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Gene Information
Gene symbol: LPAL2
Gene name: lipoprotein, Lp(a)-like 2
HGNC ID: 21210
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 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. |
| 2 | 1358344 | Apolipoprotein levels in normolipidemic non-insulin-dependent diabetes mellitus. |
| 3 | 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). |
| 4 | 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. |
| 5 | 1358344 | Apolipoprotein levels in normolipidemic non-insulin-dependent diabetes mellitus. |
| 6 | 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). |
| 7 | 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. |
| 8 | 1358344 | Apolipoprotein levels in normolipidemic non-insulin-dependent diabetes mellitus. |
| 9 | 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). |
| 10 | 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. |
| 11 | 1386533 | Apolipoprotein(a), together with apo B-100 the apolipoprotein of Lp(a), is homologeous to plasminogen but lacks fibrinolytic capacity and appeared to interfere with fibrinolysis in in vitro and ex vivo experiments. |
| 12 | 1386533 | We determined the correlations between Lp(a) and other blood lipids (serum cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides), coagulation parameters (fibrinogen, factor VII, factor VIII:C fibrin monomers, thrombin-antithrombin III) and fibrinolysis parameters (tissue plasminogen activator antigen, plasminogen activator inhibitor-1 and D-dimer) in 54 patients with essential hypertension, in 65 non-insulin-dependent diabetic patients and in 116 insulin-regulated diabetic patients. |
| 13 | 1411263 | Apolipoprotein(a) in insulin-dependent diabetic patients with and without diabetic nephropathy. |
| 14 | 1411263 | To determine whether altered levels of apolipoprotein(a) (apo(a)), the glycoprotein of the potentially atherogenic lipoprotein(a) (Lp(a)), contribute to the increased risk of ischaemic heart disease, apo(a) was determined in 50 insulin-dependent diabetic patients with diabetic nephropathy (group 1), in 50 insulin-dependent diabetic patients with microalbuminuria (group 2), in 50 insulin-dependent diabetic patients with normoalbuminuria (group 3), and in 50 healthy subjects (group 4). |
| 15 | 1411263 | Apolipoprotein(a) in insulin-dependent diabetic patients with and without diabetic nephropathy. |
| 16 | 1411263 | To determine whether altered levels of apolipoprotein(a) (apo(a)), the glycoprotein of the potentially atherogenic lipoprotein(a) (Lp(a)), contribute to the increased risk of ischaemic heart disease, apo(a) was determined in 50 insulin-dependent diabetic patients with diabetic nephropathy (group 1), in 50 insulin-dependent diabetic patients with microalbuminuria (group 2), in 50 insulin-dependent diabetic patients with normoalbuminuria (group 3), and in 50 healthy subjects (group 4). |
| 17 | 1425859 | Normal lipoprotein(a) concentrations and apolipoprotein(a) isoforms in patients with insulin-dependent diabetes mellitus. |
| 18 | 1425859 | Lipoprotein(a) [Lp(a)] is an LDL particle in which apoliporotein B-100 is attached to a large plasminogen-like protein called apolipoprotein(a) [apo(a)]. |
| 19 | 1425859 | Normal lipoprotein(a) concentrations and apolipoprotein(a) isoforms in patients with insulin-dependent diabetes mellitus. |
| 20 | 1425859 | Lipoprotein(a) [Lp(a)] is an LDL particle in which apoliporotein B-100 is attached to a large plasminogen-like protein called apolipoprotein(a) [apo(a)]. |
| 21 | 1473615 | Plasma apolipoprotein (a) is increased in type 2 (non-insulin-dependent) diabetic patients with microalbuminuria. |
| 22 | 1473615 | Because lipoprotein abnormalities have been associated with diabetic nephropathy, this study tested the hypothesis that levels of apolipoprotein (a) are elevated in patients with Type 2 diabetes and increased levels of urinary albumin loss. |
| 23 | 1473615 | Levels of apolipoprotein (a) in diabetic patients with microalbuminuria (n = 26, geometric mean 195 U/l, 95% confidence interval 117-324) and albuminuria (n = 19, 281 U/l, 165-479) were higher than in non-diabetic control subjects (n = 140, 107 U/l, 85-134, p < 0.05), and in the albuminuric group than diabetic patients without urinary albumin loss (n = 58, 114 U/l, 76-169, p < 0.05). |
| 24 | 1473615 | Plasma apolipoprotein (a) is increased in type 2 (non-insulin-dependent) diabetic patients with microalbuminuria. |
| 25 | 1473615 | Because lipoprotein abnormalities have been associated with diabetic nephropathy, this study tested the hypothesis that levels of apolipoprotein (a) are elevated in patients with Type 2 diabetes and increased levels of urinary albumin loss. |
| 26 | 1473615 | Levels of apolipoprotein (a) in diabetic patients with microalbuminuria (n = 26, geometric mean 195 U/l, 95% confidence interval 117-324) and albuminuria (n = 19, 281 U/l, 165-479) were higher than in non-diabetic control subjects (n = 140, 107 U/l, 85-134, p < 0.05), and in the albuminuric group than diabetic patients without urinary albumin loss (n = 58, 114 U/l, 76-169, p < 0.05). |
| 27 | 1473615 | Plasma apolipoprotein (a) is increased in type 2 (non-insulin-dependent) diabetic patients with microalbuminuria. |
| 28 | 1473615 | Because lipoprotein abnormalities have been associated with diabetic nephropathy, this study tested the hypothesis that levels of apolipoprotein (a) are elevated in patients with Type 2 diabetes and increased levels of urinary albumin loss. |
| 29 | 1473615 | Levels of apolipoprotein (a) in diabetic patients with microalbuminuria (n = 26, geometric mean 195 U/l, 95% confidence interval 117-324) and albuminuria (n = 19, 281 U/l, 165-479) were higher than in non-diabetic control subjects (n = 140, 107 U/l, 85-134, p < 0.05), and in the albuminuric group than diabetic patients without urinary albumin loss (n = 58, 114 U/l, 76-169, p < 0.05). |
| 30 | 1516763 | Metabolism of HDL apolipoprotein A-I and A-II in type 1 (insulin-dependent) diabetes mellitus. |
| 31 | 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. |
| 32 | 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. |
| 33 | 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). |
| 34 | 1516763 | Firstly, the rate of apolipoprotein A-II synthesis was 22% lower than in control subjects (p less than 0.05). |
| 35 | 1516763 | Metabolism of HDL apolipoprotein A-I and A-II in type 1 (insulin-dependent) diabetes mellitus. |
| 36 | 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. |
| 37 | 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. |
| 38 | 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). |
| 39 | 1516763 | Firstly, the rate of apolipoprotein A-II synthesis was 22% lower than in control subjects (p less than 0.05). |
| 40 | 1516763 | Metabolism of HDL apolipoprotein A-I and A-II in type 1 (insulin-dependent) diabetes mellitus. |
| 41 | 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. |
| 42 | 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. |
| 43 | 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). |
| 44 | 1516763 | Firstly, the rate of apolipoprotein A-II synthesis was 22% lower than in control subjects (p less than 0.05). |
| 45 | 1516763 | Metabolism of HDL apolipoprotein A-I and A-II in type 1 (insulin-dependent) diabetes mellitus. |
| 46 | 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. |
| 47 | 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. |
| 48 | 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). |
| 49 | 1516763 | Firstly, the rate of apolipoprotein A-II synthesis was 22% lower than in control subjects (p less than 0.05). |
| 50 | 1516763 | Metabolism of HDL apolipoprotein A-I and A-II in type 1 (insulin-dependent) diabetes mellitus. |
| 51 | 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. |
| 52 | 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. |
| 53 | 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). |
| 54 | 1516763 | Firstly, the rate of apolipoprotein A-II synthesis was 22% lower than in control subjects (p less than 0.05). |
| 55 | 1521727 | HDL-cholesterol, and apolipoprotein A-I remained unchanged. |
| 56 | 1521727 | Total cholesterol, LDL-cholesterol, HDL-cholesterol, apolipoprotein A-I, apolipoprotein B remained unchanged during placebo treatment. |
| 57 | 1521727 | HDL-cholesterol, and apolipoprotein A-I remained unchanged. |
| 58 | 1521727 | Total cholesterol, LDL-cholesterol, HDL-cholesterol, apolipoprotein A-I, apolipoprotein B remained unchanged during placebo treatment. |
| 59 | 1526342 | Apolipoprotein A-I-containing particles and reverse cholesterol transport in IDDM. |
| 60 | 1531990 | Lipoprotein cholesterol, apolipoprotein A-I and B and lipoprotein (a) abnormalities in men with premature coronary artery disease. |
| 61 | 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). |
| 62 | 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. |
| 63 | 1531990 | Lipoprotein cholesterol, apolipoprotein A-I and B and lipoprotein (a) abnormalities in men with premature coronary artery disease. |
| 64 | 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). |
| 65 | 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. |
| 66 | 1531990 | Lipoprotein cholesterol, apolipoprotein A-I and B and lipoprotein (a) abnormalities in men with premature coronary artery disease. |
| 67 | 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). |
| 68 | 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. |
| 69 | 1532112 | Total cholesterol, triglycerides, high- and low-density lipoprotein cholesterol, apolipoprotein A-I, apolipoprotein B and Lp(a) were compared. |
| 70 | 1545765 | Apolipoprotein A-I was reduced by 9%. |
| 71 | 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. |
| 72 | 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. |
| 73 | 1576237 | Association in vivo of glycated apolipoprotein A-I with high density lipoproteins. |
| 74 | 1576237 | In diabetic patients, hyperglycaemia results in the non-enzymatic glycation of apolipoprotein A-I, the major protein of human high density lipoproteins. |
| 75 | 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. |
| 76 | 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. |
| 77 | 1576237 | Analysis by gel chromatography of serum from donor rats shows that glycation diminishes the interaction between apolipoprotein A-I and high density lipoprotein. |
| 78 | 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. |
| 79 | 1576237 | Association in vivo of glycated apolipoprotein A-I with high density lipoproteins. |
| 80 | 1576237 | In diabetic patients, hyperglycaemia results in the non-enzymatic glycation of apolipoprotein A-I, the major protein of human high density lipoproteins. |
| 81 | 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. |
| 82 | 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. |
| 83 | 1576237 | Analysis by gel chromatography of serum from donor rats shows that glycation diminishes the interaction between apolipoprotein A-I and high density lipoprotein. |
| 84 | 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. |
| 85 | 1576237 | Association in vivo of glycated apolipoprotein A-I with high density lipoproteins. |
| 86 | 1576237 | In diabetic patients, hyperglycaemia results in the non-enzymatic glycation of apolipoprotein A-I, the major protein of human high density lipoproteins. |
| 87 | 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. |
| 88 | 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. |
| 89 | 1576237 | Analysis by gel chromatography of serum from donor rats shows that glycation diminishes the interaction between apolipoprotein A-I and high density lipoprotein. |
| 90 | 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. |
| 91 | 1576237 | Association in vivo of glycated apolipoprotein A-I with high density lipoproteins. |
| 92 | 1576237 | In diabetic patients, hyperglycaemia results in the non-enzymatic glycation of apolipoprotein A-I, the major protein of human high density lipoproteins. |
| 93 | 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. |
| 94 | 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. |
| 95 | 1576237 | Analysis by gel chromatography of serum from donor rats shows that glycation diminishes the interaction between apolipoprotein A-I and high density lipoprotein. |
| 96 | 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. |
| 97 | 1576237 | Association in vivo of glycated apolipoprotein A-I with high density lipoproteins. |
| 98 | 1576237 | In diabetic patients, hyperglycaemia results in the non-enzymatic glycation of apolipoprotein A-I, the major protein of human high density lipoproteins. |
| 99 | 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. |
| 100 | 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. |
| 101 | 1576237 | Analysis by gel chromatography of serum from donor rats shows that glycation diminishes the interaction between apolipoprotein A-I and high density lipoprotein. |
| 102 | 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. |
| 103 | 1576237 | Association in vivo of glycated apolipoprotein A-I with high density lipoproteins. |
| 104 | 1576237 | In diabetic patients, hyperglycaemia results in the non-enzymatic glycation of apolipoprotein A-I, the major protein of human high density lipoproteins. |
| 105 | 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. |
| 106 | 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. |
| 107 | 1576237 | Analysis by gel chromatography of serum from donor rats shows that glycation diminishes the interaction between apolipoprotein A-I and high density lipoprotein. |
| 108 | 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. |
| 109 | 1579407 | Apolipoprotein A-I, A-II, B, C-II, and C-III in children with insulin-dependent diabetes mellitus. |
| 110 | 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. |
| 111 | 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). |
| 112 | 1579407 | Apolipoprotein A-I, A-II, B, C-II, and C-III in children with insulin-dependent diabetes mellitus. |
| 113 | 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. |
| 114 | 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). |
| 115 | 1579407 | Apolipoprotein A-I, A-II, B, C-II, and C-III in children with insulin-dependent diabetes mellitus. |
| 116 | 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. |
| 117 | 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). |
| 118 | 1644426 | Apolipoprotein A-IV genetic polymorphism and its impact on quantitative traits in normoglycemic and non-insulin-dependent diabetic Hispanics from the San Luis Valley, Colorado. |
| 119 | 1644426 | Apolipoprotein A-IV exhibits a common two-allele polymorphism in several human populations studied to date. |
| 120 | 1644426 | Using isoelectric focusing and immunoblotting, we have analyzed plasmas from 188 non-insulin-dependent diabetic and 238 normoglycemic Hispanic individuals from the San Luis Valley, Colorado, to determine APOA4 genotype frequencies and to estimate the impact of the genotypes on quantitative traits. |
| 121 | 1644426 | Apolipoprotein A-IV genetic polymorphism and its impact on quantitative traits in normoglycemic and non-insulin-dependent diabetic Hispanics from the San Luis Valley, Colorado. |
| 122 | 1644426 | Apolipoprotein A-IV exhibits a common two-allele polymorphism in several human populations studied to date. |
| 123 | 1644426 | Using isoelectric focusing and immunoblotting, we have analyzed plasmas from 188 non-insulin-dependent diabetic and 238 normoglycemic Hispanic individuals from the San Luis Valley, Colorado, to determine APOA4 genotype frequencies and to estimate the impact of the genotypes on quantitative traits. |
| 124 | 1672575 | Blood pressure, glucose tolerance and immunoreactive insulin (IRI) response to 75 gm oral glucose load, hemoglobin A1 (Hb A1), serum lipid profile, and serum apolipoprotein were examined before and after treatment. |
| 125 | 1677323 | DNA restriction polymorphisms of the apolipoprotein AI-CIII-AIV gene cluster: a genetic determinant of atherosclerosis in type 2 (non-insulin-dependent) diabetes mellitus. |
| 126 | 1702705 | The thyroxine-binding site of human apolipoprotein-A-I: location in the N-terminal domain. |
| 127 | 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. |
| 128 | 1702705 | The thyroxine-binding site of human apolipoprotein-A-I: location in the N-terminal domain. |
| 129 | 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. |
| 130 | 1811553 | Apolipoprotein A-IV polymorphism, and its role in determining variation in lipoprotein-lipid, glucose and insulin levels in normal and non-insulin-dependent diabetic individuals. |
| 131 | 1811553 | Apolipoprotein A-IV (apo A-IV) is a major component of several lipoprotein particles and may, therefore, play an important role in lipid metabolism. |
| 132 | 1811553 | Apolipoprotein A-IV polymorphism, and its role in determining variation in lipoprotein-lipid, glucose and insulin levels in normal and non-insulin-dependent diabetic individuals. |
| 133 | 1811553 | Apolipoprotein A-IV (apo A-IV) is a major component of several lipoprotein particles and may, therefore, play an important role in lipid metabolism. |
| 134 | 1825896 | Hypertension, lipoprotein(a), and apolipoprotein A-I as risk factors for stroke in the Chinese. |
| 135 | 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. |
| 136 | 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. |
| 137 | 1825896 | Hypertension, lipoprotein(a), and apolipoprotein A-I as risk factors for stroke in the Chinese. |
| 138 | 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. |
| 139 | 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. |
| 140 | 1825896 | Hypertension, lipoprotein(a), and apolipoprotein A-I as risk factors for stroke in the Chinese. |
| 141 | 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. |
| 142 | 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. |
| 143 | 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. |
| 144 | 1838064 | Plasma lipid and apolipoprotein levels of Type 1 and Type 2 young Kuwaiti diabetic women on insulin therapy were investigated to elucidate the relationship between coronary artery disease risk factors and lipid levels. |
| 145 | 1838064 | Levels of HDL-, HDL2- and HDL3-cholesterol and plasma apolipoprotein AI were markedly decreased in both the diabetic groups compared with their control groups (all p less than 0.001 except HDL3-cholesterol in Type 1 diabetic vs control, p less than 0.05). |
| 146 | 1838064 | In Type 2 diabetic patients, HbA1c correlated positively with triglycerides (r = 0.70, p less than 0.001), cholesterol (r = 0.60, p less than 0.001), apolipoprotein B (r = 0.77, p less than 0.001), and apolipoprotein CIII (r = 0.55, p less than 0.001) and negatively with apolipoprotein AI (r = -0.49, p less than 0.001). |
| 147 | 1838064 | Plasma lipid and apolipoprotein levels of Type 1 and Type 2 young Kuwaiti diabetic women on insulin therapy were investigated to elucidate the relationship between coronary artery disease risk factors and lipid levels. |
| 148 | 1838064 | Levels of HDL-, HDL2- and HDL3-cholesterol and plasma apolipoprotein AI were markedly decreased in both the diabetic groups compared with their control groups (all p less than 0.001 except HDL3-cholesterol in Type 1 diabetic vs control, p less than 0.05). |
| 149 | 1838064 | In Type 2 diabetic patients, HbA1c correlated positively with triglycerides (r = 0.70, p less than 0.001), cholesterol (r = 0.60, p less than 0.001), apolipoprotein B (r = 0.77, p less than 0.001), and apolipoprotein CIII (r = 0.55, p less than 0.001) and negatively with apolipoprotein AI (r = -0.49, p less than 0.001). |
| 150 | 1838064 | Plasma lipid and apolipoprotein levels of Type 1 and Type 2 young Kuwaiti diabetic women on insulin therapy were investigated to elucidate the relationship between coronary artery disease risk factors and lipid levels. |
| 151 | 1838064 | Levels of HDL-, HDL2- and HDL3-cholesterol and plasma apolipoprotein AI were markedly decreased in both the diabetic groups compared with their control groups (all p less than 0.001 except HDL3-cholesterol in Type 1 diabetic vs control, p less than 0.05). |
| 152 | 1838064 | In Type 2 diabetic patients, HbA1c correlated positively with triglycerides (r = 0.70, p less than 0.001), cholesterol (r = 0.60, p less than 0.001), apolipoprotein B (r = 0.77, p less than 0.001), and apolipoprotein CIII (r = 0.55, p less than 0.001) and negatively with apolipoprotein AI (r = -0.49, p less than 0.001). |
| 153 | 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. |
| 154 | 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. |
| 155 | 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. |
| 156 | 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. |
| 157 | 1865164 | To determine the possible role of a glycaemic control in lipid metabolism in non-insulin-dependent diabetes mellitus (NIDDM) patients, serum lipid and apolipoprotein levels were measured in well-controlled and poorly controlled lean NIDDM without proteinuria and hypertension. |
| 158 | 1884882 | Apolipoprotein levels in non-insulin-dependent diabetes mellitus with clinical macroangiopathy. |
| 159 | 1900041 | Coronary artery disease and apolipoprotein A-I/C-III gene polymorphism: a study of Saudi Arabians. |
| 160 | 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. |
| 161 | 1900041 | We studied the apolipoprotein A-I/C-III gene cluster polymorphism in 97 Saudi Arabians in relation to coronary artery disease. |
| 162 | 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. |
| 163 | 1900041 | Coronary artery disease and apolipoprotein A-I/C-III gene polymorphism: a study of Saudi Arabians. |
| 164 | 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. |
| 165 | 1900041 | We studied the apolipoprotein A-I/C-III gene cluster polymorphism in 97 Saudi Arabians in relation to coronary artery disease. |
| 166 | 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. |
| 167 | 1900041 | Coronary artery disease and apolipoprotein A-I/C-III gene polymorphism: a study of Saudi Arabians. |
| 168 | 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. |
| 169 | 1900041 | We studied the apolipoprotein A-I/C-III gene cluster polymorphism in 97 Saudi Arabians in relation to coronary artery disease. |
| 170 | 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. |
| 171 | 1900041 | Coronary artery disease and apolipoprotein A-I/C-III gene polymorphism: a study of Saudi Arabians. |
| 172 | 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. |
| 173 | 1900041 | We studied the apolipoprotein A-I/C-III gene cluster polymorphism in 97 Saudi Arabians in relation to coronary artery disease. |
| 174 | 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. |
| 175 | 2022058 | Disparity between apolipoprotein E phenotypes and genotypes (as determined by polymerase chain reaction and oligonucleotide probes) in patients with non-insulin-dependent diabetes mellitus. |
| 176 | 2022058 | Apolipoprotein (apo) E phenotype and genotype frequencies, due to allelic variation at amino acids 112 and 158, have been investigated in 95 Caucasian non-insulin dependent diabetic patients (NIDDM). |
| 177 | 2040396 | Increased plasma apolipoprotein(a) levels in IDDM patients with microalbuminuria. |
| 178 | 2040396 | Patients with insulin-dependent diabetes mellitus (IDDM) have a significantly increased risk of macrovascular disease, particularly if they have persistent proteinuria. |
| 179 | 2040396 | To determine whether altered levels of apolipoprotein(a) [apo(a)], the plasminogenlike glycoprotein of the potentially atherogenic lipoprotein(a); contribute to the increased risk of atherosclerosis, apo(a) levels were measured in 107 patients with IDDM and compared with nondiabetic control subjects and male elective coronary artery graft patients. |
| 180 | 2040396 | The elevated apo(a) levels found in patients with IDDM and increased urinary albumin loss may contribute to their heightened risk of macrovascular disease. |
| 181 | 2040396 | Increased plasma apolipoprotein(a) levels in IDDM patients with microalbuminuria. |
| 182 | 2040396 | Patients with insulin-dependent diabetes mellitus (IDDM) have a significantly increased risk of macrovascular disease, particularly if they have persistent proteinuria. |
| 183 | 2040396 | To determine whether altered levels of apolipoprotein(a) [apo(a)], the plasminogenlike glycoprotein of the potentially atherogenic lipoprotein(a); contribute to the increased risk of atherosclerosis, apo(a) levels were measured in 107 patients with IDDM and compared with nondiabetic control subjects and male elective coronary artery graft patients. |
| 184 | 2040396 | The elevated apo(a) levels found in patients with IDDM and increased urinary albumin loss may contribute to their heightened risk of macrovascular disease. |
| 185 | 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. |
| 186 | 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. |
| 187 | 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). |
| 188 | 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. |
| 189 | 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. |
| 190 | 2065046 | Calcification revealed a mixed pattern, with duration, hypertension, and triglyceride to apolipoprotein A-I ratio being the statistically significant associated factors. |
| 191 | 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. |
| 192 | 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. |
| 193 | 2065046 | Calcification revealed a mixed pattern, with duration, hypertension, and triglyceride to apolipoprotein A-I ratio being the statistically significant associated factors. |
| 194 | 2066673 | To determine whether alterations in apolipoprotein composition of plasma lipoproteins were due to changes in apolipoprotein gene expression, we measured the steady state apoE mRNA levels in several tissues from both control and diabetic rabbits. |
| 195 | 2066673 | The result that apoE mRNA levels and tissue cholesterol content are altered in the diabetic cholesterol-fed rabbit suggests that insulin deficiency in the rabbit may influence apoE gene expression and tissue cholesterol homeostasis. |
| 196 | 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. |
| 197 | 2105208 | Having demonstrated that plasma low density lipoproteins (LDL) bind T4 through a specific interaction with their sole apolipoprotein, apoB-100, we tested the hypothesis that cells could internalize the LDL-T4 complex via cell surface LDL receptors. |
| 198 | 2105208 | These changes were confirmed with several different LDL preparations and were mimicked by isolated apoB-100 and apoE, the sole ligands for the LDL receptors (apoB/E receptors). |
| 199 | 2105208 | The specificity of the LDL effect was shown by the finding that T4-binding globulin, prealbumin, or serum albumin, at concentrations giving 10-90% T4 bound, failed to increase T4 uptake. |
| 200 | 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. |
| 201 | 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. |
| 202 | 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. |
| 203 | 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. |
| 204 | 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. |
| 205 | 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. |
| 206 | 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. |
| 207 | 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. |
| 208 | 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. |
| 209 | 2115989 | Lipid and apolipoprotein compositions of two species of ApoA-I containing lipoproteins in young girls with insulin-dependent diabetes mellitus. |
| 210 | 2115989 | Two species of lipoproteins containing apoA-I (A-ILp), lipoprotein containing apoA-I and apoA-II (LpA-I/A-II), and lipoprotein containing apoA-I but no apoA-II were isolated from 12 girls with insulin-dependent diabetes mellitus (IDDM) and from 19 healthy controls using affinity chromatography. |
| 211 | 2115989 | However, apolipoprotein changes of LpA-I/A-II may possibly be related to the accelerated atherosclerotic processes noted in patients with IDDM. |
| 212 | 2115989 | Lipid and apolipoprotein compositions of two species of ApoA-I containing lipoproteins in young girls with insulin-dependent diabetes mellitus. |
| 213 | 2115989 | Two species of lipoproteins containing apoA-I (A-ILp), lipoprotein containing apoA-I and apoA-II (LpA-I/A-II), and lipoprotein containing apoA-I but no apoA-II were isolated from 12 girls with insulin-dependent diabetes mellitus (IDDM) and from 19 healthy controls using affinity chromatography. |
| 214 | 2115989 | However, apolipoprotein changes of LpA-I/A-II may possibly be related to the accelerated atherosclerotic processes noted in patients with IDDM. |
| 215 | 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. |
| 216 | 2132196 | Apolipoprotein and lipid ratios in treated non-insulin dependent diabetics. |
| 217 | 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. |
| 218 | 2137219 | [Lipoprotein and apolipoprotein levels in young insulin-dependent diabetic patients. |
| 219 | 2137219 | The most significant increases of TG, TC, LDL-C and ApoB levels were observed in group 3, i.e. in patients whose diabetes was the most poorly controlled (HbA 1: 12.9 +/- 1.3 per cent; fructosamine: 4.6 +/- 0.9 mmol/l). |
| 220 | 2137219 | Thus, TG, TC, LDL-C and ApoB are increased in young diabetics whose HbA1 and fructosamine levels exceed reference values by more than 5 standard deviations. |
| 221 | 2147637 | Serum apolipoprotein B and apolipoprotein (a) showed no statistically significant changes. |
| 222 | 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). |
| 223 | 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. |
| 224 | 2182032 | Effect of different insulin regimens on plasma lipoprotein and apolipoprotein concentrations in patients with non-insulin-dependent diabetes mellitus. |
| 225 | 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. |
| 226 | 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. |
| 227 | 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. |
| 228 | 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. |
| 229 | 2318345 | Effects of omega-3 fish oils on plasma lipids, lipoprotein composition, and postheparin lipoprotein lipase in women with IDDM. |
| 230 | 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). |
| 231 | 2318345 | Weight, insulin requirements, and glycosylated hemoglobin remained stable. |
| 232 | 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. |
| 233 | 2492924 | The 27-kilodalton thyroxine (T4)-binding protein is human apolipoprotein A-I: identification of a 68-kilodalton high density lipoprotein that binds T4. |
| 234 | 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. |
| 235 | 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. |
| 236 | 2492924 | The 27-kilodalton thyroxine (T4)-binding protein is human apolipoprotein A-I: identification of a 68-kilodalton high density lipoprotein that binds T4. |
| 237 | 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. |
| 238 | 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. |
