoA(1) mRNA is synthesized primarily in the liver and small intestine, under the direction of a number of signaling molecules and tissue-specific regulatory elements. |
| 595 | 11463575 | Previously, we demonstrated that extracellular acidosis suppresses apoA(1) mRNA levels at the level of transcription. |
| 596 | 11463575 | Here we demonstrate that intracellular acidosis, in the absence of extracellular pH changes, represses apoA(1) promoter activity. |
| 597 | 11463575 | Repression occurs through a pH responsive element (pH-RE) located within the apoA(1) gene promoter. |
| 598 | 11463575 | Acidosis increases the specific DNA binding activity of a putative repressor protein within the immediate 5'-flanking region of the apoA(1) gene. |
| 599 | 11463575 | The cis-element that binds the putative repressor protein contains a negative thyroid hormone response element (nTRE) located 3' and adjacent to the apoA(1) TATA box. |
| 600 | 11463575 | Inhibition of tyrosine kinase activity and diacylglycerol-stimulated protein kinase C (PKC) signaling pathways with tyrophostin A47 and phorbol myristate acetate, respectively, did not affect the repression of apoA(1) promoter activity with acidosis. |
| 601 | 11463575 | These results suggest that transcriptional repression of the apoA(1) gene by alterations in ambient pH is associated with enhanced DNA binding activity of a repressor protein, through a mechanism which appears to be independent of de novo mRNA and protein synthesis, tyrosine kinase activity, or PKC activation. |
| 602 | 11463575 | Serum apolipoprotein A(1) (apoA(1)) concentration is inversely correlated with the risk of premature atherosclerosis. |
| 603 | 11463575 | Serum apoA(1) concentrations are regulated, in part, at the transcriptional level. |
| 604 | 11463575 | ApoA(1) mRNA is synthesized primarily in the liver and small intestine, under the direction of a number of signaling molecules and tissue-specific regulatory elements. |
| 605 | 11463575 | Previously, we demonstrated that extracellular acidosis suppresses apoA(1) mRNA levels at the level of transcription. |
| 606 | 11463575 | Here we demonstrate that intracellular acidosis, in the absence of extracellular pH changes, represses apoA(1) promoter activity. |
| 607 | 11463575 | Repression occurs through a pH responsive element (pH-RE) located within the apoA(1) gene promoter. |
| 608 | 11463575 | Acidosis increases the specific DNA binding activity of a putative repressor protein within the immediate 5'-flanking region of the apoA(1) gene. |
| 609 | 11463575 | The cis-element that binds the putative repressor protein contains a negative thyroid hormone response element (nTRE) located 3' and adjacent to the apoA(1) TATA box. |
| 610 | 11463575 | Inhibition of tyrosine kinase activity and diacylglycerol-stimulated protein kinase C (PKC) signaling pathways with tyrophostin A47 and phorbol myristate acetate, respectively, did not affect the repression of apoA(1) promoter activity with acidosis. |
| 611 | 11463575 | These results suggest that transcriptional repression of the apoA(1) gene by alterations in ambient pH is associated with enhanced DNA binding activity of a repressor protein, through a mechanism which appears to be independent of de novo mRNA and protein synthesis, tyrosine kinase activity, or PKC activation. |
| 612 | 11463575 | Serum apolipoprotein A(1) (apoA(1)) concentration is inversely correlated with the risk of premature atherosclerosis. |
| 613 | 11463575 | Serum apoA(1) concentrations are regulated, in part, at the transcriptional level. |
| 614 | 11463575 | ApoA(1) mRNA is synthesized primarily in the liver and small intestine, under the direction of a number of signaling molecules and tissue-specific regulatory elements. |
| 615 | 11463575 | Previously, we demonstrated that extracellular acidosis suppresses apoA(1) mRNA levels at the level of transcription. |
| 616 | 11463575 | Here we demonstrate that intracellular acidosis, in the absence of extracellular pH changes, represses apoA(1) promoter activity. |
| 617 | 11463575 | Repression occurs through a pH responsive element (pH-RE) located within the apoA(1) gene promoter. |
| 618 | 11463575 | Acidosis increases the specific DNA binding activity of a putative repressor protein within the immediate 5'-flanking region of the apoA(1) gene. |
| 619 | 11463575 | The cis-element that binds the putative repressor protein contains a negative thyroid hormone response element (nTRE) located 3' and adjacent to the apoA(1) TATA box. |
| 620 | 11463575 | Inhibition of tyrosine kinase activity and diacylglycerol-stimulated protein kinase C (PKC) signaling pathways with tyrophostin A47 and phorbol myristate acetate, respectively, did not affect the repression of apoA(1) promoter activity with acidosis. |
| 621 | 11463575 | These results suggest that transcriptional repression of the apoA(1) gene by alterations in ambient pH is associated with enhanced DNA binding activity of a repressor protein, through a mechanism which appears to be independent of de novo mRNA and protein synthesis, tyrosine kinase activity, or PKC activation. |
| 622 | 11463575 | Serum apolipoprotein A(1) (apoA(1)) concentration is inversely correlated with the risk of premature atherosclerosis. |
| 623 | 11463575 | Serum apoA(1) concentrations are regulated, in part, at the transcriptional level. |
| 624 | 11463575 | ApoA(1) mRNA is synthesized primarily in the liver and small intestine, under the direction of a number of signaling molecules and tissue-specific regulatory elements. |
| 625 | 11463575 | Previously, we demonstrated that extracellular acidosis suppresses apoA(1) mRNA levels at the level of transcription. |
| 626 | 11463575 | Here we demonstrate that intracellular acidosis, in the absence of extracellular pH changes, represses apoA(1) promoter activity. |
| 627 | 11463575 | Repression occurs through a pH responsive element (pH-RE) located within the apoA(1) gene promoter. |
| 628 | 11463575 | Acidosis increases the specific DNA binding activity of a putative repressor protein within the immediate 5'-flanking region of the apoA(1) gene. |
| 629 | 11463575 | The cis-element that binds the putative repressor protein contains a negative thyroid hormone response element (nTRE) located 3' and adjacent to the apoA(1) TATA box. |
| 630 | 11463575 | Inhibition of tyrosine kinase activity and diacylglycerol-stimulated protein kinase C (PKC) signaling pathways with tyrophostin A47 and phorbol myristate acetate, respectively, did not affect the repression of apoA(1) promoter activity with acidosis. |
| 631 | 11463575 | These results suggest that transcriptional repression of the apoA(1) gene by alterations in ambient pH is associated with enhanced DNA binding activity of a repressor protein, through a mechanism which appears to be independent of de novo mRNA and protein synthesis, tyrosine kinase activity, or PKC activation. |
| 632 | 11463575 | Serum apolipoprotein A(1) (apoA(1)) concentration is inversely correlated with the risk of premature atherosclerosis. |
| 633 | 11463575 | Serum apoA(1) concentrations are regulated, in part, at the transcriptional level. |
| 634 | 11463575 | ApoA(1) mRNA is synthesized primarily in the liver and small intestine, under the direction of a number of signaling molecules and tissue-specific regulatory elements. |
| 635 | 11463575 | Previously, we demonstrated that extracellular acidosis suppresses apoA(1) mRNA levels at the level of transcription. |
| 636 | 11463575 | Here we demonstrate that intracellular acidosis, in the absence of extracellular pH changes, represses apoA(1) promoter activity. |
| 637 | 11463575 | Repression occurs through a pH responsive element (pH-RE) located within the apoA(1) gene promoter. |
| 638 | 11463575 | Acidosis increases the specific DNA binding activity of a putative repressor protein within the immediate 5'-flanking region of the apoA(1) gene. |
| 639 | 11463575 | The cis-element that binds the putative repressor protein contains a negative thyroid hormone response element (nTRE) located 3' and adjacent to the apoA(1) TATA box. |
| 640 | 11463575 | Inhibition of tyrosine kinase activity and diacylglycerol-stimulated protein kinase C (PKC) signaling pathways with tyrophostin A47 and phorbol myristate acetate, respectively, did not affect the repression of apoA(1) promoter activity with acidosis. |
| 641 | 11463575 | These results suggest that transcriptional repression of the apoA(1) gene by alterations in ambient pH is associated with enhanced DNA binding activity of a repressor protein, through a mechanism which appears to be independent of de novo mRNA and protein synthesis, tyrosine kinase activity, or PKC activation. |
| 642 | 11463575 | Serum apolipoprotein A(1) (apoA(1)) concentration is inversely correlated with the risk of premature atherosclerosis. |
| 643 | 11463575 | Serum apoA(1) concentrations are regulated, in part, at the transcriptional level. |
| 644 | 11463575 | ApoA(1) mRNA is synthesized primarily in the liver and small intestine, under the direction of a number of signaling molecules and tissue-specific regulatory elements. |
| 645 | 11463575 | Previously, we demonstrated that extracellular acidosis suppresses apoA(1) mRNA levels at the level of transcription. |
| 646 | 11463575 | Here we demonstrate that intracellular acidosis, in the absence of extracellular pH changes, represses apoA(1) promoter activity. |
| 647 | 11463575 | Repression occurs through a pH responsive element (pH-RE) located within the apoA(1) gene promoter. |
| 648 | 11463575 | Acidosis increases the specific DNA binding activity of a putative repressor protein within the immediate 5'-flanking region of the apoA(1) gene. |
| 649 | 11463575 | The cis-element that binds the putative repressor protein contains a negative thyroid hormone response element (nTRE) located 3' and adjacent to the apoA(1) TATA box. |
| 650 | 11463575 | Inhibition of tyrosine kinase activity and diacylglycerol-stimulated protein kinase C (PKC) signaling pathways with tyrophostin A47 and phorbol myristate acetate, respectively, did not affect the repression of apoA(1) promoter activity with acidosis. |
| 651 | 11463575 | These results suggest that transcriptional repression of the apoA(1) gene by alterations in ambient pH is associated with enhanced DNA binding activity of a repressor protein, through a mechanism which appears to be independent of de novo mRNA and protein synthesis, tyrosine kinase activity, or PKC activation. |
| 652 | 11472752 | Plasma insulin, leptin, and soluble TNF receptors levels in relation to obesity-related atherogenic and thrombogenic cardiovascular disease risk factors among men. |
| 653 | 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. |
| 654 | 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. |