| 239 | 2492924 | The 27-kilodalton thyroxine (T4)-binding protein is human apolipoprotein A-I: identification of a 68-kilodalton high density lipoprotein that binds T4. |
| 240 | 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. |
| 241 | 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. |
| 242 | 2500699 | Apolipoprotein assays: methodological considerations and studies in non-insulin-dependent diabetes treated by diet, glibenclamide and insulin. |
| 243 | 2500699 | The apolipoprotein method selected was validated by comparing their concentrations with their corresponding lipoprotein lipid or protein in normal controls and Type 2 (non-insulin-dependent) diabetic patients. |
| 244 | 2500699 | Apolipoprotein assays: methodological considerations and studies in non-insulin-dependent diabetes treated by diet, glibenclamide and insulin. |
| 245 | 2500699 | The apolipoprotein method selected was validated by comparing their concentrations with their corresponding lipoprotein lipid or protein in normal controls and Type 2 (non-insulin-dependent) diabetic patients. |
| 246 | 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. |
| 247 | 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. |
| 248 | 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). |
| 249 | 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. |
| 250 | 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. |
| 251 | 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. |
| 252 | 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. |
| 253 | 2562831 | Insulin-receptor and apolipoprotein genes contribute to development of NIDDM in Chinese Americans. |
| 254 | 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. |
| 255 | 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). |
| 256 | 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. |
| 257 | 2562831 | Insulin-receptor and apolipoprotein genes contribute to development of NIDDM in Chinese Americans. |
| 258 | 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. |
| 259 | 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). |
| 260 | 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. |
| 261 | 2629300 | A significant correlation was demonstrated between the concentrations of cholesterol and apolipoprotein A, on the one hand, and blood glucose level, on the other, and apolipoprotein A was found to be a better indicator of lipid disturbances in the aspect of diabetes control then apolipoprotein B. |
| 262 | 2656141 | Concentrations of total cholesterol, very-low-density lipoprotein cholesterol, low-density lipoprotein (LDL) cholesterol, triglyceride (TG), LDL TG, high-density lipoprotein triglyceride (HDL TG), phospholipid, glucose, glycosylated hemoglobin (HbAtc), apolipoprotein B (apoB), LDL-apoB, and apoB/apoAl were significantly elevated in diabetic women compared with control subjects. |
| 263 | 2656141 | Despite normal body weight and insulin therapy, abnormalities in lipids, lipoprotein lipids, and apoB persisted in NIDDM patients compared with control subjects. |
| 264 | 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. |
| 265 | 2661890 | Apolipoprotein A-II (apo A-II) levels were significantly higher in the VSA group than in the C and CAD groups. |
| 266 | 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. |
| 267 | 2661890 | Apolipoprotein A-II (apo A-II) levels were significantly higher in the VSA group than in the C and CAD groups. |
| 268 | 2673217 | Insulin effects on apolipoprotein B production by normal, diabetic and treated-diabetic rat liver and cultured rat hepatocytes. |
| 269 | 2673217 | The effect of insulin on apolipoprotein (apo B) secretion was studied in 24 h recirculating liver perfusions of isolated normal, diabetic and insulin-treated diabetic rats. |
| 270 | 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. |
| 271 | 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. |
| 272 | 2776655 | We report here a new formula for estimating apolipoprotein (apo) B concentration in the low-density lipoprotein (LDL) fraction from measurements of plasma triglyceride and apoB. |
| 273 | 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. |
| 274 | 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. |
| 275 | 2894928 | The synthesis of either an abnormal insulin/proinsulin molecule or an abnormal insulin receptor can confer susceptibility to NIDDM. |
| 276 | 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. |
| 277 | 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]. |
| 278 | 2923077 | Linoleic-acid-enriched diet: long-term effects on serum lipoprotein and apolipoprotein concentrations and insulin sensitivity in noninsulin-dependent diabetic patients. |
| 279 | 2964335 | Diabetes was diagnosed and treated with insulin at this time but the patient was taking the oral contraceptive pill and also had a deficiency of apolipoprotein CII. |
| 280 | 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). |
| 281 | 3089186 | In women, HDL cholesterol, apolipoprotein A-I, and log-triglyceride values were significantly correlated with those of HbA1 and log-fasting insulin. |
| 282 | 3089186 | Although there were weaker associations in men, apolipoprotein A-I and HbA1 values were inversely related. |
| 283 | 3089186 | These data suggest that HDL cholesterol and apolipoprotein A-I levels are closely linked to glucose metabolism in nondiabetic individuals. |
| 284 | 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). |
| 285 | 3089186 | In women, HDL cholesterol, apolipoprotein A-I, and log-triglyceride values were significantly correlated with those of HbA1 and log-fasting insulin. |
| 286 | 3089186 | Although there were weaker associations in men, apolipoprotein A-I and HbA1 values were inversely related. |
| 287 | 3089186 | These data suggest that HDL cholesterol and apolipoprotein A-I levels are closely linked to glucose metabolism in nondiabetic individuals. |
| 288 | 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). |
| 289 | 3089186 | In women, HDL cholesterol, apolipoprotein A-I, and log-triglyceride values were significantly correlated with those of HbA1 and log-fasting insulin. |
| 290 | 3089186 | Although there were weaker associations in men, apolipoprotein A-I and HbA1 values were inversely related. |
| 291 | 3089186 | These data suggest that HDL cholesterol and apolipoprotein A-I levels are closely linked to glucose metabolism in nondiabetic individuals. |
| 292 | 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). |
| 293 | 3089186 | In women, HDL cholesterol, apolipoprotein A-I, and log-triglyceride values were significantly correlated with those of HbA1 and log-fasting insulin. |
| 294 | 3089186 | Although there were weaker associations in men, apolipoprotein A-I and HbA1 values were inversely related. |
| 295 | 3089186 | These data suggest that HDL cholesterol and apolipoprotein A-I levels are closely linked to glucose metabolism in nondiabetic individuals. |
| 296 | 3091343 | Effect of CS-514, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on lipoprotein and apolipoprotein in plasma of hypercholesterolemic diabetics. |
| 297 | 3094958 | Blood lipid assays repeated after 1, 3, 6, 9, and 12 months of treatment revealed consistent and statistically significant reductions of all atherogenic lipid fractions (total cholesterol, low-density lipoprotein cholesterol, and apolipoprotein B) with parallel increases of high-density lipoprotein cholesterol and apolipoprotein A. |
| 298 | 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). |
| 299 | 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. |
| 300 | 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. |
| 301 | 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. |
| 302 | 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. |
| 303 | 3112449 | [Clinical evaluation of serum apolipoprotein A-I, A-II and B levels in patients with diabetes mellitus]. |
| 304 | 3128878 | Plasma apolipoprotein C-III levels in children with type I diabetes. |
| 305 | 3134018 | Non enzymatic glycation of apolipoprotein A-I. |
| 306 | 3134018 | In diabetic patients, hyperglycaemia results in the non enzymatic glycation of many proteins including apolipoprotein A-I. |
| 307 | 3134018 | Non enzymatic glycation of apolipoprotein A-I. |
| 308 | 3134018 | In diabetic patients, hyperglycaemia results in the non enzymatic glycation of many proteins including apolipoprotein A-I. |
| 309 | 3152618 | Effects of glyburide treatment on serum lipoprotein and apolipoprotein concentrations and ratios in non-insulin-dependent diabetes mellitus. |
| 310 | 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. |
| 311 | 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. |
| 312 | 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. |
| 313 | 3172677 | In long-term diabetic females (n = 20), apolipoprotein A-I levels were also increased (p less than 0.02). |
| 314 | 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. |
| 315 | 3172677 | In long-term diabetic females (n = 20), apolipoprotein A-I levels were also increased (p less than 0.02). |
| 316 | 3223190 | Metabolic control affects plasma lipid and apolipoprotein levels in women, but not in men, with IDDM. |
| 317 | 3223190 | In order to evaluate if in insulin-dependent diabetes lipid and apolipoprotein levels are differently affected by metabolic control in men and women, we measured the concentrations of fasting plasma glucose, mean plasma glucose, glycosylated hemoglobin, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, and apolipoproteins A and B in 94 sex matched patients. |
| 318 | 3223190 | In women, total and LDL cholesterol, triglycerides and apolipoprotein A correlated positively with HbA1 but not with fasting and mean plasma glucose. |
| 319 | 3223190 | Metabolic control affects plasma lipid and apolipoprotein levels in women, but not in men, with IDDM. |
| 320 | 3223190 | In order to evaluate if in insulin-dependent diabetes lipid and apolipoprotein levels are differently affected by metabolic control in men and women, we measured the concentrations of fasting plasma glucose, mean plasma glucose, glycosylated hemoglobin, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, and apolipoproteins A and B in 94 sex matched patients. |
| 321 | 3223190 | In women, total and LDL cholesterol, triglycerides and apolipoprotein A correlated positively with HbA1 but not with fasting and mean plasma glucose. |
| 322 | 3223190 | Metabolic control affects plasma lipid and apolipoprotein levels in women, but not in men, with IDDM. |
| 323 | 3223190 | In order to evaluate if in insulin-dependent diabetes lipid and apolipoprotein levels are differently affected by metabolic control in men and women, we measured the concentrations of fasting plasma glucose, mean plasma glucose, glycosylated hemoglobin, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, and apolipoproteins A and B in 94 sex matched patients. |
| 324 | 3223190 | In women, total and LDL cholesterol, triglycerides and apolipoprotein A correlated positively with HbA1 but not with fasting and mean plasma glucose. |
| 325 | 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. |
| 326 | 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. |
| 327 | 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. |
| 328 | 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. |
| 329 | 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. |
| 330 | 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. |
| 331 | 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. |
| 332 | 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. |
| 333 | 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. |
| 334 | 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. |
| 335 | 3379342 | The apolipoprotein C-II and C-III distribution was similar to that in normolipidemic subjects. |
| 336 | 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). |
| 337 | 3384218 | The ratio of apolipoprotein A-I to B did not differ from that in control children. |
| 338 | 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). |
| 339 | 3384218 | The ratio of apolipoprotein A-I to B did not differ from that in control children. |
| 340 | 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%). |
| 341 | 3452804 | [Polymorphism of the apolipoprotein A-I gene and susceptibility to non-insulin-dependent diabetes mellitus]. |
| 342 | 3474772 | There are certain parallels between hypertriglyceridemic cholesterol-fed alloxan-diabetic rabbits and humans with familial lipoprotein lipase deficiency, familial apolipoprotein C-II deficiency and insulin-dependent diabetes mellitus in the ketoacidotic state. |
| 343 | 3521180 | Biosynthetic human insulin does not modify circulating lipid and apolipoprotein concentrations in type I diabetic patients. |
| 344 | 3521180 | Since insulin modulates key enzymes of lipid metabolism, different biological activities of biosynthetic human insulin (BHI) and conventional insulins might induce different plasma lipid and apolipoprotein patterns in diabetic patients chronically treated with the former or the latter insulin preparation. |
| 345 | 3521180 | In this study we have evaluated the effects of 3 months of therapy with BHI on plasma lipid and apolipoprotein concentrations in a group of type I diabetics previously treated with insulin of animal origin and the results have been compared with those from diabetics maintained on conventional insulin therapy. |
| 346 | 3521180 | Thus, long-term BHI treatment of type I diabetics does not cause any major change in plasma lipid and apolipoprotein patterns in comparison with animal insulin therapy, so that the validity of using BHI in the treatment of type I diabetes is confirmed. |
| 347 | 3521180 | Biosynthetic human insulin does not modify circulating lipid and apolipoprotein concentrations in type I diabetic patients. |
| 348 | 3521180 | Since insulin modulates key enzymes of lipid metabolism, different biological activities of biosynthetic human insulin (BHI) and conventional insulins might induce different plasma lipid and apolipoprotein patterns in diabetic patients chronically treated with the former or the latter insulin preparation. |
| 349 | 3521180 | In this study we have evaluated the effects of 3 months of therapy with BHI on plasma lipid and apolipoprotein concentrations in a group of type I diabetics previously treated with insulin of animal origin and the results have been compared with those from diabetics maintained on conventional insulin therapy. |
| 350 | 3521180 | Thus, long-term BHI treatment of type I diabetics does not cause any major change in plasma lipid and apolipoprotein patterns in comparison with animal insulin therapy, so that the validity of using BHI in the treatment of type I diabetes is confirmed. |
| 351 | 3521180 | Biosynthetic human insulin does not modify circulating lipid and apolipoprotein concentrations in type I diabetic patients. |
| 352 | 3521180 | Since insulin modulates key enzymes of lipid metabolism, different biological activities of biosynthetic human insulin (BHI) and conventional insulins might induce different plasma lipid and apolipoprotein patterns in diabetic patients chronically treated with the former or the latter insulin preparation. |
| 353 | 3521180 | In this study we have evaluated the effects of 3 months of therapy with BHI on plasma lipid and apolipoprotein concentrations in a group of type I diabetics previously treated with insulin of animal origin and the results have been compared with those from diabetics maintained on conventional insulin therapy. |
| 354 | 3521180 | Thus, long-term BHI treatment of type I diabetics does not cause any major change in plasma lipid and apolipoprotein patterns in comparison with animal insulin therapy, so that the validity of using BHI in the treatment of type I diabetes is confirmed. |
| 355 | 3521180 | Biosynthetic human insulin does not modify circulating lipid and apolipoprotein concentrations in type I diabetic patients. |
| 356 | 3521180 | Since insulin modulates key enzymes of lipid metabolism, different biological activities of biosynthetic human insulin (BHI) and conventional insulins might induce different plasma lipid and apolipoprotein patterns in diabetic patients chronically treated with the former or the latter insulin preparation. |
| 357 | 3521180 | In this study we have evaluated the effects of 3 months of therapy with BHI on plasma lipid and apolipoprotein concentrations in a group of type I diabetics previously treated with insulin of animal origin and the results have been compared with those from diabetics maintained on conventional insulin therapy. |
| 358 | 3521180 | Thus, long-term BHI treatment of type I diabetics does not cause any major change in plasma lipid and apolipoprotein patterns in comparison with animal insulin therapy, so that the validity of using BHI in the treatment of type I diabetes is confirmed. |
| 359 | 3730047 | Serum apolipoprotein A-II levels were lower in the male subjects with type 2 diabetes or IGT than in controls. |
| 360 | 3730047 | Insulin response, i.e., sum of immunoreactive insulin (IRI) levels at basal, 30, 60, 90 and 120 min after a 75-g oral glucose load, negatively correlated to HDL- and HDL2 cholesterol levels (r = -0.396, P less than 0.05; r = -0.482, P less than 0.001, respectively), and positively correlated to VLDL triglyceride values (r = 0.485, P less than 0.001) in the male subjects with type 2 diabetes or IGT. |
| 361 | 3781171 | Alterations in plasma levels of apolipoprotein A-IV in various clinical entities. |
| 362 | 3781171 | The serum levels of apolipoprotein A-IV (apo A-IV) were measured by rocket immunoelectrophoresis in disease-free humans, at fasting and after oral and intravenous fat administration. |
| 363 | 3781171 | Alterations in plasma levels of apolipoprotein A-IV in various clinical entities. |
| 364 | 3781171 | The serum levels of apolipoprotein A-IV (apo A-IV) were measured by rocket immunoelectrophoresis in disease-free humans, at fasting and after oral and intravenous fat administration. |
| 365 | 3865885 | In addition, defective clearance of VLDL may be involved (e.g. impaired lipoprotein-lipase activity or an altered apolipoprotein composition of triglyceride-rich particles). |
| 366 | 3923627 | Increased levels of HDL-cholesterol and apolipoprotein A-I after intensified insulin therapy for diabetes. |
| 367 | 3923627 | Levels of HDL-cholesterol and apolipoprotein A-I increased without significant changes in hemoglobin A1 (HbA1), triglyceride, or cholesterol. |
| 368 | 3923627 | These findings suggest that increases in HDL-cholesterol and apolipoprotein A-I were a result of the intensified insulin delivery. |
| 369 | 3923627 | Increased levels of HDL-cholesterol and apolipoprotein A-I after intensified insulin therapy for diabetes. |
| 370 | 3923627 | Levels of HDL-cholesterol and apolipoprotein A-I increased without significant changes in hemoglobin A1 (HbA1), triglyceride, or cholesterol. |
| 371 | 3923627 | These findings suggest that increases in HDL-cholesterol and apolipoprotein A-I were a result of the intensified insulin delivery. |
| 372 | 3923627 | Increased levels of HDL-cholesterol and apolipoprotein A-I after intensified insulin therapy for diabetes. |
| 373 | 3923627 | Levels of HDL-cholesterol and apolipoprotein A-I increased without significant changes in hemoglobin A1 (HbA1), triglyceride, or cholesterol. |
| 374 | 3923627 | These findings suggest that increases in HDL-cholesterol and apolipoprotein A-I were a result of the intensified insulin delivery. |
| 375 | 3936351 | Apolipoprotein A-I gene polymorphism and susceptibility of non-insulin-dependent diabetes mellitus. |
| 376 | 3936351 | A polymorphic DNA sequence of the apolipoprotein (apo) A-I gene region was studied in relation to non-insulin-dependent diabetes mellitus (NIDDM). |
| 377 | 3936351 | Apolipoprotein A-I gene polymorphism and susceptibility of non-insulin-dependent diabetes mellitus. |
| 378 | 3936351 | A polymorphic DNA sequence of the apolipoprotein (apo) A-I gene region was studied in relation to non-insulin-dependent diabetes mellitus (NIDDM). |
| 379 | 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. |
| 380 | 6225845 | Diabetic animals had higher HDL-apoA-I (apolipoprotein A-I) levels than did CO- and LF- but not BT-fed rats. |
| 381 | 6225845 | In LDL, apoB levels were lower and apoE levels were higher in LF-fed rats than in animals fed high fat diets. |
| 382 | 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. |
| 383 | 6229255 | No correlation between HbA1 and either HDL cholesterol or A-I and A-II was found in IDD and NIDD. |
| 384 | 6229255 | A positive correlation between HbA1 and either triglyceride or VLDL triglyceride was noted in IDD and NIDD. |
| 385 | 6229255 | There was also a positive correlation between insulin dosage in IDD and HDL cholesterol, apolipoprotein A-I and A-II. |
| 386 | 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. |
| 387 | 6229255 | No correlation between HbA1 and either HDL cholesterol or A-I and A-II was found in IDD and NIDD. |
| 388 | 6229255 | A positive correlation between HbA1 and either triglyceride or VLDL triglyceride was noted in IDD and NIDD. |
| 389 | 6229255 | There was also a positive correlation between insulin dosage in IDD and HDL cholesterol, apolipoprotein A-I and A-II. |
| 390 | 6336700 | Effect of metabolic control on lipid, lipoprotein, and apolipoprotein levels in 55 insulin-dependent diabetic patients. |
| 391 | 6393441 | In view of the high incidence of hyperlipidemia and the low sialic acid content in the membranes of diabetics, we analyzed the percentage composition of apolipoprotein CII, known as an activator of lipoprotein lipase, and a subspecies of apolipoprotein CIII, an inhibitor of lipoprotein lipase, in triglyceride-rich lipoproteins. |
| 392 | 6406724 | [Radioimmunoassay of apolipoprotein A - I and A - II of human plasma high density lipoprotein and its clinical use]. |
| 393 | 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. |
| 394 | 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). |
| 395 | 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. |
| 396 | 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). |
| 397 | 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. |
| 398 | 6436127 | Insulin and apolipoprotein A-1/C-III gene polymorphisms relating to hypertriglyceridaemia and diabetes mellitus. |
| 399 | 6436127 | Two gene specific probes have been used to identify polymorphic DNA loci on chromosome 11 close to the insulin and apoprotein A-1 genes in a genetic analysis of hypertriglyceridaemic patients with and without co-existing diabetes. |
| 400 | 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. |
| 401 | 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. |
| 402 | 6734382 | The relationship between serum lipid, lipoprotein, and apolipoprotein levels and abnormalities of renal function has been investigated in 112 insulin-dependent (type I) diabetic patients. |
| 403 | 6762034 | The application of a two-week continuous intravenous insulin infusion (CIVII) resulted in a normalisation of lipoprotein- and apolipoprotein fractions, whereas the in vivo platelet function remained unchanged. |
| 404 | 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). |
| 405 | 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. |
| 406 | 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. |
| 407 | 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). |
| 408 | 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. |
| 409 | 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. |
| 410 | 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). |
| 411 | 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. |
| 412 | 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. |
| 413 | 6793437 | High-density lipoprotein cholesterol and apolipoprotein A-I levels at diagnosis in patients with non-insulin dependent diabetes. |
| 414 | 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). |
| 415 | 6793437 | High-density lipoprotein cholesterol and apolipoprotein A-I levels at diagnosis in patients with non-insulin dependent diabetes. |
| 416 | 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). |
| 417 | 6799600 | To determine the acute effects of insulin on lipoprotein metabolism, we have followed the plasma lipoprotein lipid and apolipoprotein levels during insulin therapy for the first 24 hr in 13 patients with diabetic ketoacidosis. |
| 418 | 6799600 | Plasma apoprotein (apo) B levels were in the upper normal range (101 mg/dl) before treatment and decreased with therapy due to significant decreases in VLDL, but not IDL or LDL apoB. |
| 419 | 6814965 | High density lipoprotein cholesterol and apolipoprotein a-1 concentrations in non-insulin dependent diabetics treated by diet and chlorpropamide. |
| 420 | 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. |
| 421 | 6814965 | High density lipoprotein cholesterol and apolipoprotein a-1 concentrations in non-insulin dependent diabetics treated by diet and chlorpropamide. |
| 422 | 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. |
| 423 | 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. |
| 424 | 7098378 | From these data, the LDL-cholesterol and the atherosclerosis indices (LDL-cholesterol/HDL-cholesterol and apolipoprotein B/apolipoprotein A) were determined. |
| 425 | 7106445 | Apolipoprotein C in type 2 (non-insulin-dependent) diabetic patients with hypertriglyceridaemia. |
| 426 | 7106445 | The composition of apolipoprotein C of the very low density lipoproteins (VLDL) was examined in 23 treated Type 2 (non-insulin-dependent) diabetic patients, who had elevated VLDL concentrations. |
| 427 | 7106445 | Apolipoprotein C was separated by isoelectric focussing into apolipoprotein C-II which is known as the specific activator of lipoprotein lipase, and three apolipoprotein C-III fragments. |
| 428 | 7106445 | A regulatory role has been ascribed to the ratio of apolipoprotein C-II to apolipoprotein C-III in the removal of plasma triglycerides. |
| 429 | 7106445 | In particular, the above apolipoprotein ratio and the relative amounts of apolipoprotein C-III fragments were normal. |
| 430 | 7106445 | Apolipoprotein C in type 2 (non-insulin-dependent) diabetic patients with hypertriglyceridaemia. |
| 431 | 7106445 | The composition of apolipoprotein C of the very low density lipoproteins (VLDL) was examined in 23 treated Type 2 (non-insulin-dependent) diabetic patients, who had elevated VLDL concentrations. |
| 432 | 7106445 | Apolipoprotein C was separated by isoelectric focussing into apolipoprotein C-II which is known as the specific activator of lipoprotein lipase, and three apolipoprotein C-III fragments. |
| 433 | 7106445 | A regulatory role has been ascribed to the ratio of apolipoprotein C-II to apolipoprotein C-III in the removal of plasma triglycerides. |
| 434 | 7106445 | In particular, the above apolipoprotein ratio and the relative amounts of apolipoprotein C-III fragments were normal. |
| 435 | 7106445 | Apolipoprotein C in type 2 (non-insulin-dependent) diabetic patients with hypertriglyceridaemia. |
| 436 | 7106445 | The composition of apolipoprotein C of the very low density lipoproteins (VLDL) was examined in 23 treated Type 2 (non-insulin-dependent) diabetic patients, who had elevated VLDL concentrations. |
| 437 | 7106445 | Apolipoprotein C was separated by isoelectric focussing into apolipoprotein C-II which is known as the specific activator of lipoprotein lipase, and three apolipoprotein C-III fragments. |
| 438 | 7106445 | A regulatory role has been ascribed to the ratio of apolipoprotein C-II to apolipoprotein C-III in the removal of plasma triglycerides. |
| 439 | 7106445 | In particular, the above apolipoprotein ratio and the relative amounts of apolipoprotein C-III fragments were normal. |
| 440 | 7106445 | Apolipoprotein C in type 2 (non-insulin-dependent) diabetic patients with hypertriglyceridaemia. |
| 441 | 7106445 | The composition of apolipoprotein C of the very low density lipoproteins (VLDL) was examined in 23 treated Type 2 (non-insulin-dependent) diabetic patients, who had elevated VLDL concentrations. |
| 442 | 7106445 | Apolipoprotein C was separated by isoelectric focussing into apolipoprotein C-II which is known as the specific activator of lipoprotein lipase, and three apolipoprotein C-III fragments. |
| 443 | 7106445 | A regulatory role has been ascribed to the ratio of apolipoprotein C-II to apolipoprotein C-III in the removal of plasma triglycerides. |
| 444 | 7106445 | In particular, the above apolipoprotein ratio and the relative amounts of apolipoprotein C-III fragments were normal. |
| 445 | 7106445 | Apolipoprotein C in type 2 (non-insulin-dependent) diabetic patients with hypertriglyceridaemia. |
| 446 | 7106445 | The composition of apolipoprotein C of the very low density lipoproteins (VLDL) was examined in 23 treated Type 2 (non-insulin-dependent) diabetic patients, who had elevated VLDL concentrations. |
| 447 | 7106445 | Apolipoprotein C was separated by isoelectric focussing into apolipoprotein C-II which is known as the specific activator of lipoprotein lipase, and three apolipoprotein C-III fragments. |
| 448 | 7106445 | A regulatory role has been ascribed to the ratio of apolipoprotein C-II to apolipoprotein C-III in the removal of plasma triglycerides. |
| 449 | 7106445 | In particular, the above apolipoprotein ratio and the relative amounts of apolipoprotein C-III fragments were normal. |
| 450 | 7430134 | These particles are unusual in that they contain apolipoprotein A-I in addition to their usual complement of apolipoproteins. |
| 451 | 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). |
| 452 | 7485220 | The authors evaluated serum retinol, retinol-binding protein (RBP), and beta-carotene levels to elucidate the retinoid metabolism in non-insulin-dependent diabetes mellitus (NIDDM). |
| 453 | 7485220 | Lipid-lowering medication significantly decreased retinol, with decreasing apolipoprotein C-II but without a commensurate decrease in RBP. |
| 454 | 7485220 | The retinol levels had a positive correlation with apolipoprotein C-II in all or normolipidemic patients with diabetes and control subjects. |
| 455 | 7485220 | The authors evaluated serum retinol, retinol-binding protein (RBP), and beta-carotene levels to elucidate the retinoid metabolism in non-insulin-dependent diabetes mellitus (NIDDM). |
| 456 | 7485220 | Lipid-lowering medication significantly decreased retinol, with decreasing apolipoprotein C-II but without a commensurate decrease in RBP. |
| 457 | 7485220 | The retinol levels had a positive correlation with apolipoprotein C-II in all or normolipidemic patients with diabetes and control subjects. |
| 458 | 7508874 | Maturity-onset diabetes of the young (MODY) is a model for genetic studies of non-insulin-dependent diabetes mellitus. |
| 459 | 7508874 | We have identified 15 MODY families in which diabetes is not the result of mutations in the glucokinase gene. |
| 460 | 7508874 | Nine other candidate genes potentially implicated in insulin secretion or insulin action have been tested for linkage with MODY in these families, including glucokinase regulatory protein, hexokinase II, insulin receptor substrate 1, fatty acid-binding protein 2, glucagon-like peptide-1 receptor, apolipoprotein C-II, glycogen synthase, adenosine deaminase (a marker for the MODY gene on chromosome 20), and phosphoenolpyruvate carboxykinase. |
| 461 | 7583560 | In control subjects but not patients with diabetes, paraoxonase correlated with HDL cholesterol and apolipoprotein A-1. |
| 462 | 7587865 | Lipoprotein(a), apolipoprotein(a) polymorphism, and insulin treatment in type II diabetic patients. |
| 463 | 7589821 | Loci included the insulin-responsive (GLUT4) glucose transporter, hexokinase 2, glucagon, growth hormone, insulin receptor substrate 1 (IRS1), phosphoenolpyruvate carboxykinase, hepatic and muscle forms of pyruvate kinase, hepatic phosphofructokinase, the apolipoprotein B and the apolipoprotein A2 cluster, lipoprotein lipase, hepatic triglyceride lipase, the very-low-density-lipoprotein receptor, and the Pima insulin resistance locus on chromosome 4. |
| 464 | 7595089 | Increased proportion of plasma apoB-48 to apoB-100 in non-insulin-dependent diabetic rats: contribution of enhanced apoB mRNA editing in the liver. |
| 465 | 7595089 | To assess the alteration of apolipoprotein (apo) B mRNA editing in non-insulin-dependent diabetes mellitus (NIDDM), we measured plasma apoB-100 and apoB-48 levels and apoB mRNA editing efficiency in the liver and intestine from GK (Goto-Kakizaki) rats, a genetically NIDDM animal. |
| 466 | 7595089 | In conclusion, an enhanced apoB mRNA editing was indicated in the non-insulin-dependent diabetic rats, which might contribute to the increase of plasma apoB-48 levels. |
| 467 | 7604809 | Apolipoprotein A-I levels increased (p = 0.054) despite no significant change in the levels of high density lipoprotein cholesterol. |
| 468 | 7621978 | Non-enzymatic glycosylation of apolipoprotein A-I and its functional consequences. |
| 469 | 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. |
| 470 | 7621978 | Non-enzymatic glycosylation of apolipoprotein A-I and its functional consequences. |
| 471 | 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. |
| 472 | 7621979 | Apolipoprotein A-IV in diabetes mellitus. |
| 473 | 7621979 | Apolipoprotein A-IV is considered to play a role in triglyceride-rich lipoprotein metabolism, in reverse cholesterol transport, and in facilitation of CETP (Cholesterolyl Ester Transfer Protein) activity. |
| 474 | 7621979 | In non-insulin-dependent-diabetes, increased apoA-IV levels are found, mainly related to hypertriglyceridemia and to a lesser extent to HDL cholesterol level; apoA-IV phenotype distribution is not different from controls; in the control population, the potential protective lipid profile (characterized by increased HDL and HDL2 cholesterol levels) related to the apoA-IV 1-2 phenotype, is no longer found in NIDDM patients (the metabolic state of NIDDM appears to have effected the potential protective lipid profile related to the apoA-IV 1-2 phenotype); and plasma apoA-IV levels is associated with increased prevalence for macrovascular disease. |
| 475 | 7621979 | Apolipoprotein A-IV in diabetes mellitus. |
| 476 | 7621979 | Apolipoprotein A-IV is considered to play a role in triglyceride-rich lipoprotein metabolism, in reverse cholesterol transport, and in facilitation of CETP (Cholesterolyl Ester Transfer Protein) activity. |
| 477 | 7621979 | In non-insulin-dependent-diabetes, increased apoA-IV levels are found, mainly related to hypertriglyceridemia and to a lesser extent to HDL cholesterol level; apoA-IV phenotype distribution is not different from controls; in the control population, the potential protective lipid profile (characterized by increased HDL and HDL2 cholesterol levels) related to the apoA-IV 1-2 phenotype, is no longer found in NIDDM patients (the metabolic state of NIDDM appears to have effected the potential protective lipid profile related to the apoA-IV 1-2 phenotype); and plasma apoA-IV levels is associated with increased prevalence for macrovascular disease. |
| 478 | 7646575 | Atherogenic index and apolipoprotein B/apolipoprotein A-I ratio were also significantly decreased after 4 weeks. |
| 479 | 7648790 | Analysis of serum apolipoprotein A-I in elderly non-insulin-dependent diabetic patients. |
| 480 | 7648790 | Furthermore, serum lipids and apolipoprotein A-I and B levels were determined. |
| 481 | 7648790 | Analysis of serum apolipoprotein A-I in elderly non-insulin-dependent diabetic patients. |
| 482 | 7648790 | Furthermore, serum lipids and apolipoprotein A-I and B levels were determined. |
| 483 | 7729606 | Decreased interstitial apolipoprotein A-I levels in IDDM patients with diabetic nephropathy. |
| 484 | 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. |
| 485 | 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). |
| 486 | 7729606 | Decreased interstitial apolipoprotein A-I levels in IDDM patients with diabetic nephropathy. |
| 487 | 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. |
| 488 | 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). |
| 489 | 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. |
| 490 | 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. |
| 491 | 7758222 | It could, however, be explained by glycation of lysine residues in apolipoprotein A-I, which is the most potent activator of LCAT. |
| 492 | 7758885 | Insulin resistance and abnormal albumin excretion in non-diabetic first-degree relatives of patients with NIDDM. |
| 493 | 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. |
| 494 | 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. |
| 495 | 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. |
| 496 | 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. |
| 497 | 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. |
| 498 | 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. |
| 499 | 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. |
| 500 | 7820935 | DNA polymorphisms at the locus for human cholesteryl ester transfer protein (CETP) are associated with macro- and microangiopathy in non-insulin-dependent diabetes mellitus. |
| 501 | 7820935 | The effect of variation at the cholesteryl ester transfer protein (CETP) gene locus and in the apolipoprotein (apo) AI-CIII-AIV gene cluster on the susceptibility of individuals with non-insulin-dependent diabetes mellitus (NIDDM) to atherosclerotic vascular disease was studied in 136 male and 122 female patients with NIDDM. |
| 502 | 7825638 | Several lines of evidence suggest that a subset of women may be at increased risk of cardiovascular disease because of unfavorable alterations in insulin action and/or production, accompanying altered apolipoprotein metabolism and altered androgenicity and/or estrogenicity. |
| 503 | 7856176 | The major protein constituents of lipoprotein (a) are apolipoprotein B 100 und apolipoprotein (a) (apo(a)). |
| 504 | 7856176 | After subdivision of the diabetic patients according to different stages of diabetic nephropathy (DN), determined by urinary albumin excretion, significant relationships were found between DN and triglycerides (P = 0.04), LDL (P = 0.03) and apolipoprotein B (P = 0.008, Kruskal-Wallis test) levels. |
| 505 | 7868080 | Intracerebral and cerebrovascular beta-protein amyloid deposits are a hallmark of the pathology of both sporadic and familial Alzheimer's disease, beta 2-microglobulin-derived amyloid is a common complication of long term haemodialysis, and islet amyloid polypeptide is the fibril protein in the universal islet amyloidosis of type II diabetes mellitus. |
| 506 | 7868080 | New fibril proteins have lately been identified in hereditary amyloidosis, including variants of gelsolin, apolipoprotein AI, lysozyme and fibrinogen. |
| 507 | 7868080 | The development of radiolabelled serum amyloid P component (SAP) scintigraphy has allowed amyloid to be diagnosed non-invasively in vivo for the first time, provided unique insight into the distribution and size of amyloid deposits, and yielded novel information on the natural history and the effects of treatment. |
| 508 | 7895421 | Compared to fasting with fluid and salt replacement, fasting with no fluids was associated with higher (mean, 95% confidence interval) total serum cholesterol (8.1%, 4.3-11.9%), HDL cholesterol (7.5%, 1.8-13.1%), LDL cholesterol (10.5%, 2.2-18.8%), apolipoprotein A-1 (8.9%, 5.0-12.8%), and apolipoprotein B (10.5%, 5.2-15.8%). |
| 509 | 7923754 | Lipoprotein(a) [Lp(a)] is a plasma macromolecular complex that is assembled from low-density lipoproteins (LDL) and a large hydrophilic glycoprotein, named apolipoprotein(a) [apo(a)], linked by a disulfide bond to apolipoprotein B-100. |
| 510 | 7943306 | Acute changes in very low-density lipoprotein (VLDL) triglyceride (TG) and VLDL apolipoprotein (apo) B production were examined in 11 healthy young males in response to insulin delivered either by the peripheral venous route or secreted directly by the pancreas. |
| 511 | 7955979 | The effect of recombinant insulin-like growth factor I on ketone body, lipid and apolipoprotein concentrations and its use to treat ketoacidosis in severe insulin resistance. |
| 512 | 7956623 | Apolipoprotein A-IV levels and phenotype distribution in NIDDM. |
| 513 | 7958503 | In 356 NIDDM patients and 1,087 people with normal glucose tolerance, we investigated the association between MI risk and polymorphism at codon 360 in the apolipoprotein A-IV (apoA-IV) gene. |
| 514 | 7980694 | Apolipoprotein E2, renal failure and lipid abnormalities in non-insulin-dependent diabetes mellitus. |
| 515 | 7980694 | The association of apolipoprotein E (apo E) genetic polymorphism, particularly apo E2, with renal failure (plasma creatinine > or = 1.4 mg/dl, and urinary albumin excretion index > or = 300 mg/g.creatinine and/or persistent proteinuria) was investigated in 57 non-insulin-dependent diabetic (NIDDM) patients. |
| 516 | 7986307 | NIDDM subjects also have altered apolipoprotein concentrations, including increased apoB, apoC-III, and decreased apoA-I; in addition, apoE-2 may be over-represented in diabetic populations. |
| 517 | 7990698 | LDLs and RBC membranes were isolated from 11 insulin-dependent (IDDM) and 18 non-insulin-dependent diabetic (NIDDM) patients and exposed to a peroxidative stress by incubation with phenylhydrazine. |
| 518 | 7990698 | The following parameters were also evaluated: plasma glucose, triglycerides (TG), phospholipids (PL), total and high-density lipoprotein (HDL) cholesterol, apolipoprotein (apo) A-I, apo B, hemoglobin A1c (HbA1c), LDL PL and cholesterol, LDL fatty acid composition, and RBC membrane PL and cholesterol. |
| 519 | 8013760 | We investigated the effects of non-insulin-dependent diabetes mellitus (NIDDM) on lipoprotein(a) (Lp[a]) and apolipoprotein(a) (apo[a]) in a population of Mexican-Americans. |
| 520 | 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. |
| 521 | 8083340 | Apolipoprotein LP(a)]. |
| 522 | 8098786 | Apolipoprotein A-II levels and coronary artery disease in subjects with and without diabetes: a study with use of a specific radioimmunoassay for apolipoprotein A-II. |
| 523 | 8098786 | High-density lipoprotein cholesterol (HDL-C), apolipoprotein (apo) A-I, and apo A-II levels were measured in 1,219 normal subjects with no clinical evidence of coronary artery disease, 81 subjects without diabetes but with "significant" coronary artery disease determined by coronary arteriography, and 151 subjects with non-insulin-dependent diabetes mellitus (48 with clinical coronary artery disease and 103 without such disease). |
| 524 | 8098786 | Apolipoprotein A-II levels and coronary artery disease in subjects with and without diabetes: a study with use of a specific radioimmunoassay for apolipoprotein A-II. |
| 525 | 8098786 | High-density lipoprotein cholesterol (HDL-C), apolipoprotein (apo) A-I, and apo A-II levels were measured in 1,219 normal subjects with no clinical evidence of coronary artery disease, 81 subjects without diabetes but with "significant" coronary artery disease determined by coronary arteriography, and 151 subjects with non-insulin-dependent diabetes mellitus (48 with clinical coronary artery disease and 103 without such disease). |
| 526 | 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). |
| 527 | 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). |
| 528 | 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. |
| 529 | 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). |
| 530 | 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. |
| 531 | 8139126 | The serum concentrations of apolipoprotein C-II, C-III and E were significantly higher in the treated groups (p < 0.05). |
| 532 | 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. |
| 533 | 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. |
| 534 | 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). |
| 535 | 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. |
| 536 | 8139126 | The serum concentrations of apolipoprotein C-II, C-III and E were significantly higher in the treated groups (p < 0.05). |
| 537 | 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. |
| 538 | 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. |
| 539 | 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). |
| 540 | 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. |
| 541 | 8139126 | The serum concentrations of apolipoprotein C-II, C-III and E were significantly higher in the treated groups (p < 0.05). |
| 542 | 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. |
| 543 | 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. |
| 544 | 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). |
| 545 | 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. |
| 546 | 8139126 | The serum concentrations of apolipoprotein C-II, C-III and E were significantly higher in the treated groups (p < 0.05). |
| 547 | 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. |
| 548 | 8139482 | This study compared the lipoprotein composition of nondiabetic controls (n = 68) with that of patients with insulin-dependent diabetes mellitus ([IDDM] n = 13) and of patients with IDDM and CRF ([IDDM + CRF] n = 74). |
| 549 | 8139482 | The IDDM + CRF group had multiple abnormalities including (1) elevated TG, apolipoprotein (apo) C-II, and apo C-III levels in all lipid subfractions; (2) elevated VLDL and IDL apo B, TG, FC, cholesterol ester (CE), and phospholipid (PL) levels (with an increased CE/TG ratio in VLDL only); (3) decreased HDL-M apo A-I, apo A-II, CE, and PL levels, but an increased HDL-D apo A-I level; and (4) decreased lecithin:cholesterol acyltransferase (LCAT) activity. |
| 550 | 8141841 | We investigated the relationship between serum apolipoprotein(a) (apo(a)) and growth hormone (GH) levels in 15 patients with acromegaly before and during treatment with octreotide, a long-acting somatostatin analogue, 288-600 micrograms/day s.c., for 6 months. |
| 551 | 8141841 | There were significant reductions in serum GH (F = 7.30; P < 0.01), insulin growth factor 1 (IGF1) (F = 31.4, P < 0.001) and insulin (F = 4.57; P < 0.05) concentrations. |
| 552 | 8143357 | On the other hand, apolipoprotein C-II/C-III ratios in high and very low density lipoprotein, showed no significant differences at baseline compared with controls, suggesting that an apolipoprotein C-II deficiency or apolipoproteins Cs imbalance can be ruled out. |
| 553 | 8190178 | Apolipoprotein (a) levels and atherogenic lipid fractions in relation to the degree of urinary albumin excretion in type 2 diabetes mellitus. |
| 554 | 8190178 | The relationship between serum lipids, apolipoprotein levels including apolipoprotein (a) to albumin excretion rate (AER) in 52 (17 male, 35 female) type 2 diabetic patients was studied. |
| 555 | 8190178 | Apolipoprotein (a) levels and atherogenic lipid fractions in relation to the degree of urinary albumin excretion in type 2 diabetes mellitus. |
| 556 | 8190178 | The relationship between serum lipids, apolipoprotein levels including apolipoprotein (a) to albumin excretion rate (AER) in 52 (17 male, 35 female) type 2 diabetic patients was studied. |
| 557 | 8197611 | After correction for these 7 variables, cyclosporine blood levels remained significantly associated with high-density lipoprotein cholesterol, high-density lipoprotein3 cholesterol, apolipoprotein A-1, apolipoprotein B, low-density lipoprotein cholesterol, and the cholesterol/high-density lipoprotein cholesterol ratio. |
| 558 | 8261628 | The preferential site of non-enzymatic glycation of human apolipoprotein A-I in vivo. |
| 559 | 8265249 | Lipoprotein(a) (Lp(a)) consists of a unique apolipoprotein, apolipoprotein(a), (apo(a)) linked by a disulphide bridge to apolipoprotein B of low density lipoprotein (LDL). |
| 560 | 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. |
| 561 | 8308480 | We observed two patients with hypercholesterolaemia and tendon xanthomas associated with apolipoprotein (apoE-7) E-7, a rare variant of the apoE isoforms. |
| 562 | 8309265 | Immunomagnetic separation of subpopulations of apolipoprotein A-I. |
| 563 | 8314155 | Preliminary research on apolipoprotein A-I and A-II in patients with non-insulin-dependent diabetes mellitus (NIDDM). |
| 564 | 8314449 | Apolipoprotein(a) and cardiovascular disease in type 2 (non-insulin-dependent) diabetic patients with and without diabetic nephropathy. |
| 565 | 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). |
| 566 | 8314449 | Apolipoprotein(a) and cardiovascular disease in type 2 (non-insulin-dependent) diabetic patients with and without diabetic nephropathy. |
| 567 | 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). |
| 568 | 8318568 | Decreased activation of lecithin:cholesterol acyltransferase by glycated apolipoprotein A-I. |
| 569 | 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. |
| 570 | 8318568 | Activation by glycated apolipoprotein A-I was significantly lower at all concentrations than the activation by normal apolipoprotein A-I. |
| 571 | 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). |
| 572 | 8318568 | Decreased activation of lecithin:cholesterol acyltransferase by glycated apolipoprotein A-I. |
| 573 | 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. |
| 574 | 8318568 | Activation by glycated apolipoprotein A-I was significantly lower at all concentrations than the activation by normal apolipoprotein A-I. |
| 575 | 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). |
| 576 | 8318568 | Decreased activation of lecithin:cholesterol acyltransferase by glycated apolipoprotein A-I. |
| 577 | 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. |
| 578 | 8318568 | Activation by glycated apolipoprotein A-I was significantly lower at all concentrations than the activation by normal apolipoprotein A-I. |
| 579 | 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). |
| 580 | 8318568 | Decreased activation of lecithin:cholesterol acyltransferase by glycated apolipoprotein A-I. |
| 581 | 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. |
| 582 | 8318568 | Activation by glycated apolipoprotein A-I was significantly lower at all concentrations than the activation by normal apolipoprotein A-I. |
| 583 | 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). |
| 584 | 8349039 | Regulation of apolipoprotein A-I-containing lipoproteins in IDDM. |
| 585 | 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. |
| 586 | 8366982 | Serum apolipoprotein A II and B levels were also decreased in uremics. |
| 587 | 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. |
| 588 | 8366982 | Serum apolipoprotein A II and B levels were also decreased in uremics. |
| 589 | 8406323 | Bezafibrate affects lipid, lipo- and apolipoprotein pattern in non-insulin-dependent diabetic patients. |
| 590 | 8485116 | For apolipoprotein B predictive significance was observed in the middle-aged populations, whereas apolipoprotein A-I had a protective effect in elderly women. |
| 591 | 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. |
| 592 | 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. |
| 593 | 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. |
| 594 | 8495815 | It has been localized within the framework genetic map of chromosome 19 and is located in the region of the apolipoprotein C-II and histidine-rich calcium-binding protein genes. |
| 595 | 8534686 | Fasting serum Lp(a), total cholesterol, triglycerides, LDL-cholesterol, HDL-cholesterol, apolipoprotein-A and apolipoprotein-B levels were measured on entering the CAPD program and at 3 monthly intervals. |
| 596 | 8535357 | Apolipoprotein(a) concentrations in type 2 (non-insulin dependent) diabetic patients from Romania. |
| 597 | 8535357 | Since non-insulin-dependent diabetes mellitus (NIDDM) is characterized by an increased risk of coronary heart disease (CHD) as related to the general population, the main purpose of our study was to compare the plasma levels of apolipoprotein (a)-(apo) (a) in 30 NIDDM patients hospitalized in our department, and in 20 non-diabetic controls from Timişoara. |
| 598 | 8535357 | We found weak correlations between apo (a) and hemoglobin A1 (HbA1) (r = 0.42). |
| 599 | 8535357 | Apolipoprotein(a) concentrations in type 2 (non-insulin dependent) diabetic patients from Romania. |
| 600 | 8535357 | Since non-insulin-dependent diabetes mellitus (NIDDM) is characterized by an increased risk of coronary heart disease (CHD) as related to the general population, the main purpose of our study was to compare the plasma levels of apolipoprotein (a)-(apo) (a) in 30 NIDDM patients hospitalized in our department, and in 20 non-diabetic controls from Timişoara. |
| 601 | 8535357 | We found weak correlations between apo (a) and hemoglobin A1 (HbA1) (r = 0.42). |
| 602 | 8535356 | Apolipoprotein (a) concentrations in type 1 (insulin-dependent) diabetes mellitus. |
| 603 | 8535356 | It has been suggested that insulin-dependent diabetes mellitus (IDDM) patients have higher values of lipoprotein (a)-Lp (a) that may account for their increased atherogenic risk, as related to non-diabetic subjects. |
| 604 | 8536954 | No association of apolipoprotein A-IV codon 347 and 360 variation with atherosclerosis and lipid transport in a sample of mixed hyperlipidemics. |
| 605 | 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. |
| 606 | 8589767 | Relations of body fat and fat distribution to the serum lipid, apolipoprotein and insulin concentrations of Samoan men and women. |
| 607 | 8593945 | Among regions with multiple potential candidates is chromosome 11, which includes the apolipoprotein C3 cluster, muscle glycogen phosphorylase, two insulin-dependent diabetes loci, the sulfonylurea receptor, and ataxia telangiectasia. |
| 608 | 8609827 | Insulin-dependent diabetes mellitus (IDDM) is characterized by altered composition of atherogenic lipoproteins, especially a depletion in choline-containing phospholipids (PL) of apolipoprotein (apo) B lipoproteins (LpB). |
| 609 | 8609827 | To determine the effects of continuous intraperitoneal (IP) insulin infusion (CIPII) on this qualitative lipoprotein abnormality, we compared lipoprotein profiles of 14 IDDM patients treated by continuous subcutaneous insulin infusion (CSII) and at 2 and 4 months after treatment with CIPII using an implantable pump. |
| 610 | 8609827 | The following parameters were studies: hemoglobin A1c (HbA1c), monthly blood glucose, daily insulin dose (units per kilogram per day), total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL) and low density lipoprotein (LDL) cholesterol, apo A-I, and apo B. |
| 611 | 8609827 | These changes may be related to the route of insulin administration, which may be accompanied by a reduction of lipoprotein lipase (LPL) activity and consequently a reduction of phospholipase activity. |
| 612 | 8645362 | The goal of this study was to compare the structural and biological characteristics of apolipoprotein (apo) B-100-containing particle subfractions isolated from poorly controlled diabetic patients with insulin-dependent diabetes (IDDM), and healthy controls matched for sex, age and body mass index (BMI). |
| 613 | 8646198 | This review is aiming to study the values of apolipoprotein AI and B and plasma lipid levels (total cholesterol, HDL cholesterol, LDL cholesterol and triglyceride) in well-treated diabetic patients, and their possible relationship with hemoglobin A1, body mass index and insulin levels. |
| 614 | 8646198 | The study groups were 26 insulin-dependent diabetic (IDDM) patients, 30 non-insulin-dependent diabetic (NIDDM) subjects and 20 non diabetic subjects (controls). |
| 615 | 8646198 | Apolipoprotein AI concentrations were similar in the three groups, but apolipoprotein B values and apo B/apo AI ratio were significantly higher in IDDM as related to NIDDM patients (p < 0.001) and to non-diabetic subjects (p < 0.001). |
| 616 | 8646198 | We found a weak correlation between apo B and hemoglobin AI in IDDM (r = 0.45; 0.02 < p < 0.05), but not in NIDDM patients. |
| 617 | 8666151 | The aim of this study was to characterize abnormalities of triglyceride-rich apolipoprotein (apo) B-containing lipoproteins in type I diabetic patients with elevated albumin excretion rates (AERs). |
| 618 | 8682012 | Fibrinogen, total cholesterol, triglycerides, high and low density lipoprotein cholesterol, apolipoprotein A-1, apolipoprotein B and lipoprotein (a) were measured. |
| 619 | 8729170 | We found a rapid suppression of plasma free fatty acid (FFA) levels in response to insulin and a consistent 50-60% insulin-induced suppression of both VLDL TG and VLDL apolipoprotein (apo) B in lean insulin-sensitive individuals. |
| 620 | 8729170 | In addition, we found that chronically insulin-resistant hyperinsulinemic obese individuals were resistant to this suppressive effect of insulin on VLDL apoB production, in keeping with similar findings by others performing in vitro experiments using cultured hepatocytes isolated from insulin-resistant or hyperinsulinemic rats. |
| 621 | 8736830 | Apolipoprotein CII & CIII in non-insulin dependent diabetic patients. |
| 622 | 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. |
| 623 | 8763631 | Recent data suggest the existence of a relationship between ischemic heart diseases and apolipoprotein A-I containing lipoproteins. |
| 624 | 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). |
| 625 | 8763631 | In contrast, their lipoprotein particles containing only apolipoprotein AI without apolipoprotein AII and apoAI/apoB ratio were lowered (p < 0.001). |
| 626 | 8763631 | Also, the distribution of particles containing apolipoprotein A-I without apolipoprotein A-II in non-insulin-dependent diabetics was found abnormal. |
| 627 | 8763631 | Recent data suggest the existence of a relationship between ischemic heart diseases and apolipoprotein A-I containing lipoproteins. |
| 628 | 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). |
| 629 | 8763631 | In contrast, their lipoprotein particles containing only apolipoprotein AI without apolipoprotein AII and apoAI/apoB ratio were lowered (p < 0.001). |
| 630 | 8763631 | Also, the distribution of particles containing apolipoprotein A-I without apolipoprotein A-II in non-insulin-dependent diabetics was found abnormal. |
| 631 | 8763631 | Recent data suggest the existence of a relationship between ischemic heart diseases and apolipoprotein A-I containing lipoproteins. |
| 632 | 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). |
| 633 | 8763631 | In contrast, their lipoprotein particles containing only apolipoprotein AI without apolipoprotein AII and apoAI/apoB ratio were lowered (p < 0.001). |
| 634 | 8763631 | Also, the distribution of particles containing apolipoprotein A-I without apolipoprotein A-II in non-insulin-dependent diabetics was found abnormal. |
| 635 | 8770324 | Genetic control of apolipoprotein A-I distribution among HDL subclasses. |
| 636 | 8786017 | We studied the quantitative and qualitative characteristics of lipoprotein(a) [Lp(a)] as a function of apolipoprotein(a) [apo(a)] phenotype in 87 members (42 males, 45 females) of 20 diabetic families, 26 of whom were diagnosed with non-insulin-dependent diabetes mellitus (NIDDM) with moderate glycaemic control (HbA1c 7.1 +/- 1.2%). |
| 637 | 8786731 | Also, in insulin-dependent diabetes mellitus (IDDM) patients, elevated Lp(a) levels have been reported. |
| 638 | 8786731 | In our study population, Lp(a) concentration was not significantly correlated with either hemoglobin A1c (HbA1c) levels of apolipoprotein(a) [apo(a)] phenotype. |
| 639 | 8792770 | Fibrinopeptide A was associated with high C-reactive protein and apolipoprotein(a) and lower ankle-brachial index. |
| 640 | 8808492 | This study examines the activity of two key enzymes of reverse cholesterol transport, cholesterol ester transfer protein (CETP) and lecithin:cholesterol acyl transferase (LCAT) in 21 patients with non-insulin dependent diabetes mellitus (NIDDM) and 21 control subjects. |
| 641 | 8808492 | Serum CETP was assessed by measuring plasma-mediated cholesteryl ester transfer between pooled exogenous lipoprotein with endogenous LCAT inhibited--an estimate of CETP mass. |
| 642 | 8808492 | CETP activity was determined as cholesteryl ester transfer in the presence of the patients' lipoproteins and LCAT (endogenous assay). |
| 643 | 8808492 | There was no significant difference in CETP mass between the diabetic and non-diabetic subjects and there was no correlation between CETP mass and LCAT activity. |
| 644 | 8808492 | Serum free cholesterol from diabetic and control subjects correlated with CETP activity measured using endogenous lipoprotein assay (r = 0.77, P < 0.001 and r = 0.82, P < 0.001), and also with LCAT activity (r = 0.76, P < 0.01 and r = 0.79, P < 0.01). |
| 645 | 8808492 | In a subgroup of 10 control subjects, there was a positive correlation between LCAT activity and apolipoprotein (apo) A-I (r = 0.49, P < 0.05) and apo A-II (r = 0.51, P < 0.05) and also between CETP activity (endogenous assay) and apo A-I (r = 0.87, P = 0.001) and apo A-II (r = 0.63, P < 0.05). |
| 646 | 8808492 | Thus, serum CETP mass was normal in Type 2 diabetes but CETP activity (endogenous assay) was increased and was related to free cholesterol levels and LCAT activity in both diabetic and non-diabetic subjects. |
| 647 | 8817108 | The offspring (male and female) of NIDDM mothers had slightly lower serum apolipoprotein A-I levels than the offspring of NIDDM fathers. |
| 648 | 8829124 | In considering potentially important genetic factors, this study examined the association between genetic polymorphisms in apolipoprotein (apo) E and diabetic nephropathy in 146 patients with insulin-dependent diabetes mellitus (IDDM) of 15 to 21 years' duration. |
| 649 | 8831910 | In addition, many other factors including diabetes, haemostatic factors such as fibrinogen, factor VII, plasminogen activator inhibitors, and new factors such as apolipoprotein E4 and homocysteine, are known to increase the risk of developing clinical CVD. |
| 650 | 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. |