| 655 | 11472752 | We measured plasma insulin and leptin levels by radioimmunoassay and sTNF-R levels by ELISA. |
| 656 | 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). |
| 657 | 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. |
| 658 | 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. |
| 659 | 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. |
| 660 | 11472752 | Plasma insulin, leptin, and soluble TNF receptors levels in relation to obesity-related atherogenic and thrombogenic cardiovascular disease risk factors among men. |
| 661 | 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. |
| 662 | 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. |
| 663 | 11472752 | We measured plasma insulin and leptin levels by radioimmunoassay and sTNF-R levels by ELISA. |
| 664 | 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). |
| 665 | 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. |
| 666 | 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. |
| 667 | 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. |
| 668 | 11473048 | Glucose regulates the transcription of human genes relevant to HDL metabolism: responsive elements for peroxisome proliferator-activated receptor are involved in the regulation of phospholipid transfer protein. |
| 669 | 11473048 | Phospholipid transfer protein (PLTP) plays an important role in human plasma HDL metabolism. |
| 670 | 11473048 | In addition, high glucose increases mRNA levels for several genes that are functionally important in HDL metabolism, including human ATP-binding cassette transporter A1, apolipoprotein A-I, scavenger receptor BI, and hepatic lipase. |
| 671 | 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. |
| 672 | 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). |
| 673 | 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. |
| 674 | 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. |
| 675 | 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). |
| 676 | 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. |
| 677 | 11779886 | Apolipoprotein A-I and B and stroke events in a community-based cohort in Taiwan: report of the Chin-Shan Community Cardiovascular Study. |
| 678 | 11853190 | Apolipoprotein A-I concentration in tears in diabetic retinopathy. |
| 679 | 11916929 | A tailored therapy for the metabolic syndrome: the dual peroxisome proliferator-activated receptor-alpha/gamma agonist LY465608 ameliorates insulin resistance and diabetic hyperglycemia while improving cardiovascular risk factors in preclinical models. |
| 680 | 11916929 | Further characterization of LY465608 revealed metabolic changes distinct from a selective PPAR-gamma agonist, which were presumably due to the concomitant PPAR-alpha agonism, lower respiratory quotient, and less fat accumulation, despite a similar impact on glycemia in male ZDF rats. |
| 681 | 11916929 | In addition to these alterations in diabetic and insulin-resistant animals, LY465608 dose-dependently elevated HDL cholesterol and lowered plasma triglycerides in human apolipoprotein A-I transgenic mice, demonstrating that this compound significantly improves primary cardiovascular risk factors. |
| 682 | 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. |
| 683 | 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). |
| 684 | 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. |
| 685 | 12401722 | Relationship of phospholipid transfer protein activity to HDL and apolipoprotein B-containing lipoproteins in subjects with and without type 1 diabetes. |
| 686 | 12401722 | Patients with type 1 diabetes have greatly increased phospholipid transfer protein (PLTP) activity and have an altered HDL subclass distribution. |
| 687 | 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. |
| 688 | 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). |
| 689 | 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). |
| 690 | 12401722 | PLTP activity was also positively associated with apoB, total VLDL and LDL particle number, and IDL level in subjects with diabetes. |
| 691 | 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. |
| 692 | 12401722 | They also support a role for PLTP in the metabolism of apoB-containing lipoproteins. |
| 693 | 12486210 | Apolipoprotein A-I expression in rats is not altered by troglitazone. |
| 694 | 12486210 | Insulin is known to upregulate apolipoprotein A-I (apoA-I) promoter activity and to increase apoA1 gene expression in vivo. |
| 695 | 12486210 | Intestinal apoA-I mRNA content relative to glyceraldehyde-3 phosphate dehydrogenase (G(3)PDH) mRNA was significantly lower compared with hepatic tissue content in both control and troglitazone-treated rats. |
| 696 | 12486210 | However, peroxisome proliferator activator receptor (PPAR) agonists that have significant PPAR alpha activity in addition to their PPAR gamma effects, may well be able to induce apoA-I expression. |
| 697 | 12486210 | Apolipoprotein A-I expression in rats is not altered by troglitazone. |
| 698 | 12486210 | Insulin is known to upregulate apolipoprotein A-I (apoA-I) promoter activity and to increase apoA1 gene expression in vivo. |
| 699 | 12486210 | Intestinal apoA-I mRNA content relative to glyceraldehyde-3 phosphate dehydrogenase (G(3)PDH) mRNA was significantly lower compared with hepatic tissue content in both control and troglitazone-treated rats. |
| 700 | 12486210 | However, peroxisome proliferator activator receptor (PPAR) agonists that have significant PPAR alpha activity in addition to their PPAR gamma effects, may well be able to induce apoA-I expression. |
| 701 | 12562839 | Pre beta 1-HDL is thought to be either the initial acceptor of cellular cholesterol or virtually the first particle in the pathway of the formation of HDL from apolipoprotein A-I and cellular lipids. |
| 702 | 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. |
| 703 | 12639401 | The level of apolipoprotein B registered a significant fall together with a significant increment in the level of apolipoprotein A1. |
| 704 | 12679171 | Effect of chromium on apolipoprotein A-I expression in HepG2 cells. |
| 705 | 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. |
| 706 | 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. |
| 707 | 12766975 | The inherited amyloid neuropathies are due to mutations of three proteins: transthyretin, apolipoprotein A1, and gelsolin. |
| 708 | 12777470 | LPL was positively correlated with the apolipoprotein A-I (apoA-I), cholesterol, and phospholipid mass in total Lp(A-I), and with the apoA-I in large Lp(A-I) (r >or= 0.58, P >or= 0.001). |
| 709 | 12777470 | No correlation was detected between LPL and Lp(A-I,A-II). |
| 710 | 12948871 | Elevated levels of intracellular cholesterol stimulate the liver X receptor pathway, enhancing the expression of ABCA1, which increases intracellular trafficking of excess cholesterol to the cell surface for interaction with lipid-poor apolipoprotein A-I to form nascent HDL. |
| 711 | 12951168 | Although isolated low plasma HDL-cholesterol (HDL-c) and apolipoprotein A-I (apo A-I, the major apolipoprotein component of HDL) can occur in the absence of hypertriglyceridemia or any other features of insulin resistance, the majority of cases in which HDL-c is low are closely linked with other clinical features of insulin resistance and hypertriglyceridemia. |
| 712 | 12957326 | Plasma levels of high-density lipoprotein (HDL) cholesterol and its major protein, apolipoprotein A-I, are inversely correlated with the incidence of atherosclerotic cardiovascular disease. |
| 713 | 12957326 | Low HDL cholesterol and apolipoprotein A-I levels often are found in association with other cardiovascular risk factors, including the metabolic syndrome, insulin resistance, and type 2 diabetes mellitus. |
| 714 | 12957326 | However, overexpression of apolipoprotein A-I in animals has been shown to reduce progression and even induce regression of atherosclerosis, indicating that apolipoprotein A-I is directly protective against atherosclerosis. |
| 715 | 12957326 | A major mechanism by which apolipoprotein A-I inhibits atherosclerosis may be by promoting cholesterol efflux from macrophages and returning it to the liver for excretion, a process termed reverse cholesterol transport. |
| 716 | 12957326 | Plasma levels of high-density lipoprotein (HDL) cholesterol and its major protein, apolipoprotein A-I, are inversely correlated with the incidence of atherosclerotic cardiovascular disease. |
| 717 | 12957326 | Low HDL cholesterol and apolipoprotein A-I levels often are found in association with other cardiovascular risk factors, including the metabolic syndrome, insulin resistance, and type 2 diabetes mellitus. |
| 718 | 12957326 | However, overexpression of apolipoprotein A-I in animals has been shown to reduce progression and even induce regression of atherosclerosis, indicating that apolipoprotein A-I is directly protective against atherosclerosis. |
| 719 | 12957326 | A major mechanism by which apolipoprotein A-I inhibits atherosclerosis may be by promoting cholesterol efflux from macrophages and returning it to the liver for excretion, a process termed reverse cholesterol transport. |
| 720 | 12957326 | Plasma levels of high-density lipoprotein (HDL) cholesterol and its major protein, apolipoprotein A-I, are inversely correlated with the incidence of atherosclerotic cardiovascular disease. |
| 721 | 12957326 | Low HDL cholesterol and apolipoprotein A-I levels often are found in association with other cardiovascular risk factors, including the metabolic syndrome, insulin resistance, and type 2 diabetes mellitus. |
| 722 | 12957326 | However, overexpression of apolipoprotein A-I in animals has been shown to reduce progression and even induce regression of atherosclerosis, indicating that apolipoprotein A-I is directly protective against atherosclerosis. |
| 723 | 12957326 | A major mechanism by which apolipoprotein A-I inhibits atherosclerosis may be by promoting cholesterol efflux from macrophages and returning it to the liver for excretion, a process termed reverse cholesterol transport. |
| 724 | 12957326 | Plasma levels of high-density lipoprotein (HDL) cholesterol and its major protein, apolipoprotein A-I, are inversely correlated with the incidence of atherosclerotic cardiovascular disease. |
| 725 | 12957326 | Low HDL cholesterol and apolipoprotein A-I levels often are found in association with other cardiovascular risk factors, including the metabolic syndrome, insulin resistance, and type 2 diabetes mellitus. |
| 726 | 12957326 | However, overexpression of apolipoprotein A-I in animals has been shown to reduce progression and even induce regression of atherosclerosis, indicating that apolipoprotein A-I is directly protective against atherosclerosis. |