| 651 | 8835322 | Increased frequency of apolipoprotein epsilon 2 allele in non-insulin dependent diabetic (NIDDM) patients with nephropathy. |
| 652 | 8864946 | We studied whether the whole-body catabolism of LDL varies according to its sialic acid content by analyzing the sialic acids in total (d 1.019-1.063 g/ml), light (d 1.019-1.036 g/ml), dense (d 1.037-1.055 g/ml), and very dense (d 1.056-1.063 g/ml) LDL, and the kinetics of total and dense LDL apolipoprotein (apo) B in 20 non-insulin-dependent diabetic and 10 non-diabetic men of similar age, both groups without and with coronary artery disease (CAD). |
| 653 | 8864962 | HDL cholesterol and apolipoprotein A-I kinetics were unchanged. |
| 654 | 8865367 | The frequencies of restriction fragment length polymorphism (RFLP) of the genes for apoB, a major LDL apolipoprotein, and apoAII, a major HDL apolipoprotein, were studied in 45 Tunisian diabetics and an equal number of sex and age matched controls. |
| 655 | 8865367 | Southern blot analysis of an EcoR1 apoB polymorphism and an Msp1 apo AII polymorphism indicates that there was no statistically significant difference in the incidence of different genotypes or alleles among diabetics compared to controls. |
| 656 | 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. |
| 657 | 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). |
| 658 | 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. |
| 659 | 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. |
| 660 | 8911786 | A population association study of four candidate genes (hexokinase II, glucagon-like peptide-1 receptor, fatty acid binding protein-2, and apolipoprotein C-II) with type 2 diabetes and impaired glucose tolerance in Japanese subjects. |
| 661 | 8911786 | Each polymorphic locus near the four candidate genes, hexokinase II (HKII), glucagon-like peptide-1 receptor (GLP1R), fatty acid binding protein-2 (FABP-2), and apolipoprotein C-II (apoC-II) genes, were amplified by polymerase chain reaction (PCR) using 32P-labelled primers and each subject was genotyped for the association study. |
| 662 | 8911786 | The HKII, GLP1R, FABP-2, and apoC-II polymorphisms exhibited 18, 10, 7, and 10 alleles, respectively. |
| 663 | 8911786 | These results suggest that the HKII, GLP1R, FABP-2, and apoC-II genes are not the major inherited factors for the development of Type 2 diabetes or IGT in Japanese subjects, although minor contribution cannot be ruled out. |
| 664 | 8911786 | A population association study of four candidate genes (hexokinase II, glucagon-like peptide-1 receptor, fatty acid binding protein-2, and apolipoprotein C-II) with type 2 diabetes and impaired glucose tolerance in Japanese subjects. |
| 665 | 8911786 | Each polymorphic locus near the four candidate genes, hexokinase II (HKII), glucagon-like peptide-1 receptor (GLP1R), fatty acid binding protein-2 (FABP-2), and apolipoprotein C-II (apoC-II) genes, were amplified by polymerase chain reaction (PCR) using 32P-labelled primers and each subject was genotyped for the association study. |
| 666 | 8911786 | The HKII, GLP1R, FABP-2, and apoC-II polymorphisms exhibited 18, 10, 7, and 10 alleles, respectively. |
| 667 | 8911786 | These results suggest that the HKII, GLP1R, FABP-2, and apoC-II genes are not the major inherited factors for the development of Type 2 diabetes or IGT in Japanese subjects, although minor contribution cannot be ruled out. |
| 668 | 8916142 | AApoAII amyloid deposits studied in one senescence-accelerated mouse P1 (SAMP1), congenic mice that have the amyloidogenic apolipoprotein A-II of SAMP1 mice, and AKR mice all reacted with biotinylated 6D12 by formic acid pretreatment, whereas AA amyloid deposits did not react with the antibody. |
| 669 | 8916142 | The immunoreaction with anti-apolipoprotein A-II for amyloid deposits in senile mice was approximately homogeneous in intensity; on the other hand the reaction with biotinylated 6D12 was irregular in distribution and intensity over the amyloid deposits. |
| 670 | 8916142 | AApoAII amyloid deposits studied in one senescence-accelerated mouse P1 (SAMP1), congenic mice that have the amyloidogenic apolipoprotein A-II of SAMP1 mice, and AKR mice all reacted with biotinylated 6D12 by formic acid pretreatment, whereas AA amyloid deposits did not react with the antibody. |
| 671 | 8916142 | The immunoreaction with anti-apolipoprotein A-II for amyloid deposits in senile mice was approximately homogeneous in intensity; on the other hand the reaction with biotinylated 6D12 was irregular in distribution and intensity over the amyloid deposits. |
| 672 | 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. |
| 673 | 8971092 | Macrovascular disease is associated with increased plasma apolipoprotein A-IV levels in NIDDM. |
| 674 | 8971092 | Apolipoprotein A-IV (apoA-IV) might play an important role in lipoprotein metabolism, including modulation of triglyceride-rich lipoprotein catabolism, reverse cholesterol transport and cholesteryl ester transfer protein (CETP) activity. |
| 675 | 8971092 | Macrovascular disease is associated with increased plasma apolipoprotein A-IV levels in NIDDM. |
| 676 | 8971092 | Apolipoprotein A-IV (apoA-IV) might play an important role in lipoprotein metabolism, including modulation of triglyceride-rich lipoprotein catabolism, reverse cholesterol transport and cholesteryl ester transfer protein (CETP) activity. |
| 677 | 8985654 | Indication for genetic linkage of the phosphoenolpyruvate carboxykinase (PCK1) gene region on chromosome 20q to non-insulin-dependent diabetes mellitus. |
| 678 | 8985654 | No significant results were obtained with glycogen synthase (GSY), insulin receptor substrate-1 (IRS-1) and apolipoprotein C-II (APOC-II) genes. |
| 679 | 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. |
| 680 | 9064379 | [Apolipoprotein AI-CIII, B, and CII gene polymorphisms in patients with non-insulin dependent diabetes mellitus. |
| 681 | 9069522 | There were no significant differences in serum total cholesterol, apolipoprotein A, apolipoprotein B or lipoprotein(a) levels between the study groups. |
| 682 | 9088774 | Response of apolipoprotein AIV and lipoproteins to glycaemic control in young people with insulin-dependent diabetes mellitus. |
| 683 | 9088774 | Young people with insulin-dependent diabetes mellitus (IDDM) (n = 104, 7 to 19 years old) were classified into groups of good (I), fair (II), and poor (III) diabetic control and compared to 22 healthy controls of same origin and age range. |
| 684 | 9088774 | Neither HDL-C nor apolipoprotein AI (apo AI) were affected by glycaemic control, but phospholipids were increased in all three subgroups of IDDM subjects (p < 0.001). |
| 685 | 9088774 | Response of apolipoprotein AIV and lipoproteins to glycaemic control in young people with insulin-dependent diabetes mellitus. |
| 686 | 9088774 | Young people with insulin-dependent diabetes mellitus (IDDM) (n = 104, 7 to 19 years old) were classified into groups of good (I), fair (II), and poor (III) diabetic control and compared to 22 healthy controls of same origin and age range. |
| 687 | 9088774 | Neither HDL-C nor apolipoprotein AI (apo AI) were affected by glycaemic control, but phospholipids were increased in all three subgroups of IDDM subjects (p < 0.001). |
| 688 | 9137945 | Expression of mRNA for ovarian steroid-stimulating factor (apolipoprotein A-I and apolipoprotein A-I-like protein) in human granulosa cells. |
| 689 | 9137945 | The N-terminal sequence of the 3 bands corresponded completely with that of apolipoprotein A-I. |
| 690 | 9137945 | Expression of mRNA for ovarian steroid-stimulating factor (apolipoprotein A-I and apolipoprotein A-I-like protein) in human granulosa cells. |
| 691 | 9137945 | The N-terminal sequence of the 3 bands corresponded completely with that of apolipoprotein A-I. |
| 692 | 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). |
| 693 | 9377806 | Apolipoprotein (apo)H (also known as beta 2 glycoprotein-I) is a glycoprotein synthesized by liver cells and it is present in the blood associated with plasma lipoproteins. |
| 694 | 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. |
| 695 | 9392416 | The enzyme lipoprotein lipase, with apolipoprotein (apo)C-II as a co-factor, hydrolyzes chylomicron triglyceride allowing the delivery of free fatty acids to muscle and adipose tissue. |
| 696 | 9392416 | This particle is enriched in cholesteryl ester and fat-soluble vitamins and contains apoB-48 and apoE. |
| 697 | 9392416 | Here, it may 1) be removed directly by LDL receptors; 2) acquire additional apoE that is secreted free into the space, and then be removed directly by the LDL receptor-related protein (LRP); or 3) it may be sequestered in the space. |
| 698 | 9392416 | Sequestration occurs by binding of apoE to heparan sulfate proteoglycans and/or binding of apoB to hepatic lipase. |
| 699 | 9392500 | In 44 consecutive type 1 diabetic patients (35 men), CETP polymorphism, apolipoprotein (apo) E genotype, serum lipoproteins, serum CETP activity (measured with an exogenous substrate assay, n = 30), clinical variables, and a diet history were documented. |
| 700 | 9402091 | Apolipoprotein B, fibrinogen, HDL cholesterol, and apolipoprotein(a) phenotypes predict coronary artery disease in hemodialysis patients. |
| 701 | 9405926 | Apolipoprotein A-IV and E polymorphisms in children with IDDM. |
| 702 | 9421383 | IDDM patients treated with conventional subcutaneous insulin have an abnormal increase in cholesteryl ester transfer (CET), the proatherogenic step in reverse-cholesterol transport that results in the enrichment of the apolipoprotein (apo) B-containing lipoproteins (VLDL, LDL) with cholesteryl ester (CE). |
| 703 | 9421383 | This disturbance is closely linked to iatrogenic hyperinsulinemia and the nonphysiologic stimulation of lipoprotein lipase (LpL), a physiologic activator of CET, because lowering systemic insulin levels by administering insulin through the intraperitoneal insulin route normalizes LpL and CET. |
| 704 | 9421383 | Therefore, to determine whether hyperinsulinemia promotes CET in this setting, we studied CET, LpL, and insulin levels in 14 euglycemic normolipidemic IDDM PKT patients with near-normal kidney function (creatinine 1.5 +/- 0.4 mg/dl). |
| 705 | 9421383 | These findings indicate that PKT patients with systemically draining allografts have a persisting profile of potentially atherogenic disturbances in insulin levels, LpL, and CET that resemble IDDM patients treated with conventional subcutaneous insulin injections. |
| 706 | 9439928 | Anomalies of lipoprotein pattern and fibrinolysis in acromegalic patients: relation to growth hormone levels and insulin-like growth factor I. |
| 707 | 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. |
| 708 | 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). |
| 709 | 9450113 | Turnover of pro- and mature apolipoprotein A-I in diabetic patients and normolipidaemic controls. |
| 710 | 9544725 | In the non-diabetic group apolipoprotein[a] (365 [239-554] versus 184 [17-266] U/l; P < 0.01), total cholesterol (6.3 +/- 0.2 versus 5.6 +/- 0.2 mmol/l; P < 0.05), LDL cholesterol (4.1 +/- 0.2 versus 3.6 +/- 0.2 mmol/l; P < 0.05) and apolipoprotein B (146 +/- 8 versus 117 +/- 5 mg/dl; P < 0.05) were also found to be associated with PVD although these associations were not observed in the group with diabetes. |
| 711 | 9588450 | Effects of insulin and acipimox on VLDL1 and VLDL2 apolipoprotein B production in normal subjects. |
| 712 | 9588450 | The objective of the study was to examine the potential differential effect of insulin and acipimox (both of which reduce free fatty acid [FFA] availability) on VLDL apolipoprotein (apo) B metabolism. |
| 713 | 9589684 | Serum lipid, apolipoprotein concentration, and lipoprotein composition were determined in maternal and umbilical venous cord blood at delivery by elective Cesarean section (CS) in 10 singleton, full-term pregnancies with maternal insulin-dependent diabetes mellitus (type I DM), which predated pregnancy, and in 22 nondiabetic pregnancies. |
| 714 | 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). |
| 715 | 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. |
| 716 | 9649952 | Quantification of apolipoprotein AI-containing lipoprotein particles in non-insulin-dependent diabetes mellitus. |
| 717 | 9649952 | Quantification of LpAI (lipoprotein particles containing apolipoprotein AI not associated with apolipoprotein AII) was performed through an electroimmunoassay on serum from 49 non-insulin-dependent diabetic patients (mean age 60 +/- 9 years) and 53 age-matched control subjects of both sexes not affected by coronary heart disease. |
| 718 | 9649952 | Quantification of apolipoprotein AI-containing lipoprotein particles in non-insulin-dependent diabetes mellitus. |
| 719 | 9649952 | Quantification of LpAI (lipoprotein particles containing apolipoprotein AI not associated with apolipoprotein AII) was performed through an electroimmunoassay on serum from 49 non-insulin-dependent diabetic patients (mean age 60 +/- 9 years) and 53 age-matched control subjects of both sexes not affected by coronary heart disease. |
| 720 | 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. |
| 721 | 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). |
| 722 | 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. |
| 723 | 9699898 | We conclude that atherogenic apolipoprotein abnormalities occur in normoglycaemic relatives of non-insulin dependent diabetic patients. |
| 724 | 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. |
| 725 | 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). |
| 726 | 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. |
| 727 | 9699898 | We conclude that atherogenic apolipoprotein abnormalities occur in normoglycaemic relatives of non-insulin dependent diabetic patients. |
| 728 | 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. |
| 729 | 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). |
| 730 | 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. |
| 731 | 9699898 | We conclude that atherogenic apolipoprotein abnormalities occur in normoglycaemic relatives of non-insulin dependent diabetic patients. |
| 732 | 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. |
| 733 | 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). |
| 734 | 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. |
| 735 | 9699898 | We conclude that atherogenic apolipoprotein abnormalities occur in normoglycaemic relatives of non-insulin dependent diabetic patients. |
| 736 | 9703251 | Apolipoprotein CII, a co-factor of LPL, was not affected by STZ administration. |
| 737 | 9703251 | These results show that hypertriglyceridemia with low HDL cholesterol results from a reduction of LPL activity without affecting apolipoprotein CII after STZ administration. |
| 738 | 9703251 | Apolipoprotein CII, a co-factor of LPL, was not affected by STZ administration. |
| 739 | 9703251 | These results show that hypertriglyceridemia with low HDL cholesterol results from a reduction of LPL activity without affecting apolipoprotein CII after STZ administration. |
| 740 | 9768372 | Acarbose inhibited the postprandial decline of apolipoprotein C-II, and decreased the postprandial serum apolipoprotein C-III level. |
| 741 | 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). |
| 742 | 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). |
| 743 | 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. |
| 744 | 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). |
| 745 | 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). |
| 746 | 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. |
| 747 | 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). |
| 748 | 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). |
| 749 | 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. |
| 750 | 9836526 | In vivo evidence for increased apolipoprotein A-I catabolism in subjects with impaired glucose tolerance. |
| 751 | 9868130 | [Relationship between urinary albumin excretion and blood vessel lesion in non-insulin-dependent diabetics]. |
| 752 | 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. |
| 753 | 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. |
| 754 | 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. |
| 755 | 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. |
| 756 | 9932215 | Apolipoprotein CIII (ApoCIII) appears to play a key role in triglyceride-rich lipoprotein (TRL) metabolism. |
| 757 | 9932215 | Overexpression of the human ApoCIII gene in transgenic animals results in hypertriglyceridaemia, which can be corrected by overexpression of the ApoE gene. |
| 758 | 9932215 | ApoCIII decreases TRL catabolism by inhibiting lipoprotein lipase activity and reducing ApoE-dependent hepatic uptake of TRL and remnants. |
| 759 | 9932215 | There appears to be an interaction between ApoCIII and ApoE at the surface of the lipoprotein. |
| 760 | 9932215 | Our recent study of ApoCIII levels in TRL and intermediate-density lipoprotein isolated from hyperlipidaemic Type III and IV individuals confirmed the importance of the ApoCIII/ApoE ratio in these lipoproteins. |
| 761 | 9933608 | The studies reveal a specific HDL particle catabolic pathway that is down-regulated in ob/ob mice and suggest that HDL apolipoprotein turnover may be regulated by obesity and/or leptin signaling. |
| 762 | 10027576 | Insulin suppresses apolipoprotein(a) synthesis by primary cultures of cynomolgus monkey hepatocytes. |
| 763 | 10027576 | To investigate the biochemical background of these changes, we studied the effect of insulin on apolipoprotein(a) (apo(a)) synthesis and mRNA levels in primary cultures of cynomolgus monkey hepatocytes. |
| 764 | 10027576 | Low concentrations of insulin (10 nmol/l) had a small but significant decreasing effect (p < 0.046) on apolipoprotein(a) secretion (-16%). |
| 765 | 10027576 | Apolipoprotein B-100 secretion was 30%-36% decreased when using 10-1000 nmol/l and no change was observed for the secretion of apolipoprotein A-1 and albumin which were measured as control proteins. |
| 766 | 10027576 | Steady state apolipoprotein(a) mRNA concentrations paralleled the decrease in apolipoprotein(a) synthesis (-29% after incubating the cells for 48 h with 100 nmol/l insulin) indicating that the decreased synthesis is regulated at the (post)-transcriptional level. |
| 767 | 10027576 | Concentrations of apolipoprotein B-100 and apolipoprotein A-1 mRNA were not changed after incubation with insulin. |
| 768 | 10027576 | We conclude that high concentrations of insulin suppress apolipoprotein(a) synthesis in monkey hepatocytes at the (post)-transcriptional level. |
| 769 | 10027576 | Insulin suppresses apolipoprotein(a) synthesis by primary cultures of cynomolgus monkey hepatocytes. |
| 770 | 10027576 | To investigate the biochemical background of these changes, we studied the effect of insulin on apolipoprotein(a) (apo(a)) synthesis and mRNA levels in primary cultures of cynomolgus monkey hepatocytes. |
| 771 | 10027576 | Low concentrations of insulin (10 nmol/l) had a small but significant decreasing effect (p < 0.046) on apolipoprotein(a) secretion (-16%). |
| 772 | 10027576 | Apolipoprotein B-100 secretion was 30%-36% decreased when using 10-1000 nmol/l and no change was observed for the secretion of apolipoprotein A-1 and albumin which were measured as control proteins. |
| 773 | 10027576 | Steady state apolipoprotein(a) mRNA concentrations paralleled the decrease in apolipoprotein(a) synthesis (-29% after incubating the cells for 48 h with 100 nmol/l insulin) indicating that the decreased synthesis is regulated at the (post)-transcriptional level. |
| 774 | 10027576 | Concentrations of apolipoprotein B-100 and apolipoprotein A-1 mRNA were not changed after incubation with insulin. |
| 775 | 10027576 | We conclude that high concentrations of insulin suppress apolipoprotein(a) synthesis in monkey hepatocytes at the (post)-transcriptional level. |
| 776 | 10027576 | Insulin suppresses apolipoprotein(a) synthesis by primary cultures of cynomolgus monkey hepatocytes. |
| 777 | 10027576 | To investigate the biochemical background of these changes, we studied the effect of insulin on apolipoprotein(a) (apo(a)) synthesis and mRNA levels in primary cultures of cynomolgus monkey hepatocytes. |
| 778 | 10027576 | Low concentrations of insulin (10 nmol/l) had a small but significant decreasing effect (p < 0.046) on apolipoprotein(a) secretion (-16%). |
| 779 | 10027576 | Apolipoprotein B-100 secretion was 30%-36% decreased when using 10-1000 nmol/l and no change was observed for the secretion of apolipoprotein A-1 and albumin which were measured as control proteins. |
| 780 | 10027576 | Steady state apolipoprotein(a) mRNA concentrations paralleled the decrease in apolipoprotein(a) synthesis (-29% after incubating the cells for 48 h with 100 nmol/l insulin) indicating that the decreased synthesis is regulated at the (post)-transcriptional level. |
| 781 | 10027576 | Concentrations of apolipoprotein B-100 and apolipoprotein A-1 mRNA were not changed after incubation with insulin. |
| 782 | 10027576 | We conclude that high concentrations of insulin suppress apolipoprotein(a) synthesis in monkey hepatocytes at the (post)-transcriptional level. |
| 783 | 10027576 | Insulin suppresses apolipoprotein(a) synthesis by primary cultures of cynomolgus monkey hepatocytes. |
| 784 | 10027576 | To investigate the biochemical background of these changes, we studied the effect of insulin on apolipoprotein(a) (apo(a)) synthesis and mRNA levels in primary cultures of cynomolgus monkey hepatocytes. |
| 785 | 10027576 | Low concentrations of insulin (10 nmol/l) had a small but significant decreasing effect (p < 0.046) on apolipoprotein(a) secretion (-16%). |
| 786 | 10027576 | Apolipoprotein B-100 secretion was 30%-36% decreased when using 10-1000 nmol/l and no change was observed for the secretion of apolipoprotein A-1 and albumin which were measured as control proteins. |
| 787 | 10027576 | Steady state apolipoprotein(a) mRNA concentrations paralleled the decrease in apolipoprotein(a) synthesis (-29% after incubating the cells for 48 h with 100 nmol/l insulin) indicating that the decreased synthesis is regulated at the (post)-transcriptional level. |
| 788 | 10027576 | Concentrations of apolipoprotein B-100 and apolipoprotein A-1 mRNA were not changed after incubation with insulin. |
| 789 | 10027576 | We conclude that high concentrations of insulin suppress apolipoprotein(a) synthesis in monkey hepatocytes at the (post)-transcriptional level. |
| 790 | 10027576 | Insulin suppresses apolipoprotein(a) synthesis by primary cultures of cynomolgus monkey hepatocytes. |
| 791 | 10027576 | To investigate the biochemical background of these changes, we studied the effect of insulin on apolipoprotein(a) (apo(a)) synthesis and mRNA levels in primary cultures of cynomolgus monkey hepatocytes. |
| 792 | 10027576 | Low concentrations of insulin (10 nmol/l) had a small but significant decreasing effect (p < 0.046) on apolipoprotein(a) secretion (-16%). |
| 793 | 10027576 | Apolipoprotein B-100 secretion was 30%-36% decreased when using 10-1000 nmol/l and no change was observed for the secretion of apolipoprotein A-1 and albumin which were measured as control proteins. |
| 794 | 10027576 | Steady state apolipoprotein(a) mRNA concentrations paralleled the decrease in apolipoprotein(a) synthesis (-29% after incubating the cells for 48 h with 100 nmol/l insulin) indicating that the decreased synthesis is regulated at the (post)-transcriptional level. |
| 795 | 10027576 | Concentrations of apolipoprotein B-100 and apolipoprotein A-1 mRNA were not changed after incubation with insulin. |
| 796 | 10027576 | We conclude that high concentrations of insulin suppress apolipoprotein(a) synthesis in monkey hepatocytes at the (post)-transcriptional level. |
| 797 | 10027576 | Insulin suppresses apolipoprotein(a) synthesis by primary cultures of cynomolgus monkey hepatocytes. |
| 798 | 10027576 | To investigate the biochemical background of these changes, we studied the effect of insulin on apolipoprotein(a) (apo(a)) synthesis and mRNA levels in primary cultures of cynomolgus monkey hepatocytes. |
| 799 | 10027576 | Low concentrations of insulin (10 nmol/l) had a small but significant decreasing effect (p < 0.046) on apolipoprotein(a) secretion (-16%). |
| 800 | 10027576 | Apolipoprotein B-100 secretion was 30%-36% decreased when using 10-1000 nmol/l and no change was observed for the secretion of apolipoprotein A-1 and albumin which were measured as control proteins. |
| 801 | 10027576 | Steady state apolipoprotein(a) mRNA concentrations paralleled the decrease in apolipoprotein(a) synthesis (-29% after incubating the cells for 48 h with 100 nmol/l insulin) indicating that the decreased synthesis is regulated at the (post)-transcriptional level. |
| 802 | 10027576 | Concentrations of apolipoprotein B-100 and apolipoprotein A-1 mRNA were not changed after incubation with insulin. |
| 803 | 10027576 | We conclude that high concentrations of insulin suppress apolipoprotein(a) synthesis in monkey hepatocytes at the (post)-transcriptional level. |
| 804 | 10027576 | Insulin suppresses apolipoprotein(a) synthesis by primary cultures of cynomolgus monkey hepatocytes. |
| 805 | 10027576 | To investigate the biochemical background of these changes, we studied the effect of insulin on apolipoprotein(a) (apo(a)) synthesis and mRNA levels in primary cultures of cynomolgus monkey hepatocytes. |
| 806 | 10027576 | Low concentrations of insulin (10 nmol/l) had a small but significant decreasing effect (p < 0.046) on apolipoprotein(a) secretion (-16%). |
| 807 | 10027576 | Apolipoprotein B-100 secretion was 30%-36% decreased when using 10-1000 nmol/l and no change was observed for the secretion of apolipoprotein A-1 and albumin which were measured as control proteins. |
| 808 | 10027576 | Steady state apolipoprotein(a) mRNA concentrations paralleled the decrease in apolipoprotein(a) synthesis (-29% after incubating the cells for 48 h with 100 nmol/l insulin) indicating that the decreased synthesis is regulated at the (post)-transcriptional level. |
| 809 | 10027576 | Concentrations of apolipoprotein B-100 and apolipoprotein A-1 mRNA were not changed after incubation with insulin. |
| 810 | 10027576 | We conclude that high concentrations of insulin suppress apolipoprotein(a) synthesis in monkey hepatocytes at the (post)-transcriptional level. |
| 811 | 10198561 | [Gender differences and diabetic status in the relationship of blood apolipoprotein C-III, free fatty acids and triglycerides in subjects at risk for glucose intolerance]. |
| 812 | 10198561 | Conversely, apolipoprotein C-III (apoC-III) is an inhibitor of the catabolism of TG-rich lipoproteins. |
| 813 | 10198561 | [Gender differences and diabetic status in the relationship of blood apolipoprotein C-III, free fatty acids and triglycerides in subjects at risk for glucose intolerance]. |
| 814 | 10198561 | Conversely, apolipoprotein C-III (apoC-III) is an inhibitor of the catabolism of TG-rich lipoproteins. |
| 815 | 10376388 | The author presents a review on candidate genes of proteins involved in the metabolism of glucose, lipids and other metabolites (glucose carriers, insulin receptors, proinsulin, glucokinase, amyline, glycogen synthase). |
| 816 | 10376388 | In the metabolic dyshomeostasis of multiple metabolic syndrome participate in the process of atherogenesis also: isoforms of apolipoprotein E4, isoforms of apolipoprotein A-IV-1/1, hyperuricaemia, raised levels of the plasminogen activator inhibitor 1 (PAI-1), hyperfibrinogenaemia, hyperhomocysteinaemia and other metabolites (cytokines, endothelin etc.). |
| 817 | 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. |
| 818 | 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. |
| 819 | 10393218 | The gene for apolipoprotein apoB lies within the region, but apoB levels were similar in strains B6 and BKS. |
| 820 | 10393218 | We conclude that susceptibilities to diabetes and atherosclerosis are not conferred by the same genes in these strains and that a major gene on Chr 12, which we name Ath6, determines the difference in atherosclerosis susceptibility. |
| 821 | 10426383 | Plasma phospholipid transfer protein activity is lowered by 24-h insulin and acipimox administration: blunted response to insulin in type 2 diabetic patients. |
| 822 | 10426383 | We examined the effects of 24-h hyperinsulinemia (30 mU x kg(-1) x h(-1)) and 24-h Acipimox (250 mg/4 h) on plasma lipids as well as CETP and PLTP activities (measured with exogenous substrate assays) in eight healthy and eight type 2 diabetic subjects. |
| 823 | 10426383 | After 24 h of insulin, plasma free fatty acids (FFAs), HDL cholesterol, and plasma apolipoprotein AI decreased in healthy subjects and type 2 diabetic patients (P < 0.05). |
| 824 | 10426383 | Insulin decreased plasma PLTP activity by 17.6% after 24 h in healthy subjects (P < 0.05) and 10.2% in diabetic patients (P < 0.05 vs. baseline; P < 0.05 vs. healthy subjects). |
| 825 | 10426383 | Plasma CETP activity decreased by 9.5% after 24 h of insulin in healthy subjects (P < 0.05), but not in diabetic patients. |
| 826 | 10426383 | In healthy subjects, the PLTP responses with insulin and Acipimox were larger than the changes in CETP activity (P < 0.05). |
| 827 | 10426383 | These findings suggest that there is a metabolic link between the regulation of plasma FFA and PLTP, but not CETP. |
| 828 | 10426383 | The PLTP response to insulin is blunted in type 2 diabetes. |
| 829 | 10479666 | In addition, HDL(2) from diabetics did not protect against apolipoprotein B-100 fragmentation in LDL. |
| 830 | 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. |
| 831 | 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. |
| 832 | 10522403 | Similarity between apolipoprotein(a) and plasminogen structure suggests, that Lp(a) can be the bridge connecting the lipid metabolism and the coagulation system. |
| 833 | 10522991 | To determine whether cholesterol esterification rate (CER) and transfer of cholesteryl esters from high density lipoproteins to apolipoprotein B-containing lipoproteins are affected by menopause and HRT, plasma newly synthesized cholesteryl ester transfer (NCET) activity, CER and plasma lipids, lipoproteins, and apolipoprotein concentrations were measured in perimenopausal women (age range: 40-55 yr), including 49 premenopausal women and 32 postmenopausal women who were subsequently randomized to receive either placebo or 17-beta estradiol/norethisterone for 6 months. |
| 834 | 10559020 | Furthermore, diastolic blood pressure, total cholesterol, high density lipoprotein cholesterol, triglycerides, apolipoprotein A(1), fasting glucose, fasting insulin, waist-to-hip ratio, and body mass index were not associated with CHD risk. |
| 835 | 10565450 | Decreased activity of plasma cholesteryl ester transfer protein in children and adolescents with insulin-dependent diabetes mellitus. |
| 836 | 10565450 | The aims of the present study were to determine whether the activity of cholesteryl ester transfer protein (CETP) is altered in the plasma of children and adolescents with insulin-dependent diabetes mellitus (IDDM), and whether high-density lipoprotein-cholesterol (HDL-C) levels reflect CETP activity. |
| 837 | 10565450 | Serum triglycerides were significantly decreased, while the levels of HDL-C and apolipoprotein (apo) A1 were markedly increased, in the IDDM patients. |
| 838 | 10565450 | Plasma CETP activity was significantly lower in the IDDM patients than in the control children. |
| 839 | 10565450 | None of the anthropometric indices nor the biochemical data correlated significantly with CETP activity in the IDDM patients. |
| 840 | 10565450 | Suppression of CETP along with the putative activation of lipoprotein lipase due to peripheral hyperinsulinism appears to induce synergistically the increase in HDL-C in IDDM children. |
| 841 | 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. |
| 842 | 10591679 | There was little change in apolipoprotein A-I distribution. |
| 843 | 10612483 | We investigated in a pilot study the effect of testosterone suppression on lipoprotein metabolism, insulin, and leptin in 10 men who were treated either with cetrorelix, an antagonist of gonadotropin releasing hormone, or with placebo (P). |
| 844 | 10612483 | Compared to baseline, treatment with cetrorelix increased serum levels of apolipoprotein (apo) A-I, HDL subclass LpA-I, insulin, and leptin. |
| 845 | 10612483 | Compared to baseline and group P + P, treatment with cetrorelix in groups C + C and C + P did not lead to considerable or consistent changes in the plasma activities of lecithin:cholesterol acyltransferase (LCAT), phospholipid transfer protein (PLTP), cholesteryl ester transfer protein (CETP), lipoprotein lipase, and hepatic lipase (HL). |
| 846 | 10612483 | In conclusion, the small or absent effects of cetrorelix on LCAT, CETP, PLTP, LPL, and HL indicate that testosterone regulates HDL levels by other metabolic pathways. |
| 847 | 10612483 | The increases of insulin and leptin in response to cetrorelix suggest that testosterone influences HDL metabolism also via obesity and insulin resistance. |
| 848 | 10665339 | Lp(a) has the distinctive feature of containing apolipoprotein (a), which is a glycoprotein linked to apo B100, and has a similarity to plasminogen; it is also structurally related to LDL. |
| 849 | 10704613 | Albumin inhibits apolipoprotein AI and AII production in human hepatoblastoma cell line (Hep G2): additive effects of oleate-albumin complex. |
| 850 | 10704613 | Specifically, the hepatocellular mechanisms of the effect of albumin and fatty acids on apolipoprotein (apo) AI and AII [major proteins of high density lipoproteins (HDL)] synthesis and secretion are not known. |
| 851 | 10704613 | Albumin inhibits apolipoprotein AI and AII production in human hepatoblastoma cell line (Hep G2): additive effects of oleate-albumin complex. |
| 852 | 10704613 | Specifically, the hepatocellular mechanisms of the effect of albumin and fatty acids on apolipoprotein (apo) AI and AII [major proteins of high density lipoproteins (HDL)] synthesis and secretion are not known. |
| 853 | 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. |
| 854 | 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. |
| 855 | 10781652 | Replacement therapy with female sex hormones lowered Lp(a), HDL cholesterol and apolipoprotein A-I. |
| 856 | 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. |
| 857 | 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. |
| 858 | 10781652 | Replacement therapy with female sex hormones lowered Lp(a), HDL cholesterol and apolipoprotein A-I. |
| 859 | 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. |
| 860 | 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. |
| 861 | 10781652 | Replacement therapy with female sex hormones lowered Lp(a), HDL cholesterol and apolipoprotein A-I. |
| 862 | 10782563 | The significant reduction of baseline total cholesterol (58%), total triglycerides (80%), LDL-cholesterol (48%), apoprotein B (50%) and apolipoprotein (a) (61%) may be considered as a good response to the treatment. |
| 863 | 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. |
| 864 | 10855558 | The insulin resistance index showed significant positive correlation with the EC/FC ratio levels in Apo AI and in Apo B100, and showed significant negative correlation with the CH levels in Apo AI/apolipoprotein AI ratio and the CH levels in Apo B100/apolipoprotein B100 ratio levels in group C. |
| 865 | 10902867 | Glycated apolipoprotein A-I assay by combination of affinity chromatography and latex immunoagglutination. |
| 866 | 10902867 | The degree of glycation of plasma apolipoprotein A-I was measured by a combination of gel filtration, boronate affinity chromatography and latex immunoagglutination. |
| 867 | 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). |
| 868 | 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. |
| 869 | 10902867 | Labile glycated apolipoprotein A-I did not interfere with the measurement of glycated apolipoprotein A-I. |
| 870 | 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. |
| 871 | 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). |
| 872 | 10902867 | The method is simple, rapid and highly sensitive for determination of the glycation level of plasma apolipoprotein A-I. |
| 873 | 10902867 | Glycated apolipoprotein A-I assay by combination of affinity chromatography and latex immunoagglutination. |
| 874 | 10902867 | The degree of glycation of plasma apolipoprotein A-I was measured by a combination of gel filtration, boronate affinity chromatography and latex immunoagglutination. |
| 875 | 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). |
| 876 | 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. |
| 877 | 10902867 | Labile glycated apolipoprotein A-I did not interfere with the measurement of glycated apolipoprotein A-I. |
| 878 | 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. |
| 879 | 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). |
| 880 | 10902867 | The method is simple, rapid and highly sensitive for determination of the glycation level of plasma apolipoprotein A-I. |
| 881 | 10902867 | Glycated apolipoprotein A-I assay by combination of affinity chromatography and latex immunoagglutination. |
| 882 | 10902867 | The degree of glycation of plasma apolipoprotein A-I was measured by a combination of gel filtration, boronate affinity chromatography and latex immunoagglutination. |
| 883 | 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). |
| 884 | 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. |
| 885 | 10902867 | Labile glycated apolipoprotein A-I did not interfere with the measurement of glycated apolipoprotein A-I. |
| 886 | 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. |
| 887 | 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). |
| 888 | 10902867 | The method is simple, rapid and highly sensitive for determination of the glycation level of plasma apolipoprotein A-I. |
| 889 | 10902867 | Glycated apolipoprotein A-I assay by combination of affinity chromatography and latex immunoagglutination. |
| 890 | 10902867 | The degree of glycation of plasma apolipoprotein A-I was measured by a combination of gel filtration, boronate affinity chromatography and latex immunoagglutination. |
| 891 | 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). |
| 892 | 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. |
| 893 | 10902867 | Labile glycated apolipoprotein A-I did not interfere with the measurement of glycated apolipoprotein A-I. |
| 894 | 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. |
| 895 | 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). |
| 896 | 10902867 | The method is simple, rapid and highly sensitive for determination of the glycation level of plasma apolipoprotein A-I. |
| 897 | 10902867 | Glycated apolipoprotein A-I assay by combination of affinity chromatography and latex immunoagglutination. |
| 898 | 10902867 | The degree of glycation of plasma apolipoprotein A-I was measured by a combination of gel filtration, boronate affinity chromatography and latex immunoagglutination. |
| 899 | 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). |
| 900 | 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. |
| 901 | 10902867 | Labile glycated apolipoprotein A-I did not interfere with the measurement of glycated apolipoprotein A-I. |
| 902 | 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. |
| 903 | 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). |
| 904 | 10902867 | The method is simple, rapid and highly sensitive for determination of the glycation level of plasma apolipoprotein A-I. |
| 905 | 10902867 | Glycated apolipoprotein A-I assay by combination of affinity chromatography and latex immunoagglutination. |
| 906 | 10902867 | The degree of glycation of plasma apolipoprotein A-I was measured by a combination of gel filtration, boronate affinity chromatography and latex immunoagglutination. |
| 907 | 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). |
| 908 | 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. |
| 909 | 10902867 | Labile glycated apolipoprotein A-I did not interfere with the measurement of glycated apolipoprotein A-I. |
| 910 | 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. |
| 911 | 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). |
| 912 | 10902867 | The method is simple, rapid and highly sensitive for determination of the glycation level of plasma apolipoprotein A-I. |
| 913 | 10902867 | Glycated apolipoprotein A-I assay by combination of affinity chromatography and latex immunoagglutination. |
| 914 | 10902867 | The degree of glycation of plasma apolipoprotein A-I was measured by a combination of gel filtration, boronate affinity chromatography and latex immunoagglutination. |
| 915 | 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). |
| 916 | 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. |
| 917 | 10902867 | Labile glycated apolipoprotein A-I did not interfere with the measurement of glycated apolipoprotein A-I. |
| 918 | 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. |
| 919 | 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). |
| 920 | 10902867 | The method is simple, rapid and highly sensitive for determination of the glycation level of plasma apolipoprotein A-I. |
| 921 | 10902867 | Glycated apolipoprotein A-I assay by combination of affinity chromatography and latex immunoagglutination. |
| 922 | 10902867 | The degree of glycation of plasma apolipoprotein A-I was measured by a combination of gel filtration, boronate affinity chromatography and latex immunoagglutination. |
| 923 | 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). |
| 924 | 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. |
| 925 | 10902867 | Labile glycated apolipoprotein A-I did not interfere with the measurement of glycated apolipoprotein A-I. |
| 926 | 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. |
| 927 | 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). |
| 928 | 10902867 | The method is simple, rapid and highly sensitive for determination of the glycation level of plasma apolipoprotein A-I. |
| 929 | 10903851 | We have previously demonstrated that transthyretin amyloid fibrils contain four constituent protofilaments packed in a square array. |
| 930 | 10903851 | Here, we have used cross-correlation techniques to average electron microscopy images of multiple cross-sections in order to reconstruct the sub-structure of ex vivo amyloid fibrils composed of amyloid A protein, monoclonal immunoglobulin lambda light chain, Leu60Arg variant apolipoprotein AI, and Asp67His variant lysozyme, as well as synthetic fibrils derived from a ten-residue peptide corresponding to the A-strand of transthyretin. |
| 931 | 10905494 | Genotype/phenotype relationships in HNF-4alpha/MODY1: haploinsufficiency is associated with reduced apolipoprotein (AII), apolipoprotein (CIII), lipoprotein(a), and triglyceride levels. |
| 932 | 10905494 | Heterozygous mutations in the HNF-4alpha gene are responsible for maturity-onset diabetes of the young 1 (MODY1), which is characterized by pancreatic beta-cell-deficient insulin secretion. |
| 933 | 10905494 | In this study, we have identified HNF-4alpha target genes that are mainly expressed in the liver, including alpha1-antitrypsin, alpha1-antichymotrypsin, alpha-fetal protein, ceruloplasmin, IGF binding protein 1, transferrin, apolipoprotein(AI) [apo(AI)], apo(AII), apo(B), and apo(CIII). |
| 934 | 10905494 | Genotype/phenotype relationships in HNF-4alpha/MODY1: haploinsufficiency is associated with reduced apolipoprotein (AII), apolipoprotein (CIII), lipoprotein(a), and triglyceride levels. |
| 935 | 10905494 | Heterozygous mutations in the HNF-4alpha gene are responsible for maturity-onset diabetes of the young 1 (MODY1), which is characterized by pancreatic beta-cell-deficient insulin secretion. |
| 936 | 10905494 | In this study, we have identified HNF-4alpha target genes that are mainly expressed in the liver, including alpha1-antitrypsin, alpha1-antichymotrypsin, alpha-fetal protein, ceruloplasmin, IGF binding protein 1, transferrin, apolipoprotein(AI) [apo(AI)], apo(AII), apo(B), and apo(CIII). |
| 937 | 10924714 | Effects of age, gender, and lifestyle factors on plasma apolipoprotein A-IV concentrations. |
| 938 | 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). |
| 939 | 10952226 | The purpose of this study was to investigate whether the remnant-like particle cholesterol (RLP-C) is an independent risk factor for coronary artery disease (CAD) and non-insulin dependent diabetes mellitus (NIDDM) in the Korean population and to explore the relationship between RLP-C and other biochemical markers as well as the apolipoprotein (apo) E genotypes. |
| 940 | 10978257 | Human paraoxonase (PON1) is a calcium-dependent esterase closely associated with high density lipoprotein (HDL)-containing apolipoprotein AI (apoAI), which has been shown to confer antioxidant properties to HDL. |
| 941 | 10978257 | We have undertaken a study of the effect of the lipid-lowering drug simvastatin on serum PON1 activity (in relation to paraoxon and arylesterase activity), on apoAI-containing and apolipoprotein B (apoB)-containing lipoproteins, and on lipid peroxide concentrations in 64 (39 women and 25 men) unrelated FH patients. |
| 942 | 10996359 | Inefficiency of insulin therapy to correct apolipoprotein A-I metabolic abnormalities in non-insulin-dependent diabetes mellitus. |
| 943 | 11092505 | Lipoprotein and apolipoprotein changes were evaluated in 10-week-old Zucker diabetic fatty (ZDF) male rats following 12 weeks of insulin treatment, which normalized blood glucose and maintained weight gaining characteristic of nondiabetic Zucker fatty rats. |
| 944 | 11092505 | Insulin treatment depressed apolipoprotein (apo) A-I levels in HDL, but had little effect on total apo E, apo A-IV, or apo C, although apo C was redistributed to the VLDL fraction. |
| 945 | 11092505 | Lipoprotein and apolipoprotein changes were evaluated in 10-week-old Zucker diabetic fatty (ZDF) male rats following 12 weeks of insulin treatment, which normalized blood glucose and maintained weight gaining characteristic of nondiabetic Zucker fatty rats. |
| 946 | 11092505 | Insulin treatment depressed apolipoprotein (apo) A-I levels in HDL, but had little effect on total apo E, apo A-IV, or apo C, although apo C was redistributed to the VLDL fraction. |
| 947 | 11092511 | Effect of weight reduction on the distribution of apolipoprotein A-I in high-density lipoprotein subfractions in obese non-insulin-dependent diabetic subjects. |
| 948 | 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. |
| 949 | 11092511 | Effect of weight reduction on the distribution of apolipoprotein A-I in high-density lipoprotein subfractions in obese non-insulin-dependent diabetic subjects. |
| 950 | 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. |
| 951 | 11096142 | Lack of relationship in long-term type 1 diabetic patients between diabetic nephropathy and polymorphisms in apolipoprotein epsilon, lipoprotein lipase and cholesteryl ester transfer protein. |
| 952 | 11123853 | PPAR alpha activated by fibric acids form heterodimers with the 9-cis retinoic acid receptor (RXR). |
| 953 | 11123853 | Furthermore, they decrease triglycerides by increasing lipoprotein lipase gene expression and by decreasing apolipoprotein C-III gene expression. |
| 954 | 11123853 | Fibric acids increase high-density lipoprotein (HDL) cholesterol partly by increasing apolipoprotein A-I and apolipoprotein A-II gene expression. |
| 955 | 11123853 | PPAR alpha activated by fibric acids form heterodimers with the 9-cis retinoic acid receptor (RXR). |
| 956 | 11123853 | Furthermore, they decrease triglycerides by increasing lipoprotein lipase gene expression and by decreasing apolipoprotein C-III gene expression. |
| 957 | 11123853 | Fibric acids increase high-density lipoprotein (HDL) cholesterol partly by increasing apolipoprotein A-I and apolipoprotein A-II gene expression. |
| 958 | 11128033 | This included genes for phosphoenolpyruvate carboxykinase, beta-oxidation enzymes, lipoprotein lipase, apolipoprotein AI and uncoupling proteins. |
| 959 | 11128745 | Serum lipid, apolipoprotein, and lipoprotein lipid concentrations were investigated in mothers with poorly controlled or well-controlled type 1 diabetes as reflected by hemoglobin A1c(HbA1c) concentrations performed by isolab column chromatography and in their macrosomic (body wt = 4650 +/- 90 g) or appropriate-for-gestational-age newborns (body wt = 3616 +/- 68 g), and these levels were compared with those in healthy mothers and in their control newborns (body wt = 3290 +/- 45 g). |
| 960 | 11215482 | Previously, we developed an immunoturbidimetric assay method for lipoprotein A-I(LpA-I) on sera pre-absorbed with anti-apolipoprotein A-II. |
| 961 | 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. |
| 962 | 11215482 | Previously, we developed an immunoturbidimetric assay method for lipoprotein A-I(LpA-I) on sera pre-absorbed with anti-apolipoprotein A-II. |
| 963 | 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. |
| 964 | 11246886 | Studies with apolipoprotein A-II transgenic mice indicate a role for HDLs in adiposity and insulin resistance. |
| 965 | 11246886 | Apolipoprotein A-II (apoA-II) is the second most abundant protein in HDLs. |
| 966 | 11246886 | Studies with apolipoprotein A-II transgenic mice indicate a role for HDLs in adiposity and insulin resistance. |
| 967 | 11246886 | Apolipoprotein A-II (apoA-II) is the second most abundant protein in HDLs. |
| 968 | 11272161 | We found a strong positive correlation during the 6-h postprandial period between apolipoprotein (apo) B-48 plasma concentration and insulin plasma concentration (r2 = 0.70; P = 0.0001). |
| 969 | 11272161 | A biphasic response was observed with markedly reduced levels of plasma apoB-48 during insulin infusion, followed by a late accumulation of plasma apoB-48 and triglycerides. |
| 970 | 11272161 | Overall, the data obtained showed that portal and peripheral hyperinsulinism delays and exacerbates postprandial accumulation of intestinally derived chylomicrons in plasma and thus is involved in the regulation of apoB-48-triglyceride-rich lipoprotein metabolism, in the absence of insulin-resistance syndrome. |
| 971 | 11290824 | They formed complexes with lipoproteins in culture medium, notably binding to apolipoprotein A-I-containing particles. |
| 972 | 11344192 | In vivo evidence for the role of lipoprotein lipase activity in the regulation of apolipoprotein AI metabolism: a kinetic study in control subjects and patients with type II diabetes mellitus. |
| 973 | 11423471 | Mutations in the HNF4alpha gene are responsible for type 1 maturity-onset diabetes of the young (MODY1), which is characterized by a defect in insulin secretion. |
| 974 | 11423471 | Recent evidence has implicated AMP-activated protein kinase (AMPK) in the modulation of both insulin secretion by pancreatic beta-cells and the control of glucose-dependent gene expression in both hepatocytes and beta-cells. |
| 975 | 11423471 | Therefore, the question could be raised as to whether AMPK plays a role in these processes by modulating HNF-4alpha function. |
| 976 | 11423471 | In this study, we show that activation of AMPK by 5-amino-4-imidazolecarboxamide riboside (AICAR) in hepatocytes greatly diminished HNF-4alpha protein levels and consequently downregulates the expression of HNF-4alpha target genes. |
| 977 | 11423471 | Quantitative evaluation of HNF-4alpha target gene expression revealed diminished mRNA levels for HNF-1alpha, GLUT2, L-type pyruvate kinase, aldolase B, apolipoprotein (apo)-B, and apoCIII. |
| 978 | 11423471 | Our data clearly demonstrate that the MODY1/HNF-4alpha transcription factor is a novel target of AMPK in hepatocytes. |
| 979 | 11423471 | Accordingly, it can be suggested that in pancreatic beta-cells, AMPK also acts by decreasing HNF-4alpha protein level, and therefore insulin secretion. |
| 980 | 11426588 | The effect of bezafibrate (group A) or pravastatin (group B) on the cholesterol (CH) content of apolipoprotein AI, B100 containing particles or remnant-like particles (RLP) or urinary albumin excretion was studied over 4 years. |
| 981 | 11427203 | Baseline HDL cholesterol and phospholipids, pre beta-HDL in incubated plasma, plasma apolipoprotein (apo) AI, PLTP activity and cholesterol efflux to plasma were not different between the groups. |
| 982 | 11427203 | In both groups, HDL lipids, as well as plasma apo AI and PLTP activity decreased after 24 h of insulin (P<0.05 to P<0.01) compared to baseline and recovery, i.e. 1 week after insulin. |
| 983 | 11427207 | Lipoprotein composition was also altered, displaying impaired lipid and apolipoprotein moiety distribution in IDL, LDL, HDL(2) and HDL(3) lipoprotein fractions of Groups B and C. |
| 984 | 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.). |
| 985 | 11463575 | Serum apolipoprotein A(1) (apoA(1)) concentration is inversely correlated with the risk of premature atherosclerosis. |
| 986 | 11463575 | Serum apoA(1) concentrations are regulated, in part, at the transcriptional level. |
| 987 | 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. |
| 988 | 11463575 | Previously, we demonstrated that extracellular acidosis suppresses apoA(1) mRNA levels at the level of transcription. |
| 989 | 11463575 | Here we demonstrate that intracellular acidosis, in the absence of extracellular pH changes, represses apoA(1) promoter activity. |
| 990 | 11463575 | Repression occurs through a pH responsive element (pH-RE) located within the apoA(1) gene promoter. |
| 991 | 11463575 | Acidosis increases the specific DNA binding activity of a putative repressor protein within the immediate 5'-flanking region of the apoA(1) gene. |
| 992 | 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. |
| 993 | 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. |
| 994 | 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. |
| 995 | 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. |
| 996 | 11473048 | Phospholipid transfer protein (PLTP) plays an important role in human plasma HDL metabolism. |
| 997 | 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. |
| 998 | 11474486 | Fibrates bind to the peroxisome proliferator-activated receptor (PPAR)-alpha, and thiazolidinediones are ligands of PPAR-gamma. |
| 999 | 11474486 | To elucidate the target genes regulated by these compounds, we treated Zucker diabetic fatty rats (ZDF) for 15 days with a PPAR-alpha-specific compound, fenofibrate, a PPAR-gamma-specific ligand, rosiglitazone, and a PPAR-alpha/-gamma coagonist, GW2331, and measured the levels of several messenger RNAs (mRNAs) in liver by real-time polymerase chain reaction. |
| 1000 | 11474486 | Fenofibrate and GW2331 induced expression of acyl-coenzyme A (CoA) oxidase and enoyl-CoA hydratase and reduced apolipoprotein C-III and phosphoenolpyruvate carboxykinase mRNAs. |
| 1001 | 11474486 | Rosiglitazone modestly increased apolipoprotein C-III mRNA and had no effect on expression of the other 2 genes in the liver but increased the expression of glucose transporter 4 and phosphoenolpyruvate carboxykinase in adipose tissue. |
| 1002 | 11474486 | We identified a novel target in liver, mitogen-activated phosphokinase phosphatase 1, whose down-regulation by PPAR-alpha agonists may improve insulin sensitivity in that tissue by prolonging insulin responses. |
| 1003 | 11474486 | The results of these studies suggest that activation of PPAR-alpha as well as PPAR-gamma in therapy for type 2 diabetes will enhance glucose and triglyceride control by combining actions in hepatic and peripheral tissues. |
| 1004 | 11474486 | Fibrates bind to the peroxisome proliferator-activated receptor (PPAR)-alpha, and thiazolidinediones are ligands of PPAR-gamma. |
| 1005 | 11474486 | To elucidate the target genes regulated by these compounds, we treated Zucker diabetic fatty rats (ZDF) for 15 days with a PPAR-alpha-specific compound, fenofibrate, a PPAR-gamma-specific ligand, rosiglitazone, and a PPAR-alpha/-gamma coagonist, GW2331, and measured the levels of several messenger RNAs (mRNAs) in liver by real-time polymerase chain reaction. |
| 1006 | 11474486 | Fenofibrate and GW2331 induced expression of acyl-coenzyme A (CoA) oxidase and enoyl-CoA hydratase and reduced apolipoprotein C-III and phosphoenolpyruvate carboxykinase mRNAs. |
| 1007 | 11474486 | Rosiglitazone modestly increased apolipoprotein C-III mRNA and had no effect on expression of the other 2 genes in the liver but increased the expression of glucose transporter 4 and phosphoenolpyruvate carboxykinase in adipose tissue. |
| 1008 | 11474486 | We identified a novel target in liver, mitogen-activated phosphokinase phosphatase 1, whose down-regulation by PPAR-alpha agonists may improve insulin sensitivity in that tissue by prolonging insulin responses. |
| 1009 | 11474486 | The results of these studies suggest that activation of PPAR-alpha as well as PPAR-gamma in therapy for type 2 diabetes will enhance glucose and triglyceride control by combining actions in hepatic and peripheral tissues. |
| 1010 | 11478431 | Plasma glucose and serum insulin levels during oral glucose tolerance test (OGTT), serum lipoprotein(a), apolipoprotein (apo) A-I. apo B. cholesterol and triglycerides in serum and in lipoproteins, and LDL particle diameter were measured in thirty-eight consecutive newly-diagnosed non-diabetic untreated hypertensive men and 38 healthy male controls. |
| 1011 | 11552052 | The ratio of apolipoprotein b to apolipoprotein a-1 was shown to be associated with carotid atheroma. |
| 1012 | 11555832 | Effect of the inflammation, chronic hyperglycemia, or malabsorption on the apolipoprotein A-IV concentration in type 1 diabetes mellitus and in diabetes secondary to chronic pancreatitis. |
| 1013 | 11555832 | Inflammatory proteins (fibrinogen, ceruloplasmin, and haptoglobin) were significantly elevated in the 2 chronic pancreatitis groups. |
| 1014 | 11555832 | The apo A-IV concentration was positively correlated with hemoglobin A(1c) (HbA(1c)) percentage in each group of diabetic patients (CP-DM, r =.35; P =.046; type 1 DM, r =.53; P =.010), in both groups of diabetic patients (r =.472; P <.0001) and negatively correlated with ceruloplasmin concentration in each group of diabetic patients (CP-DM, r = -.48; P =.0052; type 1 DM, r = -.66; P =.003), in both groups of diabetic patients (r = -.561; P <.0001), and in the whole population (r = -.463; P <.0001). |
| 1015 | 11574408 | Among these leptin-regulated genes, apolipoprotein A-IV is a strong candidate for mediating the atherogenic-resistant phenotype of Lep(ob)/Lep(ob) mice. |
| 1016 | 11583309 | The study population consisted of 1,045 postinfarction patients (846 non-diabetic, 125 non-insulin- and 74 insulin-requiring diabetics) with the following blood tests performed 2 months after an index myocardial infarction: lipoprotein (a), apolipoprotein-B, apolipoprotein-A, cholesterol, HDL cholesterol, triglycerides, insulin, von Willebrand factor (vWF), fibrinogen, factor VII, D-dimer, and plasminogen activator inhibitor (PAI-1). |
| 1017 | 11583309 | After adjustment for relevant clinical covariates, non-insulin-requiring diabetes was significantly (p < 0.05) associated with elevated levels of (odd ratios per 1 log unit increase in parenthesis) vWF (1.74) and PAI-1 (1.42) whereas insulin requiring diabetes was associated with even more elevated levels of vWF (4.68), but not with increased levels of PAI-1. |
| 1018 | 11714842 | Our understanding of apolipoprotein A-II (apoA-II) physiology is much more limited than that of apoA-I. |
| 1019 | 11714842 | The increased concentration of apoB-containing lipoproteins present in apoA-II transgenic mice explains, in part, why these animals present increased atherosclerosis susceptibility. |
| 1020 | 11714842 | We suggest that the existence of apoA-II or apoA-I in HDL could be an important signal for specific interaction with HDL receptors such as cubilin or heat shock protein 60. |
| 1021 | 11723061 | Protection from obesity and insulin resistance in mice overexpressing human apolipoprotein C1. |
| 1022 | 11723061 | Using hyperinsulinemic-euglycemic clamp tests, we previously found that in APOC1 transgenic mice, the whole-body insulin-mediated glucose uptake is increased concomitant with a decreased fatty acid uptake. |
| 1023 | 11723061 | We next investigated whether APOC1 overexpression can modulate the initiation and/or development of obesity and insulin resistance. |
| 1024 | 11723061 | When crossbred on the genetically obese ob/ob background, APOC1 transgenic mice were fully protected from the development of obesity compared with ob/ob only mice, as reflected by a strong reduction in body weight (21 +/- 4 vs. 44 +/- 7 g), total adipose tissue stores (15 +/- 3 vs. 25 +/- 3% body wt), and average adipocyte size (7,689 +/- 624 vs. 15,295 +/- 1,289 microm(2)). |
| 1025 | 11723061 | Furthermore, despite elevated plasma free fatty acid and triglyceride levels, APOC1 overexpression significantly improved insulin sensitivity in ob/ob mice, as demonstrated by a strong reduction in plasma glucose and insulin levels, as well as a better performance in the glucose tolerance test. |
| 1026 | 11723061 | In conclusion, a marked reduction in the uptake of fatty acids into adipocytes may underlie the protection from obesity and insulin resistance in transgenic mice overexpressing human APOC1. |
| 1027 | 11768156 | As for lipoprotein analyses, the number of apolipoprotein B100 (ApoB100) particles is not significantly different between the two groups, and the higher content of triglycerides in NASH very low density lipoproteins (VLDL) increases the triglyceride-to-ApoB ratio and the particle size. |
| 1028 | 11768156 | A decreased enzymatic activity of LPL or a defective assembly and secretion of VLDL from hepatocytes due to a moderate reduction in microsomal triglyceride transfer protein could be involved in the overloading of VLDL. |