| 727 | 12957326 | A major mechanism by which apolipoprotein A-I inhibits atherosclerosis may be by promoting cholesterol efflux from macrophages and returning it to the liver for excretion, a process termed reverse cholesterol transport. |
| 728 | 14510906 | Association of two apolipoprotein A-I gene MspI polymorphisms with high density lipoprotein (HDL)-cholesterol levels and indices of obesity in selected healthy Chinese subjects and in patients with early-onset type 2 diabetes. |
| 729 | 14988232 | Transcriptional control of apolipoprotein A-I gene expression in diabetes. |
| 730 | 15223114 | The role of angiotensin-converting enzyme and apolipoprotein-E gene polymorphisms on lipid compositions in newborn infants with intrauterine growth restriction. |
| 731 | 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. |
| 732 | 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. |
| 733 | 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). |
| 734 | 15223225 | Males were characterized by higher uric acid and lower HDL-cholesterol and apoA(1) levels (two-way ANOVA considering jointly age and gender as main effects, P < 0.05 in every case). |
| 735 | 15259000 | Glycosylphosphatidylinositol-specific phospholipase D immunoreactivity is present in islet amyloid in type 2 diabetes. |
| 736 | 15259000 | Since GPI-PLD is synthesized by, and secreted from, pancreatic islet beta cells, the present study examined the hypothesis that GPI-PLD associates with islet amyloid. |
| 737 | 15259000 | Fibril formation from human islet amyloid polypeptide was determined in the absence or presence of GPI-PLD. |
| 738 | 15259000 | In non-diabetics, GPI-PLD immunoreactivity was present and co-localized with insulin, as opposed to co-localizing with amyloid in diabetics. |
| 739 | 15259000 | No immunoreactivity for apolipoprotein A-I was present in islet cells or islet amyloid. |
| 740 | 15259000 | Heparan sulphate proteoglycan, which is commonly present in most amyloid, bound GPI-PLD in vitro. |
| 741 | 15259000 | GPI-PLD inhibited the formation of amyloid fibrils from synthetic islet amyloid polypeptide in vitro. |
| 742 | 15259000 | GPI-PLD is therefore present in islet amyloid and appears to derive from local production from islets. |
| 743 | 15259000 | Since GPI-PLD also inhibited islet amyloid polypeptide fibril formation in vitro, it is concluded that GPI-PLD may play a role in islet amyloid formation in type 2 diabetes. |
| 744 | 15320783 | Additional targets have begun gaining prominence in the past few years -- modulation of proteins involved in reverse cholesterol transport and lipid metabolism in the vessel wall such as ApoA1/apoE/ABCA1, ACAT, and LpPLA2 and regulation of molecules involved in matrix remodeling and cell proliferation such as matrix metalloproteinases and heparan sulfate proteoglycans. |
| 745 | 15378114 | Moreover, the number of affected vessels displayed a significant positive correlation with the presence of diabetes mellitus (rs = 0.30; p < 0.0001; n = 155) and serum concentrations of lipoprotein (a) (rs = 0.25; p < 0.05; n = 67) and a negative correlation with apolipoprotein A-I serum concentration (rs = -0.27; p < 0.01; n = 67). |
| 746 | 15607389 | These beneficial effects may be responsible for coronary plaque stabilization in patients treated with recombinant Apolipoprotein A-I Milano/phospholipid complex. |
| 747 | 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). |
| 748 | 15658274 | [Lipid-poor apolipoprotein A-I, glycated apolipoprotein A-I]. |
| 749 | 15925013 | Overproduction of VLDL leads to increased plasma levels of TG which, via an exchange process mediated by cholesterol ester transfer protein (CETP), results in low levels of high density lipoprotein (HDL) cholesterol and apolipoprotein A-I, and the generation of small, dense, cholesterol ester depleted low density lipoproteins (LDL). |
| 750 | 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. |
| 751 | 15983229 | Black CC homozygotes had lower baseline lipoprotein lipase activity, HDL cholesterol, HDL3, and apolipoprotein (apo)A-1 concentrations. |
| 752 | 15983229 | White CC homozygotes had lower baseline HDL cholesterol, apoA-1, LDL cholesterol, and apoB levels that remained low post-exercise training. |
| 753 | 16005361 | Evaluation of apolipoprotein E secretion by macrophages in type 2 diabetic patients: role of HDL and apolipoprotein A-I. |
| 754 | 16005361 | It has been shown that apolipoprotein A-I (ApoA-I) stimulates the secretion of apolipoprotein E (ApoE) from human macrophages. |
| 755 | 16005361 | Evaluation of apolipoprotein E secretion by macrophages in type 2 diabetic patients: role of HDL and apolipoprotein A-I. |
| 756 | 16005361 | It has been shown that apolipoprotein A-I (ApoA-I) stimulates the secretion of apolipoprotein E (ApoE) from human macrophages. |
| 757 | 16006255 | Circulating levels of nitrated apolipoprotein A-I are increased in type 2 diabetic patients. |
| 758 | 16006255 | Since accelerated atherogenesis is a key complication of diabetes mellitus, and nitrosative stress has recently been implicated in diabetic pathology, we set out to demonstrate an increase in the circulating levels of nitrated apolipoprotein A (apoA)-I in type 2 diabetic patients and its putative correlation with metabolic biomarkers. |
| 759 | 16080911 | From the eight spots, six proteins were identified, including PEDF, ApoA-4, ApoA-1, Trip-11, PRBP, and VDBP. |
| 760 | 16155262 | Hypovitaminosis D is associated with reductions in serum apolipoprotein A-I but not with fasting lipids in British Bangladeshis. |
| 761 | 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). |
| 762 | 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. |
| 763 | 16243964 | The effect of select nutrients on serum high-density lipoprotein cholesterol and apolipoprotein A-I levels. |
| 764 | 16243964 | Multiple potential mechanisms account for the cardioprotective effects of HDL and its main protein apolipoprotein A-I (apo A-I). |
| 765 | 16243964 | The effect of select nutrients on serum high-density lipoprotein cholesterol and apolipoprotein A-I levels. |
| 766 | 16243964 | Multiple potential mechanisms account for the cardioprotective effects of HDL and its main protein apolipoprotein A-I (apo A-I). |
| 767 | 16256006 | Most consistent are greater changes in high-density lipoprotein (HDL), HDL2, and apolipoprotein A-I levels in women compared with men with high-carbohydrate or high-fat feeding. |
| 768 | 16327022 | Highly significant (P < 0.0001), positive associations were observed between PON1 activities and concentrations and HDL-cholesterol and apolipoprotein A-I (apoA-I) concentrations in cases and controls. |
| 769 | 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. |
| 770 | 16401881 | Mass kinetics of apolipoprotein A-I in interstitial fluid after administration of intravenous apolipoprotein A-I/lecithin discs in humans. |
| 771 | 16401881 | To determine these parameters for a pharmacologic dose of exogenous apolipoprotein A-I (apoA-I) given intravenously as apoA-I/lecithin discs, we measured apoA-I in plasma and prenodal leg lymph in five healthy men before, during, and after a 4 h infusion at 10 mg/kg/h. |
| 772 | 16401881 | Mass kinetics of apolipoprotein A-I in interstitial fluid after administration of intravenous apolipoprotein A-I/lecithin discs in humans. |
| 773 | 16401881 | To determine these parameters for a pharmacologic dose of exogenous apolipoprotein A-I (apoA-I) given intravenously as apoA-I/lecithin discs, we measured apoA-I in plasma and prenodal leg lymph in five healthy men before, during, and after a 4 h infusion at 10 mg/kg/h. |
| 774 | 16423621 | Ascorbic acid and alpha-tocopherol down-regulate apolipoprotein A-I gene expression in HepG2 and Caco-2 cell lines. |
| 775 | 16423621 | HepG2 cells and Caco-2 cells were treated with various concentrations of select antioxidants to study some of the molecular pathways underlying antioxidant-related changes in apolipoprotein A-I (apoA-I) expression. |
| 776 | 16423621 | Ascorbic acid and alpha-tocopherol down-regulate apolipoprotein A-I gene expression in HepG2 and Caco-2 cell lines. |
| 777 | 16423621 | HepG2 cells and Caco-2 cells were treated with various concentrations of select antioxidants to study some of the molecular pathways underlying antioxidant-related changes in apolipoprotein A-I (apoA-I) expression. |
| 778 | 16448983 | Recently, apolipoprotein A5 (APOA5) was identified as a novel member of the APOA1/C3/A4 gene cluster. |
| 779 | 16448983 | Data from mice over-expressing or lacking APOA5 provide direct evidence that this apolipoprotein plays a role in triglyceride metabolism. |
| 780 | 16448983 | Insulin and interleukins regulate APOA5 gene expression and provide novel clues for the role of this apolipoprotein. |
| 781 | 16448983 | To date, the triglyceride lowering action of apoA-V is attributed to the activation of lipoprotein lipase and an acceleration of very low density lipoprotein catabolism. |
| 782 | 16500635 | Lower serum paraoxonase-1 activity in type 2 diabetic patients correlates with nitrated apolipoprotein A-I levels. |
| 783 | 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). |
| 784 | 16603689 | Neither ATP-binding cassette transporter G1 (ABCG1)- nor scavenger receptor class B type I (SR-BI)-mediated cholesterol efflux was affected. |
| 785 | 16603689 | Cellular cholesterol efflux to apolipoprotein A-I was not significantly reduced in Cav-1(-/-) MPMs compared with wild-type MPMs. |
| 786 | 16603689 | However, ABCA1-mediated cholesterol efflux was clearly more sensitive to the inhibitory effects of glyburide in Cav-1(-/-) MPMs versus WT MPMs. |
| 787 | 16637783 | Emerging risk factors for coronary heart disease (CHD), including low concentrations of high-density lipoprotein (HDL) cholesterol and apolipoprotein A-1 (apoA-1), high levels of high-sensitivity C-reactive protein, and small dense low-density lipoprotein cholesterol particles, have been identified. |
| 788 | 16637783 | The new and emerging drug therapies include an antiobesity agent that reduces atherogenic dyslipidemia and abnormal glucose metabolism; cholesteryl ester transfer protein inhibitors that increase HDL cholesterol and apoA-1 levels; glitazars that increase HDL cholesterol and decrease triglyceride concentrations, as well as improve abnormal glucose metabolism; and the amylin analog pramlintide and the incretin mimetic exenatide, both of which reduce body weight as well as improve abnormal glucose metabolism. |
| 789 | 16637783 | The insulin-sensitizing effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers (ARBs), which may help prevent new-onset diabetes mellitus, and the beneficial effects of the ARB telmisartan on the glucose and lipid profiles also are presented. |