| 1029 | 11779886 | Apolipoprotein A-I and B and stroke events in a community-based cohort in Taiwan: report of the Chin-Shan Community Cardiovascular Study. |
| 1030 | 11795290 | Increased cholesteryl ester transfer protein and changes in lipid metabolism from initiating insulin therapy. |
| 1031 | 11795290 | Previous reports suggested that increased cholesteryl ester transfer protein (CETP) appeared in diabetic patients with hyperinsulinemia or given a lot of insulin is atherogenic. |
| 1032 | 11795290 | We investigated whether insulin always increases CETP and whether increased CETP by insulin is always atherogenic. |
| 1033 | 11795290 | In 40 patients the amount and activity of CETP were assessed before and 2 weeks after initiation of insulin therapy. |
| 1034 | 11795290 | No significant correlation was observed between changes in CETP and in lipids including HDL-cholesterol or apolipoprotein concentrations. |
| 1035 | 11795290 | This is the first prospective study to show increased CETP activity after initiation of insulin therapy. |
| 1036 | 11795290 | After initiating insulin, CETP increases without accompanying atherogenic changes in lipid metabolism. |
| 1037 | 11795290 | Based on the changes observed, CETP in itself does not have atherogenicity and the increase, but no excess, of CETP by appropriate insulin therapy cannot be atherogenic. |
| 1038 | 11803456 | Codon 311 (Cys --> Ser) polymorphism of paraoxonase-2 gene is associated with apolipoprotein E4 allele in both Alzheimer's and vascular dementias. |
| 1039 | 11803456 | The gene of an esterase enzyme, called paraoxonase (PON, EC.3.1.8.1.) is a member of a multigene family that comprises three related genes PON1, PON2, and PON3 with structural homology clustering on the chromosome 7.(1,2) The PON1 activity and the polymorphism of the PON1 and PON2 genes have been found to be associated with risk of cardiovascular diseases such as hypercholesterolaemia, non-insulin-dependent diabetes, coronary heart disease (CHD) and myocardial infaction.(3-8) The importance of cardiovascular risk factors in the pathomechanism of Alzheimer's disease (AD) and vascular dementia (VD)(9-13) prompted us to examine the genetic effect of PON2 gene codon 311 (Cys-->Ser; PON2*S) polymorphism and the relationship between the PON2*S allele and the other dementia risk factor, the apoE polymorphism in these dementias. |
| 1040 | 11853190 | Apolipoprotein A-I concentration in tears in diabetic retinopathy. |
| 1041 | 11872695 | The B2 allele was associated in a dose-dependent fashion with higher HDL cholesterol and apolipoprotein AI levels, together with lower CETP concentrations. |
| 1042 | 11877595 | Four apolipoprotein (apo) E variants have been reported to be associated with lipoprotein glomerulopathy (LPG), which is characterized by type III hyperlipoproteinemia (type III HLP) and proteinuria and frequently leads to nephrotic syndrome. |
| 1043 | 11897617 | 85-kDa cPLA(2) plays a critical role in PPAR-mediated gene transcription in human hepatoma cells. |
| 1044 | 11897617 | The HepG2 cells express both PPAR-alpha and -gamma but not PPAR-beta. |
| 1045 | 11897617 | Overexpression of cPLA(2), but not group IIA sPLA(2) in the HepG2 cells, caused a significantly increased PPAR-alpha/gamma-mediated reporter activity. |
| 1046 | 11897617 | Antisense inhibition of cPLA(2) resulted in a significantly decreased PPAR-alpha/gamma activity. |
| 1047 | 11897617 | The PPAR-alpha/gamma-induced gene transcription in the HepG2 cells was inhibited by the cPLA(2) inhibitors methyl arachidonyl fluorophosphonate and arachidonyltrifluoromethyl ketone, but not by the sPLA(2) inhibitor LY311727. |
| 1048 | 11897617 | The expression of PPAR-alpha-mediated endogenous gene apolipoprotein A-II was increased in cells with overexpression of cPLA(2), decreased in cells with antisense inhibition of cPLA(2), but unaltered in cells with overexpression of group IIA sPLA(2). |
| 1049 | 11897617 | The above results demonstrated an important role of cPLA(2), but not group IIA sPLA(2) in the control of PPAR activation. |
| 1050 | 11897617 | This study reveals a novel intracellular function of cPLA(2) in PPAR activation in HepG2 cells. |
| 1051 | 11897617 | The cPLA(2) thus may represent a potential therapeutic target for the control of PPAR-related liver and metabolic disorders such as obesity, lipid metabolic disorders, diabetes mellitus, and atherosclerosis. |
| 1052 | 11905095 | Three genetic disorders have been described in which chylomicrons accumulate in plasma: familial lipoprotein lipase deficiency, familial apolipoprotein C-II deficiency, and familial inhibitor to lipoprotein lipase. |
| 1053 | 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. |
| 1054 | 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. |
| 1055 | 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. |
| 1056 | 11932277 | Total cholesterol (TC), triglyceride, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol (LDLc), apolipoprotein A(1), apolipoprotein B, and lipoprotein (a) [Lp(a)] were measured after an overnight fast. |
| 1057 | 11934682 | Effect of IGF-I therapy on VLDL apolipoprotein B100 metabolism in type 1 diabetes mellitus. |
| 1058 | 11934682 | Secretion and clearance rates of very low density lipoprotein (VLDL) apolipoprotein B100 (apoB) determine plasma lipid concentrations. |
| 1059 | 11934682 | Type 1 diabetes is characterized by increased growth hormone (GH) secretion and decreased insulin-like growth factor (IGF) I concentrations. |
| 1060 | 11934682 | This study examined the effect of low-dose (40 microg.kg(-1).day(-1)) IGF-I therapy on VLDL apoB metabolism, VLDL composition, and the GH-IGF-I axis during euglycemia in type 1 diabetes. |
| 1061 | 11934682 | Using a stable isotope technique, VLDL apoB kinetics were estimated before and after 1 wk of IGF-I therapy in 12 patients with type 1 diabetes in a double-blind, placebo-controlled trial. |
| 1062 | 11934682 | Fasting plasma triglyceride (P < 0.03), VLDL-triglyceride concentrations (P < 0.05), and the VLDL-triglyceride-to-VLDL apoB ratio (P < 0.002) significantly decreased after IGF-I therapy, whereas VLDL apoB kinetics were not significantly affected by IGF-I therapy. |
| 1063 | 11934682 | The mean overnight insulin concentrations during euglycemia decreased by 25% after IGF-I therapy. |
| 1064 | 11934682 | IGF-I therapy changes fasting triglyceride concentrations and VLDL composition probably because of an increase in insulin sensitivity. |
| 1065 | 11934682 | Effect of IGF-I therapy on VLDL apolipoprotein B100 metabolism in type 1 diabetes mellitus. |
| 1066 | 11934682 | Secretion and clearance rates of very low density lipoprotein (VLDL) apolipoprotein B100 (apoB) determine plasma lipid concentrations. |
| 1067 | 11934682 | Type 1 diabetes is characterized by increased growth hormone (GH) secretion and decreased insulin-like growth factor (IGF) I concentrations. |
| 1068 | 11934682 | This study examined the effect of low-dose (40 microg.kg(-1).day(-1)) IGF-I therapy on VLDL apoB metabolism, VLDL composition, and the GH-IGF-I axis during euglycemia in type 1 diabetes. |
| 1069 | 11934682 | Using a stable isotope technique, VLDL apoB kinetics were estimated before and after 1 wk of IGF-I therapy in 12 patients with type 1 diabetes in a double-blind, placebo-controlled trial. |
| 1070 | 11934682 | Fasting plasma triglyceride (P < 0.03), VLDL-triglyceride concentrations (P < 0.05), and the VLDL-triglyceride-to-VLDL apoB ratio (P < 0.002) significantly decreased after IGF-I therapy, whereas VLDL apoB kinetics were not significantly affected by IGF-I therapy. |
| 1071 | 11934682 | The mean overnight insulin concentrations during euglycemia decreased by 25% after IGF-I therapy. |
| 1072 | 11934682 | IGF-I therapy changes fasting triglyceride concentrations and VLDL composition probably because of an increase in insulin sensitivity. |
| 1073 | 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. |
| 1074 | 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). |
| 1075 | 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. |
| 1076 | 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. |
| 1077 | 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). |
| 1078 | 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. |
| 1079 | 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. |
| 1080 | 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). |
| 1081 | 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. |
| 1082 | 12023854 | We have described previously the ability of a peptide derived from the apolipoprotein B100 (apoB100) moiety of low-density lipoproteins (KRAD14) to inhibit the procoagulant function of TF. |
| 1083 | 12048138 | Three polymorphisms in the peroxisome proliferator activated receptor alpha (PPARalpha) gene were investigated (L162V, G>A in intron 2 and G>C in intron 7), two in the apolipoprotein CIII (APOC3) gene (-482C>T and -455T>C) and one in the beta-fibrinogen (FIBB) gene (-455G>A). |
| 1084 | 12086920 | Phospholipid transfer protein (PLTP) is a member of the lipid transfer/lipopolysaccharide binding protein gene family. |
| 1085 | 12086920 | The phenotype of PLTP transgenic and gene knock out mice indicates that PLTP plays a major role in the metabolism of high-density lipoprotein (HDL) and apoB-containing lipoproteins and thereby influences the concentration, apolipoprotein content, and size of lipoprotein particles in plasma. |
| 1086 | 12086920 | At lease two underlined mechanisms are involved in the reduction of atherosclerosis in PLTP deficient status, 1) reduction of apoB-containing lipoprotein production and levels; and 2) increase of anti-oxidation potential. |
| 1087 | 12110948 | Mutations in hepatocyte nuclear factor 4alpha (HNF4alpha) gene associated with diabetes result in greater loss of HNF4alpha function in pancreatic beta-cells than in nonpancreatic beta-cells and in reduced activation of the apolipoprotein CIII promoter in hepatic cells. |
| 1088 | 12110948 | The R324H mutation had no effect on HNF4alpha function with either the HNF1alpha and L-type pyruvate kinase (LPK) promoters, but the D126Y and D126H mutations impaired HNF4alpha transcriptional activities in all tested cell lines. |
| 1089 | 12118856 | Apolipoprotein C-III and E polymorphisms and cardiovascular syndrome, hyperlipidemia, and insulin resistance in renal transplantation. |
| 1090 | 12118856 | In the general population, the S2 allelic variant of the apoprotein (apo) C-III gene has been associated with hypertriglyceridemia and an insulin resistant state, whereas the E4 allele of the apo E has been associated with hypercholesterolemia and atherosclerosis. |
| 1091 | 12136402 | Evaluation of apolipoprotein A-II as a positional candidate gene for familial Type II diabetes, altered lipid concentrations, and insulin resistance. |
| 1092 | 12200750 | The effect of age, body mass index, and fasting triglyceride level on postprandial lipemia is dependent on apolipoprotein E polymorphism in subjects with non-insulin-dependent diabetes mellitus. |
| 1093 | 12200750 | The aim of this study was to evaluate in non-insulin-dependent diabetes mellitus (NIDDM) subjects the respective influence of apolipoprotein (apo) E polymorphism, age, gender, weight, fasting triglyceride (TG) status, and glycemic status on postprandial lipemia. |
| 1094 | 12370857 | Recent evidence indicates that among the 2 major HDL subclasses, those without apolipoprotein A-II (LpA-I) are more antiatherogenic compared with those with apoA-II (LpA-I:A-II). |
| 1095 | 12486210 | Apolipoprotein A-I expression in rats is not altered by troglitazone. |
| 1096 | 12486210 | Insulin is known to upregulate apolipoprotein A-I (apoA-I) promoter activity and to increase apoA1 gene expression in vivo. |
| 1097 | 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. |
| 1098 | 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. |
| 1099 | 12486210 | Apolipoprotein A-I expression in rats is not altered by troglitazone. |
| 1100 | 12486210 | Insulin is known to upregulate apolipoprotein A-I (apoA-I) promoter activity and to increase apoA1 gene expression in vivo. |
| 1101 | 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. |
| 1102 | 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. |
| 1103 | 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. |
| 1104 | 12679171 | Effect of chromium on apolipoprotein A-I expression in HepG2 cells. |
| 1105 | 12684543 | Kinetics of apolipoprotein B100 (apoB100)-containing lipoproteins were determined before and after atorvastatin treatment and compared with data obtained in five normolipidemic volunteers. |
| 1106 | 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. |
| 1107 | 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. |
| 1108 | 12716736 | We investigated VLDL-triglyceride and -apolipoprotein (apo)-B production in relation to DNL and insulin sensitivity in female ob/ob mice. |
| 1109 | 12716736 | No differences in hepatic expression of genes encoding apoB and microsomal triglyceride transfer protein were found. |
| 1110 | 12716854 | Differential levels of gamma-glutamyl transferase activity and apolipoprotein CIII in men on either statin or fibrate therapy. |
| 1111 | 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). |
| 1112 | 12777470 | No correlation was detected between LPL and Lp(A-I,A-II). |
| 1113 | 12818411 | Genetic variation in the microsomal triglyceride transfer protein (MTP) affects the secretion pattern and plasma concentration of apolipoprotein (aopB)-containing lipoproteins and a common functional -493 G/T polymorphism has been reported to influence plasma lipids levels. |
| 1114 | 12818411 | Since type 2 diabetes is associated with obesity and insulin resistance, the present study investigated the effect of this polymorphism on plasma lipids, apoB and LDL subfractions in 281 Chinese type 2 diabetic subjects and 364 non-diabetic controls. |
| 1115 | 12924437 | Apolipoprotein A-IV mRNA overexpression in early preneoplastic hepatic foci induced by low-number pancreatic islet transplants in streptozotocin-diabetic rats. |
| 1116 | 12924437 | In rodents, apolipoprotein A-IV (A-IV) is synthesized in the small intestine and the liver. |
| 1117 | 12924437 | Apolipoprotein A-IV mRNA overexpression in early preneoplastic hepatic foci induced by low-number pancreatic islet transplants in streptozotocin-diabetic rats. |
| 1118 | 12924437 | In rodents, apolipoprotein A-IV (A-IV) is synthesized in the small intestine and the liver. |
| 1119 | 12934668 | VLDL and HDL2 derived from EFAD rats were depleted in apolipoprotein (apo) E and apo A-II, and enriched in apo A-I 2 h after TNF-alpha administration. |
| 1120 | 12934668 | Finally, TNF-alpha decreased adipose tissue LPL activity in both control and EFAD animals. |
| 1121 | 12934668 | The present results demonstrated that TNF-alpha can amplify or antagonize the effects of EFAD on lipid profile, lipoprotein composition, and LPL activity. |
| 1122 | 12937310 | C-reactive protein, troponin T (TnT), total, HDL, LDL, and lipoprotein(a) cholesterol, apoA2, apoB, triglyceride, fibrinogen, D-dimer, albumin, and creatinine levels and clinical characteristics at the time of entry were recorded. |
| 1123 | 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. |
| 1124 | 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. |
| 1125 | 12951628 | The regulation of hepatic VLDL secretion mainly depends on apolipoprotein (apo) B synthesis, on microsomal triglyceride transfer protein, insulin and the availability of triglycerides, free fatty acids (FFA) and cholesteryl ester. |
| 1126 | 12951628 | On the other hand, the short-term addition of insulin has been shown to inhibit VLDL-triglyceride and apoB production in vitro. |
| 1127 | 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. |
| 1128 | 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. |
| 1129 | 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. |
| 1130 | 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. |
| 1131 | 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. |
| 1132 | 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. |
| 1133 | 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. |
| 1134 | 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. |
| 1135 | 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. |
| 1136 | 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. |
| 1137 | 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. |
| 1138 | 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. |
| 1139 | 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. |
| 1140 | 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. |
| 1141 | 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. |
| 1142 | 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. |
| 1143 | 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. |
| 1144 | 14514638 | The aim of the present study was to examine intracellular events that govern lipid transport and apolipoprotein (apo) B-48-containing lipoprotein assembly in the small intestine of Psammomys obesus, a model of nutritionally induced insulin resistance and type 2 diabetes. |
| 1145 | 14572909 | Suppression of apolipoprotein AI gene expression in HepG2 cells by TNF alpha and IL-1beta. |
| 1146 | 14572909 | This presumably results in systemic insulin resistance, characterized by a pro-atherogenic plasma lipid profile and reduced apolipoprotein AI (apoAI) protein levels. |
| 1147 | 14572909 | To determine how cytokine-mediated insulin resistance suppresses apoAI gene expression, we investigated the effect of tumor necrosis factor alpha (TNF alpha) and interleukin-1beta (IL-1beta) on apoAI protein, mRNA, and transcriptional activity in the human hepatoma cell line HepG2. |
| 1148 | 14572909 | In order to determine if the effect of TNF alpha and IL-1beta occurs at the transcriptional level, HepG2 cells were transfected with a chloramphenicol acetyltransferase (CAT) reporter gene plasmid containing the full-length apoAI promoter, and after 24 h, treated with TNF alpha (30 ng/ml), IL-1beta (30 ng/ml), or both cytokines. |
| 1149 | 14572909 | CAT activity was suppressed by both cytokines (24.0+/-1.9% acetylation in control cells vs. 5.6+/-1.2% (P<0.0004), 10.2+/-1.5% (P<0.0006), and 3.9+/-0.9% acetylation (P<0.0002) in cells treated with TNF alpha, IL-1beta, and the combination of both cytokines, respectively) suggesting that cytokine-mediated suppression occurs at the transcriptional level. |
| 1150 | 14572909 | Suppression of apolipoprotein AI gene expression in HepG2 cells by TNF alpha and IL-1beta. |
| 1151 | 14572909 | This presumably results in systemic insulin resistance, characterized by a pro-atherogenic plasma lipid profile and reduced apolipoprotein AI (apoAI) protein levels. |
| 1152 | 14572909 | To determine how cytokine-mediated insulin resistance suppresses apoAI gene expression, we investigated the effect of tumor necrosis factor alpha (TNF alpha) and interleukin-1beta (IL-1beta) on apoAI protein, mRNA, and transcriptional activity in the human hepatoma cell line HepG2. |
| 1153 | 14572909 | In order to determine if the effect of TNF alpha and IL-1beta occurs at the transcriptional level, HepG2 cells were transfected with a chloramphenicol acetyltransferase (CAT) reporter gene plasmid containing the full-length apoAI promoter, and after 24 h, treated with TNF alpha (30 ng/ml), IL-1beta (30 ng/ml), or both cytokines. |
| 1154 | 14572909 | CAT activity was suppressed by both cytokines (24.0+/-1.9% acetylation in control cells vs. 5.6+/-1.2% (P<0.0004), 10.2+/-1.5% (P<0.0006), and 3.9+/-0.9% acetylation (P<0.0002) in cells treated with TNF alpha, IL-1beta, and the combination of both cytokines, respectively) suggesting that cytokine-mediated suppression occurs at the transcriptional level. |
| 1155 | 14681304 | Two polymorphisms related to thrombosis (an arg353gln polymorphism in the factor VII gene and a T11053G polymorphism in the plasminogen activator inhibitor type-1 gene) and one related to lipid metabolism [a C(-482)T polymorphism in the apolipoprotein CIII gene] achieved nominal significance, but were not found to be independent predictors after multiple comparison adjustment. |
| 1156 | 14709372 | Multivariate logistic regression analysis with adjustment for age, body mass index, and the prevalence of smoking, hypertension, diabetes mellitus, and hyperuricemia revealed that three polymorphisms [994G --> T (Val279Phe) in the platelet-activating factor acetylhydrolase gene, 242C --> T (His72Tyr) in the NADH/NADPH oxidase p22 phox gene, and 1100C --> T in the apolipoprotein C-III gene] were significantly associated with CAD in men with hypercholesterolemia. |
| 1157 | 14727946 | Nicotinic acid is the most potent agent and recent reports indicate that, in contrast to gemfibrozil, it selectively increases antiatherogenic HDL subfraction, lipoprotein (Lp) AI (without apolipoprotein AII), in patients with low plasma HDL-C levels. |
| 1158 | 14729390 | In mediating the transfer of cholesteryl esters (CE) from antiatherogenic high density lipoprotein (HDL) to proatherogenic apolipoprotein (apo)-B-containing lipoprotein particles (including very low density lipoprotein [VLDL], VLDL remnants, intermediate density lipoprotein [IDL], and low density lipoprotein [LDL]), the CE transfer protein (CETP) plays a critical role not only in the reverse cholesterol transport (RCT) pathway but also in the intravascular remodeling and recycling of HDL particles. |
| 1159 | 14729390 | In such states, CETP activity is elevated and contributes significantly to the cholesterol burden in atherogenic apoB-containing lipoproteins. |
| 1160 | 14730686 | One of the major difficulties in mining low abundance biomarkers from serum or plasma is due to the fact that a small number of proteins such as albumin, alpha2-macroglobulin, transferrin, and immunoglobulins, may represent as much as 80% of the total serum protein. |
| 1161 | 14730686 | For example, haptoglobin and hemoglobin are elevated in sera of AD, IR/D2, and CHF patients. |
| 1162 | 14730686 | The levels of several other proteins including fibrinogen and its fragments, alpha 2-macroglobulin, transthyretin, pro-platelet basic protein, protease inhibitors clade A and C, as well as proteins involved in the classical complement pathway such as complement C3, C4, and C1 inhibitor, were found to differ between IR/D2 and control sera. |
| 1163 | 14730686 | The sera levels of proteins, such as the 10 kDa subunit of vitronectin, alpha 1-acid glycoprotein, apolipoprotein B100, fragment of factor H, and histidine-rich glycoprotein were observed to be different between AD and controls. |
| 1164 | 14767868 | Since prostanoid synthesis inhibitors are commonly used in subjects with coronary heart disease we studied the effect of cyclooxygenase (COX) inhibition on apolipoprotein AI (apoAI) expression in a human hepatoma cell line (HepG2) transfected with full-length apoAI promoter attached to the chloramphenicol acetyl transferase (CAT) reporter gene. |
| 1165 | 14967823 | LXR-mediated activation of macrophage stearoyl-CoA desaturase generates unsaturated fatty acids that destabilize ABCA1. |
| 1166 | 14967823 | ATP binding cassette transporter A1 (ABCA1) mediates the transport of cholesterol and phospholipids from cells to HDL apolipoproteins and thus modulates HDL levels and atherogenesis. |
| 1167 | 14967823 | Because fatty acids are increased in diabetes, we examined their effects on ABCA1 activity in cultured macrophages. cAMP analogs and ligands for the liver X receptor/retinoid X receptor (LXR/RXR) system can induce Abca1 transcription in murine macrophages. |
| 1168 | 14967823 | When induced by cAMP, unsaturated but not saturated long-chain fatty acids inhibit apolipoprotein-mediated lipid efflux by destabilizing ABCA1 protein. |
| 1169 | 14967823 | The SCD inhibitors conjugated linoleic acid and troglitazone nearly abolished ABCA1 destabilization by palmitate and stearate but not by linoleate. |
| 1170 | 14967823 | These results suggest that LXR/RXR ligands generate ABCA1-destabilizing monounsaturated fatty acids from their saturated precursors by activating SCD. |
| 1171 | 14978155 | As renal function fails, many patients become progressively malnourished, as evidenced by reduced levels of albumin, prealbumin, and transferrin. |
| 1172 | 14978155 | Malnourished patients have increased levels of C reactive protein (CRP), interleukin-6 (IL-6), and concomitant cardiovascular disease when they reach end stage. |
| 1173 | 14978155 | Apolipoprotein C III (apo C III), a competitive inhibitor of lipoprotein lipase is increased in CKD. |
| 1174 | 14988232 | Transcriptional control of apolipoprotein A-I gene expression in diabetes. |
| 1175 | 14988251 | In vitro transcriptional induction of the human apolipoprotein A-II gene by glucose. |
| 1176 | 14988251 | Transgenic mice overproducing human apolipoprotein (apo)A-II, one of the two major apos of HDLs, display the same lipid disorders. |
| 1177 | 14988251 | In vitro transcriptional induction of the human apolipoprotein A-II gene by glucose. |
| 1178 | 14988251 | Transgenic mice overproducing human apolipoprotein (apo)A-II, one of the two major apos of HDLs, display the same lipid disorders. |
| 1179 | 15047603 | FXR expression was decreased in livers of streptozotocin-induced diabetic rats and normalized upon insulin supplementation. |
| 1180 | 15047603 | In primary rat hepatocytes, D-glucose increased FXR mRNA in a dose- and time-dependent manner, whereas insulin counteracted this effect. |
| 1181 | 15047603 | Finally, expression of the FXR target genes, SHP and apolipoprotein C-III, were additively regulated by D-glucose and FXR ligands. |
| 1182 | 15047603 | Dysregulation of FXR expression may contribute to alterations in lipid and bile acid metabolism in patients with diabetes or insulin resistance. |
| 1183 | 15059615 | Multivariate logistic regression analysis with adjustment for age, body mass index, and the prevalence of smoking, hypertension, hypercholesterolemia, and hyperuricemia revealed that the following polymorphisms were significantly (P < 0.005) associated with CAD: the 1019C -->T of the connexin 37 gene for men with type 2 diabetes; the 2445G -->A in the fatty acid-binding protein 2 gene for women with this condition; the -863C-->A in the tumor necrosis factor-alpha gene, the -219G-->T in the apolipoprotein E gene, the 1019C-->T in the connexin 37 gene for men without type 2 diabetes; and the -482C-->T in the apolipoprotein C-III gene for women without this condition. |
| 1184 | 15131762 | As these 2 disorders are associated with low high-density lipoprotein (HDL)-cholesterol, high triglycerides, and insulin resistance (IR), we examined the relation of serum adiponectin concentrations to serum lipid and lipoprotein profiles as well as IR in young healthy men. |
| 1185 | 15131762 | Serum adiponectin levels were positively associated with HDL-cholesterol, apolipoprotein (apo) A1, and low-density lipoprotein (LDL) particle size, and negatively associated with triglycerides and apo B. |
| 1186 | 15131762 | In a multiple regression analysis including all variables that showed significant univariate associations with adiponectin, associations of adiponectin with HDL-cholesterol (beta = 0.079, P =.0009), percent body fat (beta = -0.165, P =.002), and serum leptin (beta = -0.291, P =.01) were statistically significant. |
| 1187 | 15164326 | Since the anti-atherogenic protein apolipoprotein AI (apoAI) is positively regulated by insulin, at least partly through its effect on Sp1, we investigated the effect of glucosamine on apoAI gene expression in the hepatocyte cell line, HepG2. |
| 1188 | 15164326 | Similarly, apoAI promoter activity measured in HepG2 cell transfected with an apoAI reporter plasmid containing the full-length apoAI promoter including an insulin-responsive Sp1 binding site did not change with glucosamine addition. |
| 1189 | 15166779 | Apolipoprotein A-II, genetic variation on chromosome 1q21-q24, and disease susceptibility. |
| 1190 | 15175360 | Apolipoprotein A-IV (apoA-IV) has been postulated to be antiatherogenic. |
| 1191 | 15210953 | We now demonstrate that apolipoprotein CIII (apoCIII) is increased in serum from T1D patients and that this serum factor both induces increased cytoplasmic free intracellular Ca(2+) concentration ([Ca(2+)](i)) and beta cell death. |
| 1192 | 15259000 | Glycosylphosphatidylinositol-specific phospholipase D immunoreactivity is present in islet amyloid in type 2 diabetes. |
| 1193 | 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. |
| 1194 | 15259000 | Fibril formation from human islet amyloid polypeptide was determined in the absence or presence of GPI-PLD. |
| 1195 | 15259000 | In non-diabetics, GPI-PLD immunoreactivity was present and co-localized with insulin, as opposed to co-localizing with amyloid in diabetics. |
| 1196 | 15259000 | No immunoreactivity for apolipoprotein A-I was present in islet cells or islet amyloid. |
| 1197 | 15259000 | Heparan sulphate proteoglycan, which is commonly present in most amyloid, bound GPI-PLD in vitro. |
| 1198 | 15259000 | GPI-PLD inhibited the formation of amyloid fibrils from synthetic islet amyloid polypeptide in vitro. |
| 1199 | 15259000 | GPI-PLD is therefore present in islet amyloid and appears to derive from local production from islets. |
| 1200 | 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. |
| 1201 | 15364160 | Association of serum apolipoprotein C III levels and apolipoprotein C III gene Sst I polymorphism with carotid intima-media thickness in Chinese type 2 diabetic patients. |
| 1202 | 15364160 | Apolipoprotein C III (apo C III) plays a central role in regulating plasma metabolism of triglyceride-rich lipoprotein (TRL). |
| 1203 | 15364160 | Association of serum apolipoprotein C III levels and apolipoprotein C III gene Sst I polymorphism with carotid intima-media thickness in Chinese type 2 diabetic patients. |
| 1204 | 15364160 | Apolipoprotein C III (apo C III) plays a central role in regulating plasma metabolism of triglyceride-rich lipoprotein (TRL). |
| 1205 | 15375785 | Apolipoprotein C-III protein concentrations and gene polymorphisms in type 1 diabetes: associations with lipoprotein subclasses. |
| 1206 | 15375785 | Serum apolipoprotein C-III (apoCIII) concentration and apoCIII gene polymorphisms have been shown to be a risk factor for cardiovascular disease; however, the underlying mechanisms remain unclear. |
| 1207 | 15375785 | Higher apoCIII concentrations were associated (P < .0001) with increased triglycerides (r = 0.78), total (r = 0.61) and low-density lipoprotein (LDL) (r = 0.40) cholesterol, apoA-I (r = 0.26), and apoB (r = 0.50), and these relationships persisted after controlling for age, gender, body mass index (BMI), and hemoglobin A1c (HbA1c). |
| 1208 | 15375785 | Neither the T(-455) --> C polymorphism affecting an insulin response element in the apoCIII gene promoter nor a SacI polymorphism in the 3'UTR were associated with any alterations in circulating apoCIII concentrations, serum lipids, apolipoprotein concentrations, lipoprotein composition, or parameters measured by NMR lipoprotein subclass analyses. |
| 1209 | 15375785 | Apolipoprotein C-III protein concentrations and gene polymorphisms in type 1 diabetes: associations with lipoprotein subclasses. |
| 1210 | 15375785 | Serum apolipoprotein C-III (apoCIII) concentration and apoCIII gene polymorphisms have been shown to be a risk factor for cardiovascular disease; however, the underlying mechanisms remain unclear. |
| 1211 | 15375785 | Higher apoCIII concentrations were associated (P < .0001) with increased triglycerides (r = 0.78), total (r = 0.61) and low-density lipoprotein (LDL) (r = 0.40) cholesterol, apoA-I (r = 0.26), and apoB (r = 0.50), and these relationships persisted after controlling for age, gender, body mass index (BMI), and hemoglobin A1c (HbA1c). |
| 1212 | 15375785 | Neither the T(-455) --> C polymorphism affecting an insulin response element in the apoCIII gene promoter nor a SacI polymorphism in the 3'UTR were associated with any alterations in circulating apoCIII concentrations, serum lipids, apolipoprotein concentrations, lipoprotein composition, or parameters measured by NMR lipoprotein subclass analyses. |
| 1213 | 15375785 | Apolipoprotein C-III protein concentrations and gene polymorphisms in type 1 diabetes: associations with lipoprotein subclasses. |
| 1214 | 15375785 | Serum apolipoprotein C-III (apoCIII) concentration and apoCIII gene polymorphisms have been shown to be a risk factor for cardiovascular disease; however, the underlying mechanisms remain unclear. |
| 1215 | 15375785 | Higher apoCIII concentrations were associated (P < .0001) with increased triglycerides (r = 0.78), total (r = 0.61) and low-density lipoprotein (LDL) (r = 0.40) cholesterol, apoA-I (r = 0.26), and apoB (r = 0.50), and these relationships persisted after controlling for age, gender, body mass index (BMI), and hemoglobin A1c (HbA1c). |
| 1216 | 15375785 | Neither the T(-455) --> C polymorphism affecting an insulin response element in the apoCIII gene promoter nor a SacI polymorphism in the 3'UTR were associated with any alterations in circulating apoCIII concentrations, serum lipids, apolipoprotein concentrations, lipoprotein composition, or parameters measured by NMR lipoprotein subclass analyses. |
| 1217 | 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). |
| 1218 | 15585206 | This study was aimed to examine cholesteryl ester transfer protein (CETP), apolipoprotein AI and CIII gene polymorphisms, and to verify whether these genetic determinants are associated with the prevalence of myocardial infarction (MI) or type 2 diabetes. |
| 1219 | 15585206 | The TaqIB restriction fragment length polymorphism (RFLP) in intron I of the CETP gene, the MspI in the third intron of the APOAI gene, and also SstI in the 3' untranslated region of the APOCIII gene were determined using standard methods. |
| 1220 | 15585206 | Therefore, among these genetic polymorphisms, TaqIB of CETP and MspI of apolipoprotein AI appeared to help significantly to identify diabetic individuals. |
| 1221 | 15585206 | This study was aimed to examine cholesteryl ester transfer protein (CETP), apolipoprotein AI and CIII gene polymorphisms, and to verify whether these genetic determinants are associated with the prevalence of myocardial infarction (MI) or type 2 diabetes. |
| 1222 | 15585206 | The TaqIB restriction fragment length polymorphism (RFLP) in intron I of the CETP gene, the MspI in the third intron of the APOAI gene, and also SstI in the 3' untranslated region of the APOCIII gene were determined using standard methods. |
| 1223 | 15585206 | Therefore, among these genetic polymorphisms, TaqIB of CETP and MspI of apolipoprotein AI appeared to help significantly to identify diabetic individuals. |
| 1224 | 15598690 | Polymorphisms in the fatty acid-binding protein 2 and apolipoprotein C-III genes are associated with the metabolic syndrome and dyslipidemia in a South Indian population. |
| 1225 | 15598690 | The Ala54Thr polymorphism in the fatty acid-binding protein 2 (FABP2) gene as well as the T-455C and C-482T polymorphisms in the apolipoprotein C-III (APOC3) gene promoter have been associated with features of the MS in specific populations. |
| 1226 | 15598690 | Allelic frequencies in 70 controls and 110 patients with diabetes from the Chennai Urban Population Study were 52.9% for FABP2 Thr54, 73.0% for APOC3 -482T, and 80.2% for APOC3 -455C. |
| 1227 | 15598690 | Polymorphisms in the fatty acid-binding protein 2 and apolipoprotein C-III genes are associated with the metabolic syndrome and dyslipidemia in a South Indian population. |
| 1228 | 15598690 | The Ala54Thr polymorphism in the fatty acid-binding protein 2 (FABP2) gene as well as the T-455C and C-482T polymorphisms in the apolipoprotein C-III (APOC3) gene promoter have been associated with features of the MS in specific populations. |
| 1229 | 15598690 | Allelic frequencies in 70 controls and 110 patients with diabetes from the Chennai Urban Population Study were 52.9% for FABP2 Thr54, 73.0% for APOC3 -482T, and 80.2% for APOC3 -455C. |
| 1230 | 15607389 | These beneficial effects may be responsible for coronary plaque stabilization in patients treated with recombinant Apolipoprotein A-I Milano/phospholipid complex. |
| 1231 | 15636639 | Association of SNP3 polymorphism in the apolipoprotein A-V gene with plasma triglyceride level in Tunisian type 2 diabetes. |
| 1232 | 15642486 | Apolipoprotein C-III protein concentrations and gene polymorphisms in Type 1 diabetes: associations with microvascular disease complications in the DCCT/EDIC cohort. |
| 1233 | 15658274 | [Lipid-poor apolipoprotein A-I, glycated apolipoprotein A-I]. |
| 1234 | 15658276 | [Apolipoprotein C-I, C-II, C-III]. |
| 1235 | 15671223 | We measured circulating total, LDL, and HDL cholesterol, triacylglycerol, lipoprotein(a), apolipoprotein (apo) A1, apoB, hemoglobin (Hb)A1c, insulin, C-peptide, and leptin concentrations. |
| 1236 | 15671223 | Diets high in lignan intake may increase apoB-containing lipoproteins and decrease fasting insulin secretion, but these findings require confirmation. |
| 1237 | 15690318 | Laboratory parameters included plasma lipids and lipoproteins, lipoprotein (a), apolipoprotein (apo) A-I, apo B-100, apo C-III, and high-sensitivity C-reactive protein. |
| 1238 | 15715433 | Association of Sst I polymorphism in apolipoprotein C3 gene with hypertriglyceridaemia in coronary atherosclerotic heart disease and type II diabetes mellitus in Chinese population. |
| 1239 | 15715433 | Several independent population studies have reported that the apolipoprotein C3 (APOC3) Sst I polymorphism in apolipoprotein (apo) A1 /C3/A4/A5 gene cluster is associated with Hypertriglyceridaemia (HTG). |
| 1240 | 15715433 | The aim of this study is to investigate the association between the APOC3 gene Sst I polymorphism and the hypertriglyceridaemia in CHD and NIDDM in Chinese population. |
| 1241 | 15715433 | The genotype and allele frequencies of APOC3 Sst I polymorphism (S1/S2) were analyzed by PCR-restriction fragment length polymorphism in 267 CHD patients, 246 NIDDM patients and 491 unrelated healthy control individuals. |
| 1242 | 15715433 | Association of Sst I polymorphism in apolipoprotein C3 gene with hypertriglyceridaemia in coronary atherosclerotic heart disease and type II diabetes mellitus in Chinese population. |
| 1243 | 15715433 | Several independent population studies have reported that the apolipoprotein C3 (APOC3) Sst I polymorphism in apolipoprotein (apo) A1 /C3/A4/A5 gene cluster is associated with Hypertriglyceridaemia (HTG). |
| 1244 | 15715433 | The aim of this study is to investigate the association between the APOC3 gene Sst I polymorphism and the hypertriglyceridaemia in CHD and NIDDM in Chinese population. |
| 1245 | 15715433 | The genotype and allele frequencies of APOC3 Sst I polymorphism (S1/S2) were analyzed by PCR-restriction fragment length polymorphism in 267 CHD patients, 246 NIDDM patients and 491 unrelated healthy control individuals. |
| 1246 | 15734841 | Apolipoprotein C3 deficiency results in diet-induced obesity and aggravated insulin resistance in mice. |
| 1247 | 15734841 | Our aim was to study whether the absence of apolipoprotein (apo) C3, a strong inhibitor of lipoprotein lipase (LPL), accelerates the development of obesity and consequently insulin resistance. |
| 1248 | 15734841 | LPL-independent uptake of albumin-bound fatty acids did not differ. |
| 1249 | 15734841 | Absence of apoC3, the natural LPL inhibitor, enhances fatty acid uptake from plasma triglycerides in adipose tissue, which leads to higher susceptibility to diet-induced obesity followed by more severe development of insulin resistance. |
| 1250 | 15734841 | Therefore, apoC3 is a potential target for treatment of obesity and insulin resistance. |
| 1251 | 15734841 | Apolipoprotein C3 deficiency results in diet-induced obesity and aggravated insulin resistance in mice. |
| 1252 | 15734841 | Our aim was to study whether the absence of apolipoprotein (apo) C3, a strong inhibitor of lipoprotein lipase (LPL), accelerates the development of obesity and consequently insulin resistance. |
| 1253 | 15734841 | LPL-independent uptake of albumin-bound fatty acids did not differ. |
| 1254 | 15734841 | Absence of apoC3, the natural LPL inhibitor, enhances fatty acid uptake from plasma triglycerides in adipose tissue, which leads to higher susceptibility to diet-induced obesity followed by more severe development of insulin resistance. |
| 1255 | 15734841 | Therefore, apoC3 is a potential target for treatment of obesity and insulin resistance. |
| 1256 | 15735069 | Polyunsaturated fatty acids interact with the PPARA-L162V polymorphism to affect plasma triglyceride and apolipoprotein C-III concentrations in the Framingham Heart Study. |
| 1257 | 15735069 | We found significant gene-nutrient interactions between the L162V polymorphism and total PUFA intake, which modulated plasma triglycerides (TG; P < 0.05) and apolipoprotein C-III (apoC-III; P < 0.05) concentrations. |
| 1258 | 15735069 | Polyunsaturated fatty acids interact with the PPARA-L162V polymorphism to affect plasma triglyceride and apolipoprotein C-III concentrations in the Framingham Heart Study. |
| 1259 | 15735069 | We found significant gene-nutrient interactions between the L162V polymorphism and total PUFA intake, which modulated plasma triglycerides (TG; P < 0.05) and apolipoprotein C-III (apoC-III; P < 0.05) concentrations. |
| 1260 | 15754464 | Plasma PLTP activity was assayed by measuring the transfer of radiolabeled phosphatidylcholine from liposomes to HDL and high-sensitivity C-reactive protein (CRP) by immunoturbidimetric assay in 280 type 2 diabetic patients and 105 controls. |
| 1261 | 15754464 | Plasma PLTP activity (2364+/-651 nmol/ml/h versus 1880+/-586 nmol/ml/h in control, mean +/- S.D., P <0.01) and CRP (1.64(0.89-3.23)mg/l versus 0.99(0.53-2.23 mg/l, median (interquartile range), P<0.01) were increased in diabetic subjects. |
| 1262 | 15754464 | PLTP activity correlated significantly with age, BMI, HbA1c, log(CRP) and apolipoprotein AI and B in diabetic subjects. |
| 1263 | 15754464 | General linear model analysis showed that only apolipoprotein AI, age, BMI, and log(CRP) were independent determinants of PLTP activity. |
| 1264 | 15754464 | In conclusion, PLTP activity is increased in diabetes and apolipoprotein AI is a major determinant of PLTP activity. |
| 1265 | 15754464 | There is also an independent association between CRP and PLTP activity, suggesting that subclinical inflammation may influence PLTP activity in diabetes. |
| 1266 | 15754464 | Plasma PLTP activity was assayed by measuring the transfer of radiolabeled phosphatidylcholine from liposomes to HDL and high-sensitivity C-reactive protein (CRP) by immunoturbidimetric assay in 280 type 2 diabetic patients and 105 controls. |
| 1267 | 15754464 | Plasma PLTP activity (2364+/-651 nmol/ml/h versus 1880+/-586 nmol/ml/h in control, mean +/- S.D., P <0.01) and CRP (1.64(0.89-3.23)mg/l versus 0.99(0.53-2.23 mg/l, median (interquartile range), P<0.01) were increased in diabetic subjects. |
| 1268 | 15754464 | PLTP activity correlated significantly with age, BMI, HbA1c, log(CRP) and apolipoprotein AI and B in diabetic subjects. |
| 1269 | 15754464 | General linear model analysis showed that only apolipoprotein AI, age, BMI, and log(CRP) were independent determinants of PLTP activity. |
| 1270 | 15754464 | In conclusion, PLTP activity is increased in diabetes and apolipoprotein AI is a major determinant of PLTP activity. |
| 1271 | 15754464 | There is also an independent association between CRP and PLTP activity, suggesting that subclinical inflammation may influence PLTP activity in diabetes. |
| 1272 | 15754464 | Plasma PLTP activity was assayed by measuring the transfer of radiolabeled phosphatidylcholine from liposomes to HDL and high-sensitivity C-reactive protein (CRP) by immunoturbidimetric assay in 280 type 2 diabetic patients and 105 controls. |
| 1273 | 15754464 | Plasma PLTP activity (2364+/-651 nmol/ml/h versus 1880+/-586 nmol/ml/h in control, mean +/- S.D., P <0.01) and CRP (1.64(0.89-3.23)mg/l versus 0.99(0.53-2.23 mg/l, median (interquartile range), P<0.01) were increased in diabetic subjects. |
| 1274 | 15754464 | PLTP activity correlated significantly with age, BMI, HbA1c, log(CRP) and apolipoprotein AI and B in diabetic subjects. |
| 1275 | 15754464 | General linear model analysis showed that only apolipoprotein AI, age, BMI, and log(CRP) were independent determinants of PLTP activity. |
| 1276 | 15754464 | In conclusion, PLTP activity is increased in diabetes and apolipoprotein AI is a major determinant of PLTP activity. |
| 1277 | 15754464 | There is also an independent association between CRP and PLTP activity, suggesting that subclinical inflammation may influence PLTP activity in diabetes. |
| 1278 | 15806598 | Association of the apolipoprotein A-IV: 360 Gln/His polymorphism with cerebrovascular disease, obesity, and depression in a Brazilian elderly population. |
| 1279 | 15806598 | The apolipoprotein A-IV: 360 Gln/His polymorphism was investigated in 383 elderly individuals, who were participants of a longitudinal study commenced in 1991. |
| 1280 | 15806598 | Association of the apolipoprotein A-IV: 360 Gln/His polymorphism with cerebrovascular disease, obesity, and depression in a Brazilian elderly population. |
| 1281 | 15806598 | The apolipoprotein A-IV: 360 Gln/His polymorphism was investigated in 383 elderly individuals, who were participants of a longitudinal study commenced in 1991. |
| 1282 | 15877301 | Intestinal assembly and secretion of highly dense/lipid-poor apolipoprotein B48-containing lipoprotein particles in the fasting state: evidence for induction by insulin resistance and exogenous fatty acids. |
| 1283 | 15877301 | Emerging evidence suggests that overproduction of intestinally derived apolipoprotein (apo) B48-containing lipoprotein particles may be an important contributor to both fasting and postprandial dyslipidemia in insulin-resistant states. |
| 1284 | 15877301 | Mechanisms regulating the assembly and secretion of apoB48-containing lipoproteins are not fully understood particularly in the diabetic/insulin-resistant intestine. |
| 1285 | 15877301 | Both intracellular and secreted apoB48 particles were examined in intestinal enterocytes isolated from normal or insulin-resistant fructose-fed hamsters, as well as in enterocytes treated with exogenous oleic acid. |
| 1286 | 15877301 | A marked enhancement in assembly of apoB48-containing lipoproteins was also observed in the microsomal lumen of fructose-fed hamster enterocytes, suggesting facilitated assembly and secretion of dense intestinal lipoprotein particles in insulin-resistant states. |
| 1287 | 15877301 | The production of these small, dense, and potentially atherogenic apoB48 particles can be stimulated by increased free fatty acid flux as well as in insulin-resistant diabetes. |
| 1288 | 15900219 | Paraoxonase-1 promoter polymorphism C--107T and serum apolipoprotein AI interact to modulate serum paraoxonase-1 status. |
| 1289 | 15919788 | Inhibition of microsomal triglyceride transfer protein expression and apolipoprotein B100 secretion by the citrus flavonoid naringenin and by insulin involves activation of the mitogen-activated protein kinase pathway in hepatocytes. |
| 1290 | 15919788 | Microsomal triglyceride transfer protein (MTP) is necessary for hepatocyte assembly and secretion of apolipoprotein (apo)B100-containing lipoproteins. |
| 1291 | 15919788 | The citrus flavonoid naringenin, like insulin, decreased MTP expression in HepG2 cells, resulting in inhibition of apoB100 secretion; however, the mechanism for naringenin is independent of insulin receptor substrate-1/2. |
| 1292 | 15919788 | Recently, it was reported that insulin decreased MTP expression in HepG2 cells via the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) (MAPK(erk)) pathway. |
| 1293 | 15919788 | Inhibition of MAPK kinase (MEK) 1/2 in HepG2 cells significantly attenuated the naringenin- and insulin-induced reduction in MTP expression. |
| 1294 | 15919788 | Both naringenin and insulin increased ERK1/2 phosphorylation, which was completely inhibited by MEK1/2 inhibition and enhanced by inhibition of MAPK(p38), a negative regulator of MAPK(erk) activity. |
| 1295 | 15919788 | Inhibition of MEK1/2 significantly attenuated both the naringenin- and insulin-induced decrease in apoB100 secretion demonstrating a direct link between MAPK(erk) activation and apoB100 secretion. |
| 1296 | 15919788 | Furthermore, both compounds increased MAPK(p38) activation, and therefore inhibition of MAPK(p38) amplified thenaringenin- and insulin-induced decrease in apoB100 secretion. |
| 1297 | 15919788 | We conclude that MAPK(erk) signaling in hepatocytes is critical for inhibition of apoB100 secretion by naringenin and insulin. |
| 1298 | 15919788 | Inhibition of microsomal triglyceride transfer protein expression and apolipoprotein B100 secretion by the citrus flavonoid naringenin and by insulin involves activation of the mitogen-activated protein kinase pathway in hepatocytes. |
| 1299 | 15919788 | Microsomal triglyceride transfer protein (MTP) is necessary for hepatocyte assembly and secretion of apolipoprotein (apo)B100-containing lipoproteins. |
| 1300 | 15919788 | The citrus flavonoid naringenin, like insulin, decreased MTP expression in HepG2 cells, resulting in inhibition of apoB100 secretion; however, the mechanism for naringenin is independent of insulin receptor substrate-1/2. |
| 1301 | 15919788 | Recently, it was reported that insulin decreased MTP expression in HepG2 cells via the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) (MAPK(erk)) pathway. |
| 1302 | 15919788 | Inhibition of MAPK kinase (MEK) 1/2 in HepG2 cells significantly attenuated the naringenin- and insulin-induced reduction in MTP expression. |
| 1303 | 15919788 | Both naringenin and insulin increased ERK1/2 phosphorylation, which was completely inhibited by MEK1/2 inhibition and enhanced by inhibition of MAPK(p38), a negative regulator of MAPK(erk) activity. |
| 1304 | 15919788 | Inhibition of MEK1/2 significantly attenuated both the naringenin- and insulin-induced decrease in apoB100 secretion demonstrating a direct link between MAPK(erk) activation and apoB100 secretion. |
| 1305 | 15919788 | Furthermore, both compounds increased MAPK(p38) activation, and therefore inhibition of MAPK(p38) amplified thenaringenin- and insulin-induced decrease in apoB100 secretion. |
| 1306 | 15919788 | We conclude that MAPK(erk) signaling in hepatocytes is critical for inhibition of apoB100 secretion by naringenin and insulin. |
| 1307 | 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). |
| 1308 | 15961791 | A sandwich enzyme-linked immunosorbent assay for human plasma apolipoprotein A-V concentration. |
| 1309 | 15961791 | Apolipoprotein A-V (apoA-V) is a recently discovered apolipoprotein that appears to have a role in plasma triglyceride (TG) transport. |
| 1310 | 15961791 | The ELISA was then used to quantify plasma apoA-V in 196 healthy subjects and 106 patients with insulin-resistant diabetes mellitus. |
| 1311 | 15961791 | A sandwich enzyme-linked immunosorbent assay for human plasma apolipoprotein A-V concentration. |
| 1312 | 15961791 | Apolipoprotein A-V (apoA-V) is a recently discovered apolipoprotein that appears to have a role in plasma triglyceride (TG) transport. |
| 1313 | 15961791 | The ELISA was then used to quantify plasma apoA-V in 196 healthy subjects and 106 patients with insulin-resistant diabetes mellitus. |
| 1314 | 15983222 | The ATP-binding cassette transporter A1 (ABCA1) is an atheroprotective cell protein that mediates cholesterol transport from cells to apolipoprotein (apo) A-I, the major protein in HDL. |
| 1315 | 15983222 | These results raise the possibility that reactive carbonyl-mediated damage to ABCA1 promotes accumulation of cholesterol in arterial macrophages and thus contribute to the increased cardiovascular disease associated with diabetes, insulin resistance, and other inflammatory conditions. |
| 1316 | 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. |
| 1317 | 15983229 | Black CC homozygotes had lower baseline lipoprotein lipase activity, HDL cholesterol, HDL3, and apolipoprotein (apo)A-1 concentrations. |
| 1318 | 15983229 | White CC homozygotes had lower baseline HDL cholesterol, apoA-1, LDL cholesterol, and apoB levels that remained low post-exercise training. |
| 1319 | 15995172 | The sdLDLs of both types of patients were enriched in apolipoprotein C-III (apoC-III) and were depleted of apoC-I, apoA-I, and apoE compared with matched healthy controls with the A phenotype. |
| 1320 | 16005361 | Evaluation of apolipoprotein E secretion by macrophages in type 2 diabetic patients: role of HDL and apolipoprotein A-I. |
| 1321 | 16005361 | It has been shown that apolipoprotein A-I (ApoA-I) stimulates the secretion of apolipoprotein E (ApoE) from human macrophages. |
| 1322 | 16005361 | Evaluation of apolipoprotein E secretion by macrophages in type 2 diabetic patients: role of HDL and apolipoprotein A-I. |
| 1323 | 16005361 | It has been shown that apolipoprotein A-I (ApoA-I) stimulates the secretion of apolipoprotein E (ApoE) from human macrophages. |
| 1324 | 16006255 | Circulating levels of nitrated apolipoprotein A-I are increased in type 2 diabetic patients. |
| 1325 | 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. |
| 1326 | 16006255 | Circulating levels of nitrated apolipoprotein A-I are increased in type 2 diabetic patients. |
| 1327 | 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. |
| 1328 | 16014756 | The aim of this work was to study the influence of atorvastatin on apoAI and apoE kinetics and to determine whether its hypocholesterolemic and hypotriglyceridemic effects could be related to changes in this apolipoprotein metabolism. |
| 1329 | 16014756 | The increased number of apoE per VLDL particle suggests that atorvastatin could enhance the direct catabolism of triglyceride-rich VLDL through apoE receptor pathways. |
| 1330 | 16039297 | Since the recently discovered apolipoprotein (apo) AV was identified as a modulator of triglyceride (TG) metabolism, the aim of the study was to determine the postprandial apoAV profile of Type 2 diabetic patients. |
| 1331 | 16039297 | Postprandial apoAV was elevated in diabetic patients but no correlation was observed either with plasma TG concentration or with the intensity of lipoprotein lipase-dependent lipolysis. |
| 1332 | 16091481 | Comparison of apolipoprotein B100 metabolism between continuous subcutaneous and intraperitoneal insulin therapy in type 1 diabetes. |
| 1333 | 16125536 | At baseline and the end of the study, subjects gave blood tests for the determination of Lp(a), CRP, homocysteine, fibrinogen, serum lipids, apolipoprotein (apo) A-I, and apo B. |
| 1334 | 16142021 | Combination of apolipoprotein E2 and lipoprotein lipase heterozygosity causes severe hypertriglyceridemia during pregnancy. |
| 1335 | 16142021 | The occurrence of marked hypertriglyceridemia (HTG) is rare and may result from combination of heterozygote mutation in the lipoprotein lipase (LPL) gene and apolipoprotein E2 isoform, as reported in this case. |
| 1336 | 16142021 | Combination of apolipoprotein E2 and lipoprotein lipase heterozygosity causes severe hypertriglyceridemia during pregnancy. |
| 1337 | 16142021 | The occurrence of marked hypertriglyceridemia (HTG) is rare and may result from combination of heterozygote mutation in the lipoprotein lipase (LPL) gene and apolipoprotein E2 isoform, as reported in this case. |
| 1338 | 16155262 | Hypovitaminosis D is associated with reductions in serum apolipoprotein A-I but not with fasting lipids in British Bangladeshis. |
| 1339 | 16188578 | Hypoadiponectinemia of 1.7 microg/ml was also revealed, which may, in part, account for the insulin resistance and decreased LPL activity. |
| 1340 | 16188578 | In conclusion, the clustering of apolipoprotein E4/4 and hypoadiponectinemia, in addition to insulin resistance and poor glycemic control, might have resulted in hypertriglyceridemia with eruptive xanthomatosis in this subject. |
| 1341 | 16223942 | Mechanisms of mutual functional interactions between HNF-4alpha and HNF-1alpha revealed by mutations that cause maturity onset diabetes of the young. |
| 1342 | 16223942 | HNF-4alpha and HNF-1alpha cooperatively activate genes with binding sites for both factors, whereas suppressive interactions occur at regulatory sequences with a binding site for only one factor. |
| 1343 | 16223942 | The liver fatty acid binding protein gene (Fabp1) has binding sites for both factors, and chromatin precipitation assays were utilized to demonstrate that HNF-4alpha increased HNF-1alpha Fabp1 promoter occupancy during cooperative transcriptional activation. |
| 1344 | 16223942 | The HNF4 P2 promoter contains a HNF-1 but not HNF-4 binding site, and HNF-4alpha suppressed HNF-1alpha HNF4 P2 activation and decreased promoter HNF-1alpha occupancy. |
| 1345 | 16223942 | The apolipoprotein C III (APOC3) promoter contains a HNF-4 but not HNF-1 binding site, and HNF-1alpha suppressed HNF-4alpha APOC3 activation and decreased HNF-4alpha promoter occupancy. |
| 1346 | 16223942 | Maturity onset diabetes of the young (MODY) as well as defects in hepatic lipid metabolism result from mutations in either HNF-4alpha or HNF-1alpha. |
| 1347 | 16223942 | We found that MODY missense mutant R127W HNF-4alpha retained wild-type individual Fabp1 activation and bound to HNF-1alpha better than wild-type HNF-4alpha, yet did not cooperate with HNF-1alpha or increase HNF-1alpha Fabp1 promoter occupancy. |
| 1348 | 16223942 | The HNF-1alpha R131Q MODY mutant also retained wild-type Fabp1 activation and bound to HNF-4alpha as well as the wild type but was defective in both suppressing HNF-4alpha APOC3 activation and decreasing HNF-4alpha promoter occupancy. |
| 1349 | 16236546 | Members of the steroid receptor superfamily are known to alter the transcription of apolipoprotein AI (apo AI), the major apoprotein of high-density lipoprotein (HDL). |
| 1350 | 16243964 | The effect of select nutrients on serum high-density lipoprotein cholesterol and apolipoprotein A-I levels. |
| 1351 | 16243964 | Multiple potential mechanisms account for the cardioprotective effects of HDL and its main protein apolipoprotein A-I (apo A-I). |
| 1352 | 16243964 | The effect of select nutrients on serum high-density lipoprotein cholesterol and apolipoprotein A-I levels. |
| 1353 | 16243964 | Multiple potential mechanisms account for the cardioprotective effects of HDL and its main protein apolipoprotein A-I (apo A-I). |
| 1354 | 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. |
| 1355 | 16295048 | To elucidate the association of apoE with lipid abnormalities with respect to gender, serum lipid and apolipoprotein levels were compared among apo e2 (e2/2 and e3/2), e3 (e3/3) and e4 (e4/3 and e4/4) groups of T2DM and control subjects. |
| 1356 | 16298371 | Increased apolipoprotein C-III levels associated with insulin resistance contribute to dyslipidemia in normoglycemic and diabetic subjects from a triethnic population. |
| 1357 | 16298371 | Despite the major role of insulin in regulating apolipoprotein C-III (apo C-III) production, little is known about the relationship between apo C-III and insulin resistance. |
| 1358 | 16298371 | Increased apolipoprotein C-III levels associated with insulin resistance contribute to dyslipidemia in normoglycemic and diabetic subjects from a triethnic population. |
| 1359 | 16298371 | Despite the major role of insulin in regulating apolipoprotein C-III (apo C-III) production, little is known about the relationship between apo C-III and insulin resistance. |
| 1360 | 16319046 | The aim of this study was to evaluate the effect of a low-saturated-fat, low-cholesterol diet on plasma lipopoproteins, pre beta-high density lipoprotein (HDL) formation, lecithin:cholesterol acyltransferase (LCAT), cholesteryl ester transfer protein (CETP) and phospholipid transfer protein (PLTP) activities, as well as on the ability of plasma to stimulate cellular cholesterol efflux. |
| 1361 | 16319046 | Plasma LCAT, CETP and PLTP activities were assayed by exogenous substrate methods. |
| 1362 | 16319046 | The changes in plasma total cholesterol, very low and low-density lipoprotein (VLDL+LDL) cholesterol, HDL cholesterol, HDL phospholipids, apolipoprotein (apo) A-I, plasma LCAT activity and PLTP activity were not significant. |
| 1363 | 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. |
| 1364 | 16343038 | To evaluate the influence of cholesterol ester transfer protein (CETP) TaqIB polymorphism, lipoprotein lipase (LPL) PvuII and HindIII polymorphisms, hepatic lipase (LIPC) G-250A polymorphism and apolipoprotein C-III (APOC3) SstI gene polymorphism on lipid levels in dyslipidemia of the metabolic syndrome, 150 patients with dyslipidemia of metabolic syndrome were included. 96 % of patients had type 2 diabetes. |
| 1365 | 16343038 | The apoB level was significantly higher in patients with S1S1 genotype of APOC3 SstI polymorphism when compared with S1S2 group (1.10+/-0.26 vs. 0.98+/-0.21 g/l, p=0.02). |
| 1366 | 16343038 | Similarly, patients with H-H- genotype of LPL HindIII polymorphism had significantly higher mean apoB, compared with H+H- and H+H+ group (1.35+/-0.30 vs. 1.10+/-0.26 g/l, p=0.02). |
| 1367 | 16343038 | In the multiple stepwise linear regression analysis, apoB level seemed to be influenced by APOC3 SstI genotype, which explained 6 % of its variance. |
| 1368 | 16343038 | The present study has shown that the S1 allele of APOC3 SstI polymorphism and the H- allele of LPL HindIII polymorphism might have a small effect on apoB levels in the Central European Caucasian population with dyslipidemia of metabolic syndrome. |
| 1369 | 16375582 | The -1131T-->C polymorphism of the apolipoprotein A-V gene (APO A-V) is tightly linked to lipid metabolism and has been associated with increased triglyceride levels and familial dyslipidemia. |
| 1370 | 16399206 | Insulin, insulin-degrading enzyme and amyloid-beta peptide in Alzheimer's disease: review and hypothesis. |
| 1371 | 16399206 | The link between hyperinsulinaemia and AD may be insulin-degrading enzyme (IDE). |