| 790 | 16637783 | Emerging risk factors for coronary heart disease (CHD), including low concentrations of high-density lipoprotein (HDL) cholesterol and apolipoprotein A-1 (apoA-1), high levels of high-sensitivity C-reactive protein, and small dense low-density lipoprotein cholesterol particles, have been identified. |
| 791 | 16637783 | The new and emerging drug therapies include an antiobesity agent that reduces atherogenic dyslipidemia and abnormal glucose metabolism; cholesteryl ester transfer protein inhibitors that increase HDL cholesterol and apoA-1 levels; glitazars that increase HDL cholesterol and decrease triglyceride concentrations, as well as improve abnormal glucose metabolism; and the amylin analog pramlintide and the incretin mimetic exenatide, both of which reduce body weight as well as improve abnormal glucose metabolism. |
| 792 | 16637783 | The insulin-sensitizing effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers (ARBs), which may help prevent new-onset diabetes mellitus, and the beneficial effects of the ARB telmisartan on the glucose and lipid profiles also are presented. |
| 793 | 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. |
| 794 | 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). |
| 795 | 16781717 | The apolipoprotein gene cluster (APOA1/C3/A4/A5) was recently associated with triglycerides (TG) and high-density lipoprotein cholesterol (HDL-C) in non-diabetic population. |
| 796 | 16781717 | In addition, APOC3 promoter polymorphism -455T/C showed significant associations with fasting TG levels (P=0.006), whereas APOA4 +347T/A showed significant associations with lower levels of HDL-C (P=0.017). |
| 797 | 16968945 | Indeed, formation of HDL particles with attenuated antiatherogenic activity is mechanistically related to core lipid enrichment in triglycerides and cholesteryl ester depletion, altered apolipoprotein A-I (apoA-I) conformation, replacement of apoA-I by serum amyloid A, and covalent modification of HDL protein components by oxidation and glycation. |
| 798 | 16990839 | Apolipoprotein A-I mimetic peptides and their role in atherosclerosis prevention. |
| 799 | 16990839 | The importance of apolipoprotein A-I (apoA-I) in atherosclerosis was established by testing in animal models, and its potential usefulness in humans has been confirmed in preliminary studies. |
| 800 | 16990839 | Apolipoprotein A-I mimetic peptides and their role in atherosclerosis prevention. |
| 801 | 16990839 | The importance of apolipoprotein A-I (apoA-I) in atherosclerosis was established by testing in animal models, and its potential usefulness in humans has been confirmed in preliminary studies. |
| 802 | 17059798 | Most consistent are greater changes in high-density lipoprotein (HDL), HDL(2), and apolipoprotein A-I levels in women compared with men with high-carbohydrate or high-fat feeding. |
| 803 | 17082477 | Oxidative modification of the apolipoprotein A-I inhibits reverse cholesterol transport. |
| 804 | 17174291 | Establishment and evaluation of 2 monoclonal antibodies against oxidized apolipoprotein A-I (apoA-I) and its application to determine blood oxidized apoA-I levels. |
| 805 | 17199733 | Metabolism of high density lipoprotein apolipoprotein A-I and cholesteryl ester in insulin resistant dog: a stable isotope study. |
| 806 | 17216278 | The impact of glycation on apolipoprotein A-I structure and its ability to activate lecithin:cholesterol acyltransferase. |
| 807 | 17287470 | Although ATP-binding cassette transporter A1 (ABCA1) is well known for its role in cholesterol efflux and HDL formation, it is expressed in various tissues, where it may have different functions. |
| 808 | 17287470 | The variant was significantly associated not only with decreased HDL cholesterol and apolipoprotein A-I levels but also with obesity (odds ratio 2.527, P = 0.005), the metabolic syndrome (1.893, P = 0.0007), and type 2 diabetes (4.527, P = 0.003). |
| 809 | 17525004 | PON1 activity is inversely related to LDL apoB carbonyl content in patients with coronary artery disease. |
| 810 | 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. |
| 811 | 17525004 | All subjects were assayed for apoB carbonyl content, LDL-malondialdehyde (LDL-MDA), PON1 activity, and lipid and apolipoprotein levels. |
| 812 | 17525004 | A significantly (p < 0.01) negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 813 | 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. |
| 814 | 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. |
| 815 | 17525004 | A significantly negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 816 | 17639303 | Apolipoprotein A-I stimulates AMP-activated protein kinase and improves glucose metabolism. |
| 817 | 17697528 | Study of ATP-binding cassette transporter A1 (ABCA1)-mediated cellular cholesterol efflux in diabetic golden hamsters. |
| 818 | 17697528 | The effects of cyclic adenosine monophosphate (cAMP) and atorvastatin on macrophage adenosine triphosphate (ATP)-binding cassette transporter A1 (ABCA1)-mediated cholesterol efflux were investigated in a diabetic animal model. |
| 819 | 17697528 | Peritoneal macrophages were incubated with apolipoprotein A-1 (apoA-1), 8-bromoadenosine-3',5'-cyclic monophosphate (8-br-cAMP), and atorvastatin in vitro. |
| 820 | 17872455 | Pioglitazone stimulates apolipoprotein A-I production without affecting HDL removal in HepG2 cells: involvement of PPAR-alpha. |
| 821 | 17884441 | A novel peroxisome proliferator--activated receptor alpha/gamma dual agonist ameliorates dyslipidemia and insulin resistance in prediabetic rhesus monkeys. |
| 822 | 17884441 | Plasma triglyceride and apolipoprotein B-100 levels decreased, whereas apolipoprotein A-I increased during TAK-559 treatment. |
| 823 | 18160070 | The relation of leptin and insulin with obesity-related cardiovascular risk factors in US adults. |
| 824 | 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. |
| 825 | 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. |
| 826 | 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. |
| 827 | 18160070 | However, leptin levels were not independently associated with CRP and fibrinogen in men and CRP in women when adjusted for WC. |
| 828 | 18160070 | Positive associations of leptin and insulin with fibrinogen in women, independent of WC, were noted. |
| 829 | 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. |
| 830 | 18160070 | However, we cannot rule out the possibility that leptin and insulin influence cardiovascular risk in women through independent effects on fibrinogen concentrations. |
| 831 | 18202432 | Methionine (Met) residues in apolipoprotein A-I (apoA-I), the major apolipoprotein of HDL, reduce peroxides in HDL lipids, forming methionine sulfoxide [Met(O)]. |
| 832 | 18271034 | We report that incubation of ABLC with recombinant human apolipoprotein A-I (apoA-I) induces solubilization of ABLC by transforming the micron sized phospholipid/AMB assemblies into discrete nanoscale disk-shaped complexes termed nanodisks (ND). |
| 833 | 18277343 | ApoB/ApoA1 ratio and subclinical atherosclerosis. |
| 834 | 18332268 | Human apolipoprotein A-I gene transfer reduces the development of experimental diabetic cardiomyopathy. |
| 835 | 18417073 | One way to accomplish this is through the use of apolipoprotein A-I mimetic peptides, which remove oxidation products from lipoproteins and cell membranes, returning normal structure and function to low-density lipoprotein and HDL. |
| 836 | 18437350 | Effects of cross-link breakers, glycation inhibitors and insulin sensitisers on HDL function and the non-enzymatic glycation of apolipoprotein A-I. |
| 837 | 18457010 | Triglycerides, HDL-cholesterol, apolipoprotein B, apolipoprotein A1, glucose and HOMA index, were measured too. |
| 838 | 18480348 | Newly developed pharmacological agents include apolipoprotein A-I mimetics and the cholesteryl ester transfer protein (CETP) inhibitors, JTT-705 and torcetrapib, the latter of which has been recently withdrawn from clinical testing because of serious adverse effects. |
| 839 | 18521458 | Apolipoprotein B/apolipoprotein A-I ratio in relation to various definitions of metabolic syndrome among Saudi patients with type 2 diabetes mellitus. |
| 840 | 18595673 | Plasma sRAGE were negatively and significantly correlated with BMI, waist/hip circumference ratio and fasting glycemia, while a positive correlation was observed with apolipoprotein A-I. |
| 841 | 18622028 | Enhancing apolipoprotein A-I-dependent cholesterol efflux elevates cholesterol export from macrophages in vivo. |
| 842 | 18622028 | Eight proteins potentially involved in cholesterol efflux [ABCA1, ABCG1, CYP27A1, phospholipid transfer protein (PLTP), scavenger receptor type BI (SR-BI), caveolin-1, cholesteryl ester transfer protein, and apolipoprotein A-I (apoA-I)] were overexpressed alone or in combination in RAW 264.7 macrophages. |
| 843 | 18622028 | When apoA-I was used as an acceptor, overexpression of the combination of ABCA1, CYP27A1, PLTP, and SR-BI (Combination I) enhanced the efflux by 4.3-fold. |
| 844 | 18622028 | When HDL was used as an acceptor, overexpression of caveolin-1 or a combination of caveolin-1 and SR-BI (Combination II) was the most active, doubling the efflux to HDL, without affecting the efflux to apoA-I. |
| 845 | 18622028 | Enhancing apolipoprotein A-I-dependent cholesterol efflux elevates cholesterol export from macrophages in vivo. |
| 846 | 18622028 | Eight proteins potentially involved in cholesterol efflux [ABCA1, ABCG1, CYP27A1, phospholipid transfer protein (PLTP), scavenger receptor type BI (SR-BI), caveolin-1, cholesteryl ester transfer protein, and apolipoprotein A-I (apoA-I)] were overexpressed alone or in combination in RAW 264.7 macrophages. |
| 847 | 18622028 | When apoA-I was used as an acceptor, overexpression of the combination of ABCA1, CYP27A1, PLTP, and SR-BI (Combination I) enhanced the efflux by 4.3-fold. |
| 848 | 18622028 | When HDL was used as an acceptor, overexpression of caveolin-1 or a combination of caveolin-1 and SR-BI (Combination II) was the most active, doubling the efflux to HDL, without affecting the efflux to apoA-I. |
| 849 | 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. |
| 850 | 18758514 | Human macrophages cultured with P-407 exhibit a concentration-dependent reduction in cholesterol efflux to apolipoprotein A1 (apoA1) linked to downregulation of the ATP-binding cassette transporter A1 (ABCA1). |
| 851 | 18758514 | Activators of peroxisome proliferator-activated receptor gamma (PPARgamma), as well as PPARalpha, increase expression of liver X receptor alpha (LXRalpha) in macrophages and promote the expression of ABCA1, which, in turn, mediates cholesterol efflux to apoA1. |
| 852 | 18758514 | Because thiazolidinedione drugs (PPARgamma agonists) improve glycemic control in type 2 diabetes by reducing blood glucose concentrations, P-407 was also evaluated for its potential to alter plasma insulin and blood glucose concentrations in wild-type (C57BL/6) and PPARgamma-deficient mice. |
| 853 | 18758514 | Human macrophages cultured with P-407 exhibit a concentration-dependent reduction in cholesterol efflux to apolipoprotein A1 (apoA1) linked to downregulation of the ATP-binding cassette transporter A1 (ABCA1). |
| 854 | 18758514 | Activators of peroxisome proliferator-activated receptor gamma (PPARgamma), as well as PPARalpha, increase expression of liver X receptor alpha (LXRalpha) in macrophages and promote the expression of ABCA1, which, in turn, mediates cholesterol efflux to apoA1. |
| 855 | 18758514 | Because thiazolidinedione drugs (PPARgamma agonists) improve glycemic control in type 2 diabetes by reducing blood glucose concentrations, P-407 was also evaluated for its potential to alter plasma insulin and blood glucose concentrations in wild-type (C57BL/6) and PPARgamma-deficient mice. |
| 856 | 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. |
| 857 | 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. |
| 858 | 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. |
| 859 | 18991244 | Consumption of omega-3 enriched eggs resulted in higher levels of ApoA1, lower ApoB/ApoA1 ratio and lower plasma glucose. |
| 860 | 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. |
| 861 | 18991244 | Consumption of omega-3 enriched eggs resulted in higher levels of ApoA1, lower ApoB/ApoA1 ratio and lower plasma glucose. |
| 862 | 18993152 | Furthermore, niacin significantly increased the large alpha-1 apolipoprotein A-I-containing HDL subspecies (12 to 17 nm). |
| 863 | 19080728 | Apolipoprotein A-I mimetic peptides. |
| 864 | 19080728 | Recent publications reveal the mechanism of action of apolipoprotein A-I (apoA-I) mimetic peptides to be the remarkable binding affinity that oxidized lipids have for these peptides compared with apoA-I. |
| 865 | 19080728 | The apoA-I mimetic peptide 4F increased the formation of pre-beta high-density lipoprotein, increased cholesterol efflux, and reduced lipoprotein oxidation in vitro; it increased antioxidants and vascular repair in type 1 diabetic rats; it improved vasodilation, oxidative stress, myocardial inflammation, and angiogenic potential in a mouse model of scleroderma; it reduced renal inflammation in low-density lipoprotein receptor-null mice fed a Western diet; it reduced arthritis in a rat model; it reduced adiposity, increased adiponectin levels, and improved insulin sensitivity in obese mice; and it improved high-density lipoprotein inflammatory properties in humans with coronary heart disease. |
| 866 | 19080728 | Apolipoprotein A-I mimetic peptides. |
| 867 | 19080728 | Recent publications reveal the mechanism of action of apolipoprotein A-I (apoA-I) mimetic peptides to be the remarkable binding affinity that oxidized lipids have for these peptides compared with apoA-I. |
| 868 | 19080728 | The apoA-I mimetic peptide 4F increased the formation of pre-beta high-density lipoprotein, increased cholesterol efflux, and reduced lipoprotein oxidation in vitro; it increased antioxidants and vascular repair in type 1 diabetic rats; it improved vasodilation, oxidative stress, myocardial inflammation, and angiogenic potential in a mouse model of scleroderma; it reduced renal inflammation in low-density lipoprotein receptor-null mice fed a Western diet; it reduced arthritis in a rat model; it reduced adiposity, increased adiponectin levels, and improved insulin sensitivity in obese mice; and it improved high-density lipoprotein inflammatory properties in humans with coronary heart disease. |
| 869 | 19103817 | Newly developed pharmacological agents include apolipoprotein A-I mimetics and the cholesteryl ester transfer protein (CETP) inhibitors, JTT-705 and torcetrapib, the latter of which has been recently withdrawn from clinical testing because of serious adverse effects. |
| 870 | 19125585 | The expression of apolipoprotein A-I was reduced by 4.2-fold, and galectin-1 was increased 4.8 times in diabetic samples. |
| 871 | 19168444 | An in vivo kinetic study of HDL-apolipoprotein A-I (apoA-I) with (13)C leucine was performed at the end of each treatment period. |
| 872 | 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. |
| 873 | 19264209 | Anti-IL-5 and anti-IL-6 antibodies were effective for the treatment of respectively hypereosinophilic syndrome and rheumatoid arthritis. |
| 874 | 19273745 | We investigated the role of high-density lipoprotein (HDL) on Ang II type 1 receptor (AT1R) regulation and subsequent Ang II-mediated signaling under diabetic conditions. |
| 875 | 19273745 | To investigate the effect of HDL on AT1R expression in vivo, apolipoprotein A-I gene transfer was performed 5 days after streptozotocin injection. |
| 876 | 19273745 | Six weeks after apolipoprotein A-I gene transfer, the 1.9-fold (P=0.001) increase of HDL cholesterol was associated with a 4.7-fold (P<0.05) reduction in diabetes mellitus-induced aortic AT1R expression. |
| 877 | 19273745 | Apolipoprotein A-I transfer improved NO bioavailability as indicated by ameliorated acetylcholine-dependent vasodilation in the streptozotocin-Ad.hapoA-I group compared with streptozotocin-induced diabetes mellitus. |
| 878 | 19273745 | We investigated the role of high-density lipoprotein (HDL) on Ang II type 1 receptor (AT1R) regulation and subsequent Ang II-mediated signaling under diabetic conditions. |
| 879 | 19273745 | To investigate the effect of HDL on AT1R expression in vivo, apolipoprotein A-I gene transfer was performed 5 days after streptozotocin injection. |
| 880 | 19273745 | Six weeks after apolipoprotein A-I gene transfer, the 1.9-fold (P=0.001) increase of HDL cholesterol was associated with a 4.7-fold (P<0.05) reduction in diabetes mellitus-induced aortic AT1R expression. |
| 881 | 19273745 | Apolipoprotein A-I transfer improved NO bioavailability as indicated by ameliorated acetylcholine-dependent vasodilation in the streptozotocin-Ad.hapoA-I group compared with streptozotocin-induced diabetes mellitus. |
| 882 | 19273745 | We investigated the role of high-density lipoprotein (HDL) on Ang II type 1 receptor (AT1R) regulation and subsequent Ang II-mediated signaling under diabetic conditions. |
| 883 | 19273745 | To investigate the effect of HDL on AT1R expression in vivo, apolipoprotein A-I gene transfer was performed 5 days after streptozotocin injection. |
| 884 | 19273745 | Six weeks after apolipoprotein A-I gene transfer, the 1.9-fold (P=0.001) increase of HDL cholesterol was associated with a 4.7-fold (P<0.05) reduction in diabetes mellitus-induced aortic AT1R expression. |
| 885 | 19273745 | Apolipoprotein A-I transfer improved NO bioavailability as indicated by ameliorated acetylcholine-dependent vasodilation in the streptozotocin-Ad.hapoA-I group compared with streptozotocin-induced diabetes mellitus. |
| 886 | 19332654 | Maturation of apolipoprotein A-I: unrecognized health benefit or a forgotten rudiment? |
| 887 | 19388968 | Carotid intima-media thickness and apolipoprotein B/apolipoprotein A-I ratio in middle-aged patients with Type 2 diabetes. |
| 888 | 19408098 | APOA1 polymorphisms were associated with age-related morbidities, as well as with triglycerides, total cholesterol, HDL, VLDL, LDL, creatinine, urea, albumin, glycated hemoglobin and fasting glucose serum levels. |
| 889 | 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. |
| 890 | 19539140 | In addition to high-density lipoprotein cholesterol, apolipoprotein A-I therapies and the promotion of cholesterol efflux from macrophages by the ABCA1 and ABCG1 transporter systems hold great promise and may be available for therapeutic application in the near future. |
| 891 | 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. |
| 892 | 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. |
| 893 | 19605528 | SPI did not affect serum total cholesterol, HDL cholesterol, triacylglycerol, apolipoprotein B, or apolipoprotein A-I. |
| 894 | 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. |
| 895 | 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. |
| 896 | 19605528 | SPI did not affect serum total cholesterol, HDL cholesterol, triacylglycerol, apolipoprotein B, or apolipoprotein A-I. |
| 897 | 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. |
| 898 | 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. |
| 899 | 19605528 | SPI did not affect serum total cholesterol, HDL cholesterol, triacylglycerol, apolipoprotein B, or apolipoprotein A-I. |
| 900 | 19628574 | The comparative analysis of beta-cells from wild-type and LDL receptor-deficient mice revealed that the inhibitory effect of LDL on insulin secretion but not proliferation requires the LDL receptor. |
| 901 | 19628574 | HDL was found to modulate the survival of both human and murine islets by decreasing basal as well as IL-1beta and glucose-induced apoptosis. |
| 902 | 19628574 | IL-1beta-induced beta-cell apoptosis was also inhibited in the presence of either the delipidated protein or the deproteinated lipid moieties of HDL, apolipoprotein A1 (the main protein component of HDL), or sphingosine-1-phosphate (a bioactive sphingolipid mostly carried by HDL). |
| 903 | 19628574 | In murine beta-cells, the protective effect of HDL against IL-1beta-induced apoptosis was also observed in the absence of the HDL receptor scavenger receptor class B type 1. |
| 904 | 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. |
| 905 | 19965573 | Percentage increase in apolipoprotein A-I was virtually identical to that of HDL-C at all doses of the three statins. |
| 906 | 20059975 | Fructated apolipoprotein A-I showed severe structural modification and loss of beneficial functions in lipid-free and lipid-bound state with acceleration of atherosclerosis and senescence. |
| 907 | 20110571 | Nonenzymatic glycation impairs the antiinflammatory properties of apolipoprotein A-I. |
| 908 | 20116212 | Apolipoprotein A-I positively associated with diabetes in women independently of apolipoprotein E genotype and apolipoprotein B levels. |
| 909 | 20125002 | The promise of apolipoprotein A-I mimetics. |
| 910 | 20130116 | Our results show that diabetic animals exhibited a lower intestinal CHOL uptake, which was associated with a decrease in 1) the gene and protein expression of Niemann-Pick C1 like 1 that plays a pivotal role in CHOL incorporation in the enterocytes; and 2) mRNA of ATP-binding cassette transporters (ABC)A1 that mediates CHOL efflux from intestinal cells to apolipoprotein A-I and high-density lipoprotein. |
| 911 | 20130116 | On the other hand, in diabetic animals, a significant mRNA decrease was noticed in intestinal ABCG5 and ABCG8 responsible for the secretion of absorbed CHOL back into the lumen. |
| 912 | 20130116 | Furthermore, jejunal PCSK9 protein was diminished and low-density lipoprotein receptor was raised, along with a significant down-regulation in jejunal 3-hydroxy-3-methylglutaryl-coenzyme A reductase in P. obesus with T2D. |
| 913 | 20130116 | In the liver, there was 1) an augmentation in the protein mass of Niemann-Pick C1 like 1, SR-BI, and annexin 2; 2) an up-regulation of SR-BI mRNA; 3) a fall in ABCG8 protein content as well as in ABCG5 and ABCA1 mRNA; and 4) an augmentation in liver X receptors alpha and peroxisome proliferator-activated receptors beta/delta mRNA, together with a drop in sterol regulatory element binding protein-2 protein. |
| 914 | 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. |
| 915 | 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. |
| 916 | 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. |
| 917 | 20211930 | Lower HDL-C and apolipoprotein A-I are related to higher glomerular filtration rate in subjects without kidney disease. |
| 918 | 20213498 | The ApoB/ApoA1 ratio is associated with metabolic syndrome and its components in a Chinese population. |
| 919 | 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. |
| 920 | 20213498 | The high ApoB/ApoA1 group was defined as the gender-specific upper quartile of the ApoB/ApoA1 ratio. |
| 921 | 20213498 | The ApoB/ApoA1 ratio was significantly higher in subjects with MS, compared to those without (p < 0.05). |
| 922 | 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. |
| 923 | 20213498 | The ApoB/ApoA1 ratio increased significantly as the number of MS components increased (p < 0.05). |
| 924 | 20213498 | Taken together, these data demonstrate that the ApoB/ApoA1 ratio is strongly associated with MS and its components in an urban Chinese population. |
| 925 | 20213498 | The ApoB/ApoA1 ratio is associated with metabolic syndrome and its components in a Chinese population. |
| 926 | 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. |
| 927 | 20213498 | The high ApoB/ApoA1 group was defined as the gender-specific upper quartile of the ApoB/ApoA1 ratio. |
| 928 | 20213498 | The ApoB/ApoA1 ratio was significantly higher in subjects with MS, compared to those without (p < 0.05). |
| 929 | 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. |
| 930 | 20213498 | The ApoB/ApoA1 ratio increased significantly as the number of MS components increased (p < 0.05). |
| 931 | 20213498 | Taken together, these data demonstrate that the ApoB/ApoA1 ratio is strongly associated with MS and its components in an urban Chinese population. |
| 932 | 20213498 | The ApoB/ApoA1 ratio is associated with metabolic syndrome and its components in a Chinese population. |
| 933 | 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. |
| 934 | 20213498 | The high ApoB/ApoA1 group was defined as the gender-specific upper quartile of the ApoB/ApoA1 ratio. |
| 935 | 20213498 | The ApoB/ApoA1 ratio was significantly higher in subjects with MS, compared to those without (p < 0.05). |
| 936 | 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. |
| 937 | 20213498 | The ApoB/ApoA1 ratio increased significantly as the number of MS components increased (p < 0.05). |
| 938 | 20213498 | Taken together, these data demonstrate that the ApoB/ApoA1 ratio is strongly associated with MS and its components in an urban Chinese population. |
| 939 | 20213498 | The ApoB/ApoA1 ratio is associated with metabolic syndrome and its components in a Chinese population. |
| 940 | 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. |
| 941 | 20213498 | The high ApoB/ApoA1 group was defined as the gender-specific upper quartile of the ApoB/ApoA1 ratio. |
| 942 | 20213498 | The ApoB/ApoA1 ratio was significantly higher in subjects with MS, compared to those without (p < 0.05). |
| 943 | 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. |
| 944 | 20213498 | The ApoB/ApoA1 ratio increased significantly as the number of MS components increased (p < 0.05). |
| 945 | 20213498 | Taken together, these data demonstrate that the ApoB/ApoA1 ratio is strongly associated with MS and its components in an urban Chinese population. |
| 946 | 20213498 | The ApoB/ApoA1 ratio is associated with metabolic syndrome and its components in a Chinese population. |
| 947 | 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. |
| 948 | 20213498 | The high ApoB/ApoA1 group was defined as the gender-specific upper quartile of the ApoB/ApoA1 ratio. |
| 949 | 20213498 | The ApoB/ApoA1 ratio was significantly higher in subjects with MS, compared to those without (p < 0.05). |
| 950 | 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. |
| 951 | 20213498 | The ApoB/ApoA1 ratio increased significantly as the number of MS components increased (p < 0.05). |
| 952 | 20213498 | Taken together, these data demonstrate that the ApoB/ApoA1 ratio is strongly associated with MS and its components in an urban Chinese population. |
| 953 | 20213498 | The ApoB/ApoA1 ratio is associated with metabolic syndrome and its components in a Chinese population. |
| 954 | 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. |
| 955 | 20213498 | The high ApoB/ApoA1 group was defined as the gender-specific upper quartile of the ApoB/ApoA1 ratio. |
| 956 | 20213498 | The ApoB/ApoA1 ratio was significantly higher in subjects with MS, compared to those without (p < 0.05). |
| 957 | 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. |
| 958 | 20213498 | The ApoB/ApoA1 ratio increased significantly as the number of MS components increased (p < 0.05). |
| 959 | 20213498 | Taken together, these data demonstrate that the ApoB/ApoA1 ratio is strongly associated with MS and its components in an urban Chinese population. |
| 960 | 20213498 | The ApoB/ApoA1 ratio is associated with metabolic syndrome and its components in a Chinese population. |
| 961 | 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. |
| 962 | 20213498 | The high ApoB/ApoA1 group was defined as the gender-specific upper quartile of the ApoB/ApoA1 ratio. |
| 963 | 20213498 | The ApoB/ApoA1 ratio was significantly higher in subjects with MS, compared to those without (p < 0.05). |
| 964 | 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. |
| 965 | 20213498 | The ApoB/ApoA1 ratio increased significantly as the number of MS components increased (p < 0.05). |
| 966 | 20213498 | Taken together, these data demonstrate that the ApoB/ApoA1 ratio is strongly associated with MS and its components in an urban Chinese population. |
| 967 | 20368963 | Single nucleotide polymorphism (SNP) in adiponectin gene has been associated with insulin resistance, diabetes, and cardiovascular disease (CVD). |
| 968 | 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. |
| 969 | 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. |
| 970 | 20374257 | Several cellular membrane transporters, including ABCA1 and ABCG1, as well as scavenger receptor (SR)-BI receptor, are believed to facilitate the active efflux of cholesterol to lipid-poor apolipoprotein A-I and mature HDL, respectively. |
| 971 | 20395699 | Apolipoprotein A-I mimetic peptides: a potential new therapy for the prevention of atherosclerosis. |
| 972 | 20395699 | The beneficial effects of high-density lipoprotein (HDL) on atherosclerosis have largely been attributed to its major protein, apolipoprotein A-I (apoA-I). |
| 973 | 20395699 | In a rat model of diabetes, D-4F increased arterial concentrations of heme oxygenase-1 (HO-1) and superoxide dismutase, decreased superoxide levels, reduced levels of circulating endothelial cells, decreased endothelial cell fragmentation, and restored arterial vasoreactivity to normal. |
| 974 | 20395699 | Apolipoprotein A-I mimetic peptides: a potential new therapy for the prevention of atherosclerosis. |
| 975 | 20395699 | The beneficial effects of high-density lipoprotein (HDL) on atherosclerosis have largely been attributed to its major protein, apolipoprotein A-I (apoA-I). |
| 976 | 20395699 | In a rat model of diabetes, D-4F increased arterial concentrations of heme oxygenase-1 (HO-1) and superoxide dismutase, decreased superoxide levels, reduced levels of circulating endothelial cells, decreased endothelial cell fragmentation, and restored arterial vasoreactivity to normal. |
| 977 | 20508181 | Structure/function relationships of apolipoprotein a-I mimetic peptides: implications for antiatherogenic activities of high-density lipoprotein. |
| 978 | 20538481 | Among traditional cardiovascular risk factors, apolipoprotein (apo)B/apoA1 ratio is considered to have the strongest predictive value for ischemic stroke. |
| 979 | 20538481 | In this case-control study, we evaluated apoB/apoA1 ratio as a predictor of ischemic stroke in a cohort of elderly subjects. |
| 980 | 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. |
| 981 | 20538481 | Stroke patients exhibited a higher apoB/apoA1 ratio than controls (1.04±0.33 vs 0.86±0.22; P<.001). |
| 982 | 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). |
| 983 | 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). |
| 984 | 20538481 | Our findings support elevated apoB/apoA1 ratio as an independent predictor of ischemic stroke in individuals over age 70. |
| 985 | 20538481 | Among traditional cardiovascular risk factors, apolipoprotein (apo)B/apoA1 ratio is considered to have the strongest predictive value for ischemic stroke. |
| 986 | 20538481 | In this case-control study, we evaluated apoB/apoA1 ratio as a predictor of ischemic stroke in a cohort of elderly subjects. |
| 987 | 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. |
| 988 | 20538481 | Stroke patients exhibited a higher apoB/apoA1 ratio than controls (1.04±0.33 vs 0.86±0.22; P<.001). |
| 989 | 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). |
| 990 | 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). |
| 991 | 20538481 | Our findings support elevated apoB/apoA1 ratio as an independent predictor of ischemic stroke in individuals over age 70. |
| 992 | 20538481 | Among traditional cardiovascular risk factors, apolipoprotein (apo)B/apoA1 ratio is considered to have the strongest predictive value for ischemic stroke. |
| 993 | 20538481 | In this case-control study, we evaluated apoB/apoA1 ratio as a predictor of ischemic stroke in a cohort of elderly subjects. |
| 994 | 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. |
| 995 | 20538481 | Stroke patients exhibited a higher apoB/apoA1 ratio than controls (1.04±0.33 vs 0.86±0.22; P<.001). |
| 996 | 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). |
| 997 | 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). |
| 998 | 20538481 | Our findings support elevated apoB/apoA1 ratio as an independent predictor of ischemic stroke in individuals over age 70. |
| 999 | 20538481 | Among traditional cardiovascular risk factors, apolipoprotein (apo)B/apoA1 ratio is considered to have the strongest predictive value for ischemic stroke. |
| 1000 | 20538481 | In this case-control study, we evaluated apoB/apoA1 ratio as a predictor of ischemic stroke in a cohort of elderly subjects. |
| 1001 | 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. |
| 1002 | 20538481 | Stroke patients exhibited a higher apoB/apoA1 ratio than controls (1.04±0.33 vs 0.86±0.22; P<.001). |
| 1003 | 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). |
| 1004 | 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). |
| 1005 | 20538481 | Our findings support elevated apoB/apoA1 ratio as an independent predictor of ischemic stroke in individuals over age 70. |
| 1006 | 20538481 | Among traditional cardiovascular risk factors, apolipoprotein (apo)B/apoA1 ratio is considered to have the strongest predictive value for ischemic stroke. |
| 1007 | 20538481 | In this case-control study, we evaluated apoB/apoA1 ratio as a predictor of ischemic stroke in a cohort of elderly subjects. |
| 1008 | 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. |
| 1009 | 20538481 | Stroke patients exhibited a higher apoB/apoA1 ratio than controls (1.04±0.33 vs 0.86±0.22; P<.001). |
| 1010 | 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). |
| 1011 | 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). |
| 1012 | 20538481 | Our findings support elevated apoB/apoA1 ratio as an independent predictor of ischemic stroke in individuals over age 70. |
| 1013 | 20538481 | Among traditional cardiovascular risk factors, apolipoprotein (apo)B/apoA1 ratio is considered to have the strongest predictive value for ischemic stroke. |
| 1014 | 20538481 | In this case-control study, we evaluated apoB/apoA1 ratio as a predictor of ischemic stroke in a cohort of elderly subjects. |
| 1015 | 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. |
| 1016 | 20538481 | Stroke patients exhibited a higher apoB/apoA1 ratio than controls (1.04±0.33 vs 0.86±0.22; P<.001). |
| 1017 | 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). |
| 1018 | 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). |
| 1019 | 20538481 | Our findings support elevated apoB/apoA1 ratio as an independent predictor of ischemic stroke in individuals over age 70. |
| 1020 | 20538481 | Among traditional cardiovascular risk factors, apolipoprotein (apo)B/apoA1 ratio is considered to have the strongest predictive value for ischemic stroke. |
| 1021 | 20538481 | In this case-control study, we evaluated apoB/apoA1 ratio as a predictor of ischemic stroke in a cohort of elderly subjects. |
| 1022 | 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. |
| 1023 | 20538481 | Stroke patients exhibited a higher apoB/apoA1 ratio than controls (1.04±0.33 vs 0.86±0.22; P<.001). |
| 1024 | 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). |
| 1025 | 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). |
| 1026 | 20538481 | Our findings support elevated apoB/apoA1 ratio as an independent predictor of ischemic stroke in individuals over age 70. |
| 1027 | 20625478 | Levels of some isoforms including plasma retinol binding protein, transthyretin, Apolipoprotein A1, and kininogen showed significant changes as early as 4 weeks which coincided with the very early development of glucose intolerance. |
| 1028 | 20674218 | The distinct effect of T2DM induction on the pattern of rat serum includes the down-regulation of Apolipoprotein E, Apolipoprotein A-I, Ig gamma-2A chain C region, and up-regulation of Transthyretin (TTR), Haptoglobin (Hp), Serum amyloid P-componen (SAP), Prothrombin. |
| 1029 | 20683626 | Negative correlation between serum syndecan-1 and apolipoprotein A1 in patients with type 2 diabetes mellitus. |
| 1030 | 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. |
| 1031 | 20683626 | Serum syndecan-1 level correlated negatively with apoA1 (r = -0.46, P = 0.003). |
| 1032 | 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. |
| 1033 | 20683626 | Negative correlation between serum syndecan-1 and apolipoprotein A1 in patients with type 2 diabetes mellitus. |
| 1034 | 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. |
| 1035 | 20683626 | Serum syndecan-1 level correlated negatively with apoA1 (r = -0.46, P = 0.003). |
| 1036 | 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. |
| 1037 | 20683626 | Negative correlation between serum syndecan-1 and apolipoprotein A1 in patients with type 2 diabetes mellitus. |
| 1038 | 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. |
| 1039 | 20683626 | Serum syndecan-1 level correlated negatively with apoA1 (r = -0.46, P = 0.003). |
| 1040 | 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. |
| 1041 | 20683626 | Negative correlation between serum syndecan-1 and apolipoprotein A1 in patients with type 2 diabetes mellitus. |
| 1042 | 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. |
| 1043 | 20683626 | Serum syndecan-1 level correlated negatively with apoA1 (r = -0.46, P = 0.003). |
| 1044 | 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. |
| 1045 | 20826564 | Apolipoprotein A-I mimetic peptides prevent atherosclerosis development and reduce plaque inflammation in a murine model of diabetes. |
| 1046 | 21042216 | Apolipoprotein A-I mimetic peptides. |
| 1047 | 21257004 | Comparison of high-density lipoprotein cholesterol to apolipoprotein A-I and A-II to predict coronary calcium and the effect of insulin resistance. |
| 1048 | 21257004 | It was hypothesized that metabolic factors, including insulin resistance and type 2 diabetes, would confound the association of HDL cholesterol with coronary artery calcification (CAC) and that apolipoprotein A-I (apoA-I) and/or apolipoprotein A-II (apoA-II) would add to HDL cholesterol in predicting CAC. |
| 1049 | 21257004 | Comparison of high-density lipoprotein cholesterol to apolipoprotein A-I and A-II to predict coronary calcium and the effect of insulin resistance. |
| 1050 | 21257004 | It was hypothesized that metabolic factors, including insulin resistance and type 2 diabetes, would confound the association of HDL cholesterol with coronary artery calcification (CAC) and that apolipoprotein A-I (apoA-I) and/or apolipoprotein A-II (apoA-II) would add to HDL cholesterol in predicting CAC. |
| 1051 | 21330603 | Lipid-free apolipoprotein A-I and discoidal reconstituted high-density lipoproteins differentially inhibit glucose-induced oxidative stress in human macrophages. |
| 1052 | 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. |
| 1053 | 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. |
| 1054 | 21474825 | Neutrophil activation is attenuated by high-density lipoprotein and apolipoprotein A-I in in vitro and in vivo models of inflammation. |
| 1055 | 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). |
| 1056 | 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. |
| 1057 | 21528490 | HD patients had moderate hypertriglyceridemia, normocholesterolemia, low HDL-C, apolipoprotein A-I (apoA-I) and HDL particle concentrations as well as PON-1 activity, and increased ox-LDL and anti-ox-LDL levels. |
| 1058 | 21598304 | Apolipoprotein A-I mimetic peptide L-4F prevents myocardial and coronary dysfunction in diabetic mice. |
| 1059 | 21598304 | The apolipoprotein A-I mimetic peptide L-4F is a putative anti-diabetic drug, has antioxidant and anti-inflammatory proprieties and improves endothelial function. |
| 1060 | 21598304 | In obese mice L-4F increases adiponectin levels, improving insulin sensitivity, and reducing visceral adiposity. |
| 1061 | 21598304 | Glucose, insulin, adiponectin, and pro-inflammatory cytokines (IL-1β, TNF-α, MCP-1) were measured in plasma and HO-1, pAMPK, peNOS, iNOS, adiponectin, and superoxide in cardiac tissue. |
| 1062 | 21598304 | In db/db mice L-4F decreased accumulation of subcutaneous and total fat, and increased insulin sensitivity and adiponectin levels while lowering inflammatory cytokines (P < 0.05). |
| 1063 | 21598304 | These changes were associated with increased cardiac expression of HO-1, pAMPK, peNOS, and adiponectin and decreased levels of superoxide and iNOS (P < 0.01). |
| 1064 | 21598304 | These effects were associated with stimulation of HO-1 resulting in increased levels of anti-inflammatory, anti-oxidative, and vasodilatatory action through a mechanism involving increased levels of adiponectin, pAMPK, and peNOS. |
| 1065 | 21598304 | Apolipoprotein A-I mimetic peptide L-4F prevents myocardial and coronary dysfunction in diabetic mice. |
| 1066 | 21598304 | The apolipoprotein A-I mimetic peptide L-4F is a putative anti-diabetic drug, has antioxidant and anti-inflammatory proprieties and improves endothelial function. |
| 1067 | 21598304 | In obese mice L-4F increases adiponectin levels, improving insulin sensitivity, and reducing visceral adiposity. |
| 1068 | 21598304 | Glucose, insulin, adiponectin, and pro-inflammatory cytokines (IL-1β, TNF-α, MCP-1) were measured in plasma and HO-1, pAMPK, peNOS, iNOS, adiponectin, and superoxide in cardiac tissue. |
| 1069 | 21598304 | In db/db mice L-4F decreased accumulation of subcutaneous and total fat, and increased insulin sensitivity and adiponectin levels while lowering inflammatory cytokines (P < 0.05). |
| 1070 | 21598304 | These changes were associated with increased cardiac expression of HO-1, pAMPK, peNOS, and adiponectin and decreased levels of superoxide and iNOS (P < 0.01). |
| 1071 | 21598304 | These effects were associated with stimulation of HO-1 resulting in increased levels of anti-inflammatory, anti-oxidative, and vasodilatatory action through a mechanism involving increased levels of adiponectin, pAMPK, and peNOS. |
| 1072 | 21603009 | As a result, impaired anti-inflammatory and atheroprotective function developed in middle-aged and elderly obese individuals emerging as dysfunction of apolipoprotein A-I and HDL particles. |
| 1073 | 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. |
| 1074 | 22001232 | Individuals with Tangier disease also have elevated plasma TG concentrations and a near absence of HDL, resulting from mutations in ATP binding cassette transporter A1 (ABCA1), which facilitates the efflux of cellular phospholipid and free cholesterol to assemble with apolipoprotein A-I (apoA-I), forming nascent HDL particles. |
| 1075 | 22001232 | Silencing ABCA1 in McArdle rat hepatoma cells results in diminished assembly of large (>10nm) nascent HDL particles, diminished PI3 kinase activation, and increased secretion of large, TG-enriched VLDL1 particles. |
| 1076 | 22020260 | Acyl-CoA synthetase 1 is required for oleate and linoleate mediated inhibition of cholesterol efflux through ATP-binding cassette transporter A1 in macrophages. |
| 1077 | 22020260 | We have recently shown that diabetes associated with increased plasma lipids reduces cholesterol efflux and levels of the reverse cholesterol transporter ABCA1 (ATP-binding cassette transporter A1) in mouse macrophages, which likely contributes to macrophage lipid accumulation in diabetes. |
| 1078 | 22020260 | We therefore investigated whether acyl-CoA synthetase 1 (ACSL1), a key enzyme mediating acyl-CoA synthesis in macrophages, could directly influence ABCA1 levels and cholesterol efflux in these cells. |
| 1079 | 22020260 | Mouse macrophages deficient in ACSL1 exhibited reduced sensitivity to oleate- and linoleate-mediated ABCA1 degradation, which resulted in increased ABCA1 levels and increased apolipoprotein A-I-dependent cholesterol efflux in the presence of these fatty acids, as compared with wildtype mouse macrophages. |
| 1080 | 22020260 | Conversely, overexpression of ACSL1 resulted in reduced ABCA1 levels and reduced cholesterol efflux in the presence of unsaturated fatty acids. |
| 1081 | 22020260 | Thus, the reduced ABCA1 and cholesterol efflux in macrophages subjected to conditions of diabetes and elevated fatty load may, at least in part, be mediated by ACSL1. |
| 1082 | 22118750 | The emerging evidence for vitamin D-mediated regulation of apolipoprotein A-I synthesis. |
| 1083 | 22118750 | This process is inhibited by high-density lipoprotein (HDL), the main protein component of which is apolipoprotein A-I (apo A-I). |
| 1084 | 22118750 | The emerging evidence for vitamin D-mediated regulation of apolipoprotein A-I synthesis. |
| 1085 | 22118750 | This process is inhibited by high-density lipoprotein (HDL), the main protein component of which is apolipoprotein A-I (apo A-I). |
| 1086 | 22219194 | Myeloperoxidase targets apolipoprotein A-I, the major high density lipoprotein protein, for site-specific oxidation in human atherosclerotic lesions. |
| 1087 | 22278086 | Apolipoprotein A-I mimetics and high-density lipoprotein function. |
| 1088 | 22359512 | After a correction for multiple comparisons (P-value<2.2×10(-9)), we observed four novel loci significantly associated with phospholipids (PAQR9, AGPAT1, PKD2L1, PDXDC1) and two with sphingolipids (PLD2 and APOE) explaining up to 3.1% of the variance. |
| 1089 | 22359512 | Further analysis of the top findings with respect to within class molar proportions uncovered three additional loci for phospholipids (PNLIPRP2, PCDH20, and ABDH3) suggesting their involvement in either fatty acid elongation/saturation processes or fatty acid specific turnover mechanisms. |
| 1090 | 22359512 | Among those, 14 loci (KCNH7, AGPAT1, PNLIPRP2, SYT9, FADS1-2-3, DLG2, APOA1, ELOVL2, CDK17, LIPC, PDXDC1, PLD2, LASS4, and APOE) mapped into the glycerophospholipid and 12 loci (ILKAP, ITGA9, AGPAT1, FADS1-2-3, APOA1, PCDH20, LIPC, PDXDC1, SGPP1, APOE, LASS4, and PLD2) to the sphingolipid pathways. |
| 1091 | 22363922 | The Association between Apolipoprotein A-II and Metabolic Syndrome in Korean Adults: A Comparison Study of Apolipoprotein A-I and Apolipoprotein B. |
| 1092 | 22364131 | Data obtained from patients with early RA suggest that serum triglycerides, a proxy of disease activity as markers of systemic inflammation, impaired function of apolipoprotein A-I and HDL particles, and mediating hypertension are determinants of the excess cardiovascular risk. |
| 1093 | 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. |
| 1094 | 22407494 | Long-term RT ameliorated glycemic control, insulin sensitivity and ApoB/ApoA-I ratio in individuals with T2DM. |
| 1095 | 22431312 | Studies in gene-targeted mice, however, have also indicated that increasing HDL-cholesterol plasma levels can either limit (e.g. apolipoprotein A-I) or accelerate (e.g. |
| 1096 | 22678621 | Lower protein representations in diabetic subjects were associated with Tamm-Horsfall urinary glycoprotein, apolipoprotein A-I, apolipoprotein E, α2-thiol proteinase inhibitor, and human complement regulatory protein CD59, while higher protein representations were found for α-1-microglobulin, zinc-α2 glycoprotein, α-1B glycoprotein, and retinol-binding protein 4. |
| 1097 | 22802942 | In particular, apolipoprotein A-I (ApoA1) concentration gradually increased between 18 to 50 years of age, the levels of fibrinogen alpha (FGA) decreased over the same age span, while albumin (ALB) was significantly degraded in middle-aged individuals. |
| 1098 | 22802942 | Plasma proteins such as FGA, ALB and ApoA1 are significantly correlated with age in the Chinese Han population and could be employed as indicative ageing-related biomarkers. |
| 1099 | 22802942 | In particular, apolipoprotein A-I (ApoA1) concentration gradually increased between 18 to 50 years of age, the levels of fibrinogen alpha (FGA) decreased over the same age span, while albumin (ALB) was significantly degraded in middle-aged individuals. |
| 1100 | 22802942 | Plasma proteins such as FGA, ALB and ApoA1 are significantly correlated with age in the Chinese Han population and could be employed as indicative ageing-related biomarkers. |
| 1101 | 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. |
| 1102 | 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. |
| 1103 | 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). |
| 1104 | 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). |
| 1105 | 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. |
| 1106 | 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. |
| 1107 | 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. |
| 1108 | 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). |
| 1109 | 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). |
| 1110 | 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. |
| 1111 | 22982462 | Regulation of pattern recognition receptors by the apolipoprotein A-I mimetic peptide 4F. |
| 1112 | 23029614 | The known associations in the general population of physical activity with high-density-lipoprotein cholesterol subfractions and apolipoprotein A-I are more pronounced in hemodialysis patients than in peritoneal dialysis patients even after adjusting for these confounding factors. |
| 1113 | 23029614 | The changes in lipids and lipoproteins in hemodialysis patients could be caused by changes in activity levels of lipoprotein lipase, insulin sensitivity, and/or glucose metabolism. |
| 1114 | 23039759 | Although plasma high density lipoprotein (HDL) and apolipoprotein A-I (apoA-I) are inversely correlated to obesity, whether HDLs have anti-obesity effect remains unclear until a recent study reporting the direct anti-obesity effect of apoA-I and its mimetic peptide. |
| 1115 | 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). |
| 1116 | 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. |
| 1117 | 23060933 | Serum adiponectin levels were decreased and leptin, resistin and visfatin levels were increased in T2DM patients compared to controls. |
| 1118 | 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. |
| 1119 | 23093701 | These include pyruvate kinase M1/M2, apolipoprotein A-I, albumin, peroxiredoxin 2, annexin A2, α-1-B-glycoprotein, flotillin-1 and haptoglobin. |
| 1120 | 23154241 | Endoplasmic reticulum stress in HepG2 cells inhibits apolipoprotein A-I secretion. |
| 1121 | 23426429 | A comparison of the theoretical relationship between HDL size and the ratio of HDL cholesterol to apolipoprotein A-I with experimental results from the Women's Health Study. |
| 1122 | 23440769 | Semiquantitative analysis of apolipoprotein A-I modified by advanced glycation end products in diabetes mellitus. |
| 1123 | 23591583 | Increased apolipoprotein A-I levels mediate the development of prehypertension among Turks. |
| 1124 | 23671850 | The hypocholesterolemic effect of germinated brown rice involves the upregulation of the apolipoprotein A1 and low-density lipoprotein receptor genes. |
| 1125 | 23671850 | Our results showed that the upregulation of apolipoprotein A1 and low-density lipoprotein receptor genes was involved in the hypocholesterolemic effects of GBR. |
| 1126 | 23671850 | The hypocholesterolemic effect of germinated brown rice involves the upregulation of the apolipoprotein A1 and low-density lipoprotein receptor genes. |
| 1127 | 23671850 | Our results showed that the upregulation of apolipoprotein A1 and low-density lipoprotein receptor genes was involved in the hypocholesterolemic effects of GBR. |
| 1128 | 23696124 | In this review article, we discuss the clinical relevance of the high density lipoprotein (HDL) proteome and Apolipoprotein A-I PTMs to T2DM and CVD as well as provide illustrative MSIA and MRM data on HDL proteins from T2DM patients to provide examples of how these MS approaches can be applied to gain new insight regarding cardiovascular risk factors. |
| 1129 | 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. |
| 1130 | 23741493 | Apolipoprotein A-I glycation by glucose and reactive aldehydes alters phospholipid affinity but not cholesterol export from lipid-laden macrophages. |
| 1131 | 23741493 | Cholesterol efflux to control or glycated lipid-free apoA-I, or discoidal reconstituted HDL containing glycated apoA-I (drHDL), was examined using cholesterol-loaded murine (J774A.1) macrophages treated to increase expression of ATP binding cassette transporters A1 (ABCA1) or G1 (ABCG1). |
| 1132 | 23741493 | Cholesterol efflux from J774A.1 macrophages to glycated lipid-free apoA-I via ABCA1 or glycated drHDL via an ABCG1-dependent mechanism was unaltered, as was efflux to minimally modified apoA-I from people with Type 1 diabetes, or controls. |
| 1133 | 23741493 | Overall these studies demonstrate that glycation of lipid-free apoA-I, particularly late glycation, modifies its structure, its capacity to bind phospholipids and but not ABCA1- or ABCG1-dependent cholesterol efflux from macrophages. |
| 1134 | 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. |
| 1135 | 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. |
| 1136 | 23874769 | An apolipoprotein A-I mimetic peptide designed with a reductionist approach stimulates reverse cholesterol transport and reduces atherosclerosis in mice. |
| 1137 | 23874769 | Apolipoprotein A-I (apoA-I) mimetic peptides are considered a promising novel therapeutic approach to prevent and/or treat atherosclerosis. |
| 1138 | 23874769 | An apolipoprotein A-I mimetic peptide designed with a reductionist approach stimulates reverse cholesterol transport and reduces atherosclerosis in mice. |
| 1139 | 23874769 | Apolipoprotein A-I (apoA-I) mimetic peptides are considered a promising novel therapeutic approach to prevent and/or treat atherosclerosis. |
| 1140 | 23994331 | Serum amyloid A is independently related to apolipoprotein A-I but not to HDL-cholesterol in patients with angina pectoris. |
| 1141 | 23996585 | These proteins were found to be associated with neuropathy (α1-antitrypsin), ataxia (apolipoprotein A-I), oxidative stress (albumin), altered lipid metabolism (apolipoprotein C-II, C-III), etc. |