| 1372 | 16399206 | This enzyme degrades both insulin and amylin, peptides related to the pathology of type 2 diabetes, along with amyloid-beta peptide (Abeta), a short peptide found in excess in the AD brain. |
| 1373 | 16399206 | We review the current evidence, which suggests that hyperinsulinaemia may elevate Abeta through insulin's competition with Abeta for IDE. |
| 1374 | 16399206 | The deficiency of IDE can be caused by genetic variation or by the diversion of IDE from the metabolism of Abeta to the metabolism of insulin. |
| 1375 | 16399206 | It is intriguing to notice that both hyperinsulinaemia and IDE gene variations are related to the risk of AD when the Apolipoprotein E4 (ApoE4) allele, the major risk factor of late-onset AD, is not present. |
| 1376 | 16401881 | Mass kinetics of apolipoprotein A-I in interstitial fluid after administration of intravenous apolipoprotein A-I/lecithin discs in humans. |
| 1377 | 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. |
| 1378 | 16401881 | Mass kinetics of apolipoprotein A-I in interstitial fluid after administration of intravenous apolipoprotein A-I/lecithin discs in humans. |
| 1379 | 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. |
| 1380 | 16423621 | Ascorbic acid and alpha-tocopherol down-regulate apolipoprotein A-I gene expression in HepG2 and Caco-2 cell lines. |
| 1381 | 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. |
| 1382 | 16423621 | Ascorbic acid and alpha-tocopherol down-regulate apolipoprotein A-I gene expression in HepG2 and Caco-2 cell lines. |
| 1383 | 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. |
| 1384 | 16448983 | Recently, apolipoprotein A5 (APOA5) was identified as a novel member of the APOA1/C3/A4 gene cluster. |
| 1385 | 16448983 | Data from mice over-expressing or lacking APOA5 provide direct evidence that this apolipoprotein plays a role in triglyceride metabolism. |
| 1386 | 16448983 | Insulin and interleukins regulate APOA5 gene expression and provide novel clues for the role of this apolipoprotein. |
| 1387 | 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. |
| 1388 | 16475830 | Inhibition of apolipoprotein AI gene expression by tumor necrosis factor alpha: roles for MEK/ERK and JNK signaling. |
| 1389 | 16475830 | Plasma high-density lipoprotein and apolipoprotein AI (apoAI) levels are suppressed by tumor necrosis factor alpha. |
| 1390 | 16475830 | Exogenous ERK1 and ERK2 expression suppressed basal apoAI promoter activity; however, only ERK2 enhanced the ability of TNF alpha to suppress apoAI promoter activity. |
| 1391 | 16475830 | Exogenous expression of all three MEK isoforms (MEK1, MEK2A, and MEK2E) suppressed basal apoAI promoter activity and further aggravated TNF alpha-related apoAI promoter activity inhibition. |
| 1392 | 16475830 | Treatment with SB202190 (p38 MAP kinase inhibitor) alone significantly increased apoAI promoter activity; however, in the presence of TNF alpha, apoAI promoter activity was suppressed to an extent similar to that in cells not treated with SB202190. |
| 1393 | 16475830 | ApoAI promoter activity increased in cells treated with the specific JNK inhibitor SP600125, but unlike SB202190 treatment, the level of TNF alpha-related apoAI promoter inhibition was reduced by 50%. |
| 1394 | 16475830 | Similarly, the level of TNF alpha-related apoAI promoter inhibition was reduced in cells transfected with JNK1 siRNA. |
| 1395 | 16475830 | Finally, treatment of cells with the NF-kappaB inhibitors BAY and SN-50 or overexpression of NF-kappaB subunits p50 and p65 had no effect on the ability of TNF alpha to repress apoAI promoter activity. |
| 1396 | 16475830 | These results suggest that TNF alpha suppresses apoAI promoter activity through both the MEK/ERK and JNK pathways but is not mediated by either p38 MAP kinase activity or NF-kappaB activation. |
| 1397 | 16475830 | Inhibition of apolipoprotein AI gene expression by tumor necrosis factor alpha: roles for MEK/ERK and JNK signaling. |
| 1398 | 16475830 | Plasma high-density lipoprotein and apolipoprotein AI (apoAI) levels are suppressed by tumor necrosis factor alpha. |
| 1399 | 16475830 | Exogenous ERK1 and ERK2 expression suppressed basal apoAI promoter activity; however, only ERK2 enhanced the ability of TNF alpha to suppress apoAI promoter activity. |
| 1400 | 16475830 | Exogenous expression of all three MEK isoforms (MEK1, MEK2A, and MEK2E) suppressed basal apoAI promoter activity and further aggravated TNF alpha-related apoAI promoter activity inhibition. |
| 1401 | 16475830 | Treatment with SB202190 (p38 MAP kinase inhibitor) alone significantly increased apoAI promoter activity; however, in the presence of TNF alpha, apoAI promoter activity was suppressed to an extent similar to that in cells not treated with SB202190. |
| 1402 | 16475830 | ApoAI promoter activity increased in cells treated with the specific JNK inhibitor SP600125, but unlike SB202190 treatment, the level of TNF alpha-related apoAI promoter inhibition was reduced by 50%. |
| 1403 | 16475830 | Similarly, the level of TNF alpha-related apoAI promoter inhibition was reduced in cells transfected with JNK1 siRNA. |
| 1404 | 16475830 | Finally, treatment of cells with the NF-kappaB inhibitors BAY and SN-50 or overexpression of NF-kappaB subunits p50 and p65 had no effect on the ability of TNF alpha to repress apoAI promoter activity. |
| 1405 | 16475830 | These results suggest that TNF alpha suppresses apoAI promoter activity through both the MEK/ERK and JNK pathways but is not mediated by either p38 MAP kinase activity or NF-kappaB activation. |
| 1406 | 16500635 | Lower serum paraoxonase-1 activity in type 2 diabetic patients correlates with nitrated apolipoprotein A-I levels. |
| 1407 | 16505251 | Genetic variation within the apolipoprotein CIII (apoCIII) gene alters apoCIII levels, which are increased in type 1 diabetes and induce beta-cell apoptosis. |
| 1408 | 16505860 | Formation of small, dense HDL particles with attenuated antiatherogenic activity can be mechanistically related to HDL enrichment in triglycerides and in serum amyloid A, depletion of cholesteryl esters, covalent modification of HDL apolipoproteins and attenuated antiatherogenic function of apolipoprotein AI. |
| 1409 | 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). |
| 1410 | 16596812 | Apolipoprotein (apo)B that constitutes the essential structural protein of these lipoproteins exists in two forms, the full length form apoB-100 and the carboxy-terminal truncated apoB-48. |
| 1411 | 16603689 | Neither ATP-binding cassette transporter G1 (ABCG1)- nor scavenger receptor class B type I (SR-BI)-mediated cholesterol efflux was affected. |
| 1412 | 16603689 | Cellular cholesterol efflux to apolipoprotein A-I was not significantly reduced in Cav-1(-/-) MPMs compared with wild-type MPMs. |
| 1413 | 16603689 | However, ABCA1-mediated cholesterol efflux was clearly more sensitive to the inhibitory effects of glyburide in Cav-1(-/-) MPMs versus WT MPMs. |
| 1414 | 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. |
| 1415 | 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. |
| 1416 | 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. |
| 1417 | 16644688 | Intestinal insulin resistance and aberrant production of apolipoprotein B48 lipoproteins in an animal model of insulin resistance and metabolic dyslipidemia: evidence for activation of protein tyrosine phosphatase-1B, extracellular signal-related kinase, and sterol regulatory element-binding protein-1c in the fructose-fed hamster intestine. |
| 1418 | 16644688 | Intestinal lipoprotein production in chow-fed hamsters was responsive to the inhibitory effects of insulin, and a decrease in circulating levels of triglyceride-rich apolipoprotein (apo)B48-containing lipoproteins occurred 60 min after insulin administration. |
| 1419 | 16644688 | However, fructose-fed hamster intestine was not responsive to the insulin-induced downregulation of apoB48-lipoprotein production, suggesting insulin insensitivity at the level of the intestine. |
| 1420 | 16644688 | Enterocytes from the fructose-fed hamster exhibited normal activity of the insulin receptor but reduced levels of insulin receptor substrate-1 phosphorylation and mass and Akt protein mass. |
| 1421 | 16644688 | Conversely, the protein mass of the p110 subunit of phosphatidylinositol 3-kinase, protein tyrosine phosphatase-1B, and basal levels of phosphorylated extracellular signal-related kinase (ERK) were significantly increased in the fructose-fed hamster intestine. |
| 1422 | 16644688 | Modulating the ERK pathway through in vivo inhibition of mitogen-activated protein/ERK kinase 1/2, the upstream activator of ERK1/2, we observed a significant decrease in intestinal apoB48 synthesis and secretion. |
| 1423 | 16644688 | Interestingly, enhanced basal ERK activity in the fructose-fed hamster intestine was accompanied by an increased activation of sterol regulatory element-binding protein. |
| 1424 | 16644688 | In summary, these data suggest that insulin insensitivity at the level of the intestine and aberrant insulin signaling are important underlying factors in intestinal overproduction of highly atherogenic apoB48-containing lipoproteins in the insulin-resistant state. |
| 1425 | 16644688 | Basal activation of the ERK pathway may be an important contributor to the aberrant insulin signaling and lipoprotein overproduction in this model. |
| 1426 | 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. |
| 1427 | 16770585 | The apolipoprotein A-IV Gln360His polymorphism predicts progression of coronary artery calcification in patients with type 1 diabetes. |
| 1428 | 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. |
| 1429 | 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). |
| 1430 | 16873686 | To examine the effect of alpha-lipoic acid, a potent natural antioxidant, on atherosclerosis in diabetic mice, 3-month-old apolipoprotein (apo) E-deficient (apoE(-/-)) mice were made diabetic by administering streptozotocin (STZ). |
| 1431 | 16901410 | The mechanism for these effects is still being clarified, but may involve enhancement of triglyceride clearance (in the case of pioglitazone), alteration of apolipoprotein C-III levels, reduction of hepatic lipase, and increase in ATP binding cassette A1 (ABCA1) activity. |
| 1432 | 16917759 | The apolipoprotein A-V genotype and plasma apolipoprotein A-V and triglyceride levels: prospective risk of type 2 diabetes. |
| 1433 | 16929032 | Apolipoprotein A-IV is regulated by nutritional and metabolic stress: involvement of glucocorticoids, HNF-4 alpha, and PGC-1 alpha. |
| 1434 | 16929032 | Apolipoprotein A-IV (apoA-IV) is a 46 kDa glycoprotein that associates with triglyceride-rich and high density lipoproteins. |
| 1435 | 16929032 | Reporter gene analysis of the murine and human apoA-IV/C-III promoters revealed a conserved cooperative activation by the hepatic nuclear factor-4 alpha (HNF-4 alpha) and the peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha) but no evidence of a direct regulatory role for the glucocorticoid receptor. |
| 1436 | 16929032 | Consistent with these in vitro data, induction of apoA-IV in response to fasting was accompanied by increases in HNF-4 alpha and PGC-1 alpha expression and was abolished in liver-specific HNF-4 alpha-deficient mice. |
| 1437 | 16929032 | Together, these results indicate that the induction of apoA-IV expression in fasting and diabetes likely involves PGC-1 alpha-mediated coactivation of HNF-4 alpha in addition to glucocorticoid-dependent actions. |
| 1438 | 16929032 | Apolipoprotein A-IV is regulated by nutritional and metabolic stress: involvement of glucocorticoids, HNF-4 alpha, and PGC-1 alpha. |
| 1439 | 16929032 | Apolipoprotein A-IV (apoA-IV) is a 46 kDa glycoprotein that associates with triglyceride-rich and high density lipoproteins. |
| 1440 | 16929032 | Reporter gene analysis of the murine and human apoA-IV/C-III promoters revealed a conserved cooperative activation by the hepatic nuclear factor-4 alpha (HNF-4 alpha) and the peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha) but no evidence of a direct regulatory role for the glucocorticoid receptor. |
| 1441 | 16929032 | Consistent with these in vitro data, induction of apoA-IV in response to fasting was accompanied by increases in HNF-4 alpha and PGC-1 alpha expression and was abolished in liver-specific HNF-4 alpha-deficient mice. |
| 1442 | 16929032 | Together, these results indicate that the induction of apoA-IV expression in fasting and diabetes likely involves PGC-1 alpha-mediated coactivation of HNF-4 alpha in addition to glucocorticoid-dependent actions. |
| 1443 | 16949016 | Several enteroendocrine cells produce numerous peptides codifying either orexigenic (ghrelin, orexins) or anorexigenic signals (pancreatic polypeptide, peptide YY, cholecystokinin, amylin, bombesin homologs, apolipoprotein A-IV, glucose-dependent insulinotropic polypeptide, glucagon-like peptide 1, oxyntomodulin), which interact in a complex network with other peripheral signals of energy balance and with different neuropeptides involved in the central control of appetite and energy homeostasis. |
| 1444 | 16949383 | ESR1 rs3798577 was significantly associated with circulating estradiol concentrations, indicators of ovarian aging, high-density lipoprotein (HDL) cholesterol, apolipoprotein A-1, insulin sensitivity, and lumbar spine BMD. |
| 1445 | 16956892 | ApoO, a novel apolipoprotein, is an original glycoprotein up-regulated by diabetes in human heart. |
| 1446 | 16956892 | Chondroitinase ABC deglycosylation analysis or cell incubation with p-nitrophenyl-beta-d-xyloside indicated that apolipoprotein O belongs to the proteoglycan family. |
| 1447 | 16956892 | Naringenin or CP-346086 treatments indicated that apolipoprotein O secretion requires microsomal triglyceride transfer protein activity. |
| 1448 | 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. |
| 1449 | 16990839 | Apolipoprotein A-I mimetic peptides and their role in atherosclerosis prevention. |
| 1450 | 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. |
| 1451 | 16990839 | Apolipoprotein A-I mimetic peptides and their role in atherosclerosis prevention. |
| 1452 | 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. |
| 1453 | 17018885 | Reduction of plasma triglycerides in apolipoprotein C-II transgenic mice overexpressing lipoprotein lipase in muscle. |
| 1454 | 17018885 | LPL and its specific physiological activator, apolipoprotein C-II (apoC-II), regulate the hydrolysis of triglycerides (TGs) from circulating TG-rich lipoproteins. |
| 1455 | 17018885 | Reduction of plasma triglycerides in apolipoprotein C-II transgenic mice overexpressing lipoprotein lipase in muscle. |
| 1456 | 17018885 | LPL and its specific physiological activator, apolipoprotein C-II (apoC-II), regulate the hydrolysis of triglycerides (TGs) from circulating TG-rich lipoproteins. |
| 1457 | 17018886 | Plasma levels of apolipoprotein A-V (apoA-V), apoC-II, and apoC-III were measured in the fasting state and 2 h postprandially. |
| 1458 | 17058629 | Other parameters demonstrating greater improvement with ezetimibe included triglycerides, apolipoprotein (Apo)B/Apo A-I ratio, high-density lipoprotein cholesterol (HDL-C), and C-reactive protein. |
| 1459 | 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. |
| 1460 | 17082477 | Oxidative modification of the apolipoprotein A-I inhibits reverse cholesterol transport. |
| 1461 | 17102149 | Apolipoprotein C-III is excluded from the most abundant LDL (i.e., that of intermediate density: 1.034 < d < 1.050 g/ml) but associated with both small and large LDL(-). |
| 1462 | 17141785 | No change in apolipoprotein AI metabolism when subcutaneous insulin infusion is replaced by intraperitoneal insulin infusion in type 1 diabetic patients. |
| 1463 | 17141785 | This stable isotope kinetic study was designed to compare HDL apolipoprotein (apo) AI metabolism in seven type 1 diabetic patients first treated by continuous subcutaneous insulin infusion by an external pump and then 3 months after the beginning of intraperitoneal insulin infusion by an implantable pump. |
| 1464 | 17141785 | No change in apolipoprotein AI metabolism when subcutaneous insulin infusion is replaced by intraperitoneal insulin infusion in type 1 diabetic patients. |
| 1465 | 17141785 | This stable isotope kinetic study was designed to compare HDL apolipoprotein (apo) AI metabolism in seven type 1 diabetic patients first treated by continuous subcutaneous insulin infusion by an external pump and then 3 months after the beginning of intraperitoneal insulin infusion by an implantable pump. |
| 1466 | 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. |
| 1467 | 17192696 | Apolipoprotein (apo) J, clusterin, is ubiquitously expressed in many tissues, and is a component of high-density lipoproteins (HDLs). |
| 1468 | 17199733 | Metabolism of high density lipoprotein apolipoprotein A-I and cholesteryl ester in insulin resistant dog: a stable isotope study. |
| 1469 | 17216278 | The impact of glycation on apolipoprotein A-I structure and its ability to activate lecithin:cholesterol acyltransferase. |
| 1470 | 17259391 | Tumor necrosis factor-alpha induces intestinal insulin resistance and stimulates the overproduction of intestinal apolipoprotein B48-containing lipoproteins. |
| 1471 | 17259391 | There is growing evidence suggesting intestinal insulin resistance and overproduction of apolipoprotein (apo) B48-containing chylomicrons in insulin-resistant states. |
| 1472 | 17259391 | In the current study, we investigated the potential role of the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the development of insulin resistance and aberrant lipoprotein metabolism in the small intestine in a Syrian golden hamster model. |
| 1473 | 17259391 | TNF-alpha infusion decreased whole-body insulin sensitivity, based on in vivo euglycemic clamp studies in chow-fed hamsters. |
| 1474 | 17259391 | Analysis of intestinal tissue in TNF-alpha-treated hamsters indicated impaired phosphorylation of insulin receptor-beta, insulin receptor substrate-1, Akt, and Shc and increased phosphorylation of p38, extracellular signal-related kinase-1/2, and Jun NH(2)-terminal kinase. |
| 1475 | 17259391 | TNF-alpha infusion also increased intestinal production of total apoB48, triglyceride-rich lipoprotein apoB48, and serum triglyceride levels in both fasting and postprandial (fat load) states. |
| 1476 | 17259391 | The effects of TNF-alpha on plasma apoB48 levels could be blocked by the p38 inhibitor SB203580. |
| 1477 | 17259391 | Ex vivo experiments using freshly isolated enterocytes also showed TNF-alpha-induced p38 phosphorylation and intestinal apoB48 overproduction, effects that could be blocked by SB203580. |
| 1478 | 17259391 | Interestingly, TNF-alpha increased the mRNA and protein mass of intestinal microsomal triglyceride transfer protein without altering apoB mRNA levels. |
| 1479 | 17259391 | Enterocytes were found to have detectable levels of both TNF-alpha receptor types (p55 and p75), and antibodies against either of the two TNF-alpha receptors partially blocked the stimulatory effect of TNF-alpha on apoB48 production and p38 phosphorylation. |
| 1480 | 17259391 | In summary, these data suggest that intestinal insulin resistance can be induced in hamsters by TNF-alpha infusion, and it is accompanied by intestinal overproduction of apoB48-containing lipoproteins. |
| 1481 | 17259391 | TNF-alpha-induced stimulation of intestinal lipoprotein production appears to be mediated via TNF-alpha receptors and the p38 mitogen-activated protein kinase pathway. |
| 1482 | 17267050 | Serum amyloid A (SAA), a HDL apolipoprotein is a risk marker for cardiovascular disease. |
| 1483 | 17267050 | TNF-alpha, IL-1beta, IL-8 and IL-1ra levels were measured by ELISA in the culture supernatants and in serum of subjects. |
| 1484 | 17267050 | We make the novel observation that neutrophils and monocytes of diabetics are more responsive to SAA for the induction of the proinflammatory cytokine IL-1beta and the proangiogenic and chemotactic protein IL-8. |
| 1485 | 17267050 | Incremental TNF-alpha production was also found to occur when monocytes were stimulated with SAA. |
| 1486 | 17269729 | Among these identified proteins, two proteins which might be useful as diagnostic biomarkers of type 2 diabetics with nephropathy were verified by Western blotting: extracellular glutathione peroxidase (eGPx) and apolipoprotein (ApoE) were found to exhibit a progressive reduction in MA and CRF groups. |
| 1487 | 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. |
| 1488 | 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). |
| 1489 | 17310220 | A preliminary survey by protein analysis rather than classical nucleic acid sequencing methods has suggested a correlation between a newly discovered T45S variant of apolipoprotein C1 (ApoC1), found only in persons with American Indian or Mexican ancestry, and elevated body mass index (BMI). |
| 1490 | 17379001 | Marked decrease of apolipoprotein A-V in both diabetic and nondiabetic patients with end-stage renal disease. |
| 1491 | 17401142 | The C terminus of apolipoprotein A-V modulates lipid-binding activity. |
| 1492 | 17401142 | Human apolipoprotein A-V (apoA-V) is a potent modulator of plasma triacylglycerol (TG) levels. |
| 1493 | 17401142 | To probe different regions of this 343-amino-acid protein, four single Trp apoA-V variants were prepared. |
| 1494 | 17401142 | The C terminus of apolipoprotein A-V modulates lipid-binding activity. |
| 1495 | 17401142 | Human apolipoprotein A-V (apoA-V) is a potent modulator of plasma triacylglycerol (TG) levels. |
| 1496 | 17401142 | To probe different regions of this 343-amino-acid protein, four single Trp apoA-V variants were prepared. |
| 1497 | 17460328 | Apolipoprotein A-V association with intracellular lipid droplets. |
| 1498 | 17460328 | Apolipoprotein A-V (apoA-V) plays a key role in the regulation of triglyceride (TG) metabolism. |
| 1499 | 17460328 | Given the very low concentration of apoA-V in plasma, we hypothesized that apoA-V may influence plasma TG levels by affecting the assembly and/or secretion of apoB-containing lipoproteins. |
| 1500 | 17460328 | When apoA-V was overexpressed in cultured Hep3B cells, neither the amount of apoB secreted nor the density distribution of apoB-containing lipoproteins was affected. |
| 1501 | 17460328 | Fluorescence microscopy and cell lysate immunoprecipitation studies revealed that apoA-V is not associated with apoB intracellularly, yet immunoprecipitation of apoA-V from the cell culture medium resulted in coprecipitation of apoB. |
| 1502 | 17460328 | These data suggest that the apoA-V association with apoB-containing lipoproteins is a postsecretory event. |
| 1503 | 17460328 | Apolipoprotein A-V association with intracellular lipid droplets. |
| 1504 | 17460328 | Apolipoprotein A-V (apoA-V) plays a key role in the regulation of triglyceride (TG) metabolism. |
| 1505 | 17460328 | Given the very low concentration of apoA-V in plasma, we hypothesized that apoA-V may influence plasma TG levels by affecting the assembly and/or secretion of apoB-containing lipoproteins. |
| 1506 | 17460328 | When apoA-V was overexpressed in cultured Hep3B cells, neither the amount of apoB secreted nor the density distribution of apoB-containing lipoproteins was affected. |
| 1507 | 17460328 | Fluorescence microscopy and cell lysate immunoprecipitation studies revealed that apoA-V is not associated with apoB intracellularly, yet immunoprecipitation of apoA-V from the cell culture medium resulted in coprecipitation of apoB. |
| 1508 | 17460328 | These data suggest that the apoA-V association with apoB-containing lipoproteins is a postsecretory event. |
| 1509 | 17485571 | The increase of apolipoprotein A-V during postprandial lipemia parallels the response of triglyceride-rich lipoproteins in type 2 diabetes: no relationship between apoA-V and postheparin plasma lipolytic activity. |
| 1510 | 17495607 | Characterization of apolipoprotein A-V structure and mode of plasma triacylglycerol regulation. |
| 1511 | 17525004 | PON1 activity is inversely related to LDL apoB carbonyl content in patients with coronary artery disease. |
| 1512 | 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. |
| 1513 | 17525004 | All subjects were assayed for apoB carbonyl content, LDL-malondialdehyde (LDL-MDA), PON1 activity, and lipid and apolipoprotein levels. |
| 1514 | 17525004 | A significantly (p < 0.01) negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 1515 | 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. |
| 1516 | 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. |
| 1517 | 17525004 | A significantly negative coefficient of correlation was observed between apoB carbonyl content and PON1 activity in both patients and controls. |
| 1518 | 17639303 | Apolipoprotein A-I stimulates AMP-activated protein kinase and improves glucose metabolism. |
| 1519 | 17697528 | Study of ATP-binding cassette transporter A1 (ABCA1)-mediated cellular cholesterol efflux in diabetic golden hamsters. |
| 1520 | 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. |
| 1521 | 17697528 | Peritoneal macrophages were incubated with apolipoprotein A-1 (apoA-1), 8-bromoadenosine-3',5'-cyclic monophosphate (8-br-cAMP), and atorvastatin in vitro. |
| 1522 | 17726453 | Allelic variation in ApoC3, ApoA5 and LPL genes and first and second generation antipsychotic effects on serum lipids in patients with schizophrenia. |
| 1523 | 17726453 | We have investigated in an exploratory study whether polymorphisms in the apolipoprotein C-III (ApoC3), apolipoprotein A-V gene (ApoA5) and lipoprotein lipase genes influence differential lipid response to treatment with three second generation antipsychotics-olanzapine, clozapine and risperidone-or treatment with a first generation antipsychotic. |
| 1524 | 17729183 | Novel therapies to increase apolipoprotein AI and HDL for the treatment of atherosclerosis. |
| 1525 | 17729183 | Apolipoprotein AI (apoAI) is the major protein component of HDL, and thus has an important role in the treatment of atherosclerosis. |
| 1526 | 17729183 | Novel therapies to increase apolipoprotein AI and HDL for the treatment of atherosclerosis. |
| 1527 | 17729183 | Apolipoprotein AI (apoAI) is the major protein component of HDL, and thus has an important role in the treatment of atherosclerosis. |
| 1528 | 17823625 | Blood samples were collected before and after treatment for analysis of serum glucose, insulin, lipid profile, apolipoprotein (apo) A1, apo B, and fibrinogen. |
| 1529 | 17848837 | Apolipoprotein E and lipoprotein lipase gene polymorphisms interaction on the atherogenic combined expression of hypertriglyceridemia and hyperapobetalipoproteinemia phenotypes. |
| 1530 | 17848837 | Apolipoprotein (apo) E and lipoprotein lipase (LPL) genes are involved in the catabolism of triglycerides (TG)-rich apoB-containing lipoproteins (VLDL). |
| 1531 | 17848837 | Several apoE and LPL gene variants affecting CAD risk, plasma TG or apoB concentrations have an allelic frequency of >5% in the general population. |
| 1532 | 17848837 | This study examined the combined effect of frequent apoE and LPL gene polymorphisms on the expression of hyperTG and hyperapoB. |
| 1533 | 17848837 | ApoE (E2, E3, and E4) and LPL (D9N, N291S, G188E, and P207L) were genotyped and fasting lipid profiles were assessed among 1,441 French-Canadian subjects. |
| 1534 | 17848837 | Multivariate analyses were performed to estimate the relationship between apoE and LPL gene variants and the risk of hyperTG (TG>1.7 mmol/l) and hyperapoB (apoB>0.9 g/l). |
| 1535 | 17872455 | Pioglitazone stimulates apolipoprotein A-I production without affecting HDL removal in HepG2 cells: involvement of PPAR-alpha. |
| 1536 | 17872464 | For atherosclerotic background we used low-density lipoprotein receptor-deficient mice synthetizing only apolipoprotein B100 (LDLR(-/-) ApoB(100/100)). |
| 1537 | 17872464 | Diabetic background was obtained from transgenic mice overexpressing insulin-like growth factor-II (IGF-II) in pancreatic beta cells. |
| 1538 | 17872464 | Results indicated that IGF-II transgenic LDLR(-/-)ApoB(100/100) mice demonstrated insulin resistance, hyperglycemia, and mild hyperinsulinemia compared with hypercholesterolemic LDLR(-/-)ApoB(100/100) controls. |
| 1539 | 17872464 | In addition, old IGF-II/LDLR(-/-)ApoB(100/100) mice displayed significantly increased lesion calcification, which was more related to insulin resistance than glucose levels, and significantly higher baseline expression in aorta of several genes related to calcification and inflammation. |
| 1540 | 17872464 | Lipid levels of IGF-II/LDLR(-/-)ApoB(100/100) mice did not differ from LDLR(-/-)ApoB(100/100) controls at any time. |
| 1541 | 17884441 | A novel peroxisome proliferator--activated receptor alpha/gamma dual agonist ameliorates dyslipidemia and insulin resistance in prediabetic rhesus monkeys. |
| 1542 | 17884441 | Plasma triglyceride and apolipoprotein B-100 levels decreased, whereas apolipoprotein A-I increased during TAK-559 treatment. |
| 1543 | 17907111 | This randomised, double-blind, parallel-group study assessed the effects of addition of the dual peroxisome proliferator-activated receptor (PPAR) alpha/gamma agonist, tesaglitazar, for 24 weeks to the therapeutic regimen of 392 poorly controlled (glycosylated haemoglobin [HbA1C] 7.5-10%) insulin-treated, type 2 diabetes patients. |
| 1544 | 17907111 | After 24 weeks, tesaglitazar caused greater improvements from baseline in triglycerides (p<0.0001), high-density lipoprotein cholesterol (HDL-C) (p<0.001), non-HDL-C (p<0.05), apolipoprotein (apo)A-I (p<0.05) and apoB levels (p<0.01) than placebo. |
| 1545 | 17923573 | Apolipoprotein A-II is inversely associated with risk of future coronary artery disease. |
| 1546 | 18056685 | Effect of apolipoprotein A-V on plasma triglyceride, lipoprotein size, and composition in genetically engineered mice. |
| 1547 | 18056685 | Transgenic (Tg) mice that overexpress the human apolipoprotein A-V gene (APOA5) yet lack an endogenous mouse apoa5 gene (APOA5 Tg mice) were generated. |
| 1548 | 18056685 | Subsequently, the effect of human apoA-V expression on plasma triglyceride (TG) concentration and lipoprotein and apolipoprotein distribution was determined and compared with that in mice deficient in apoA-V (apoa5(-/-) mice). |
| 1549 | 18056685 | SDS-PAGE analysis of the d < 1.063 g/ml plasma fraction revealed that the apoB-100/apoB-48 ratio was 14-fold higher in APOA5 Tg versus apoa5(-/-) mice and that the apoE/total apoB ratio was 7-fold greater in APOA5 Tg versus apoa5(-/-) mice. |
| 1550 | 18056685 | It is anticipated that a reduction in apoB-100/apoB-48 ratio as well as that for apoE/apoB would impair the uptake of VLDL and remnants in apoa5(-/-) mice, thereby contributing to increased plasma TG levels. |
| 1551 | 18056685 | Effect of apolipoprotein A-V on plasma triglyceride, lipoprotein size, and composition in genetically engineered mice. |
| 1552 | 18056685 | Transgenic (Tg) mice that overexpress the human apolipoprotein A-V gene (APOA5) yet lack an endogenous mouse apoa5 gene (APOA5 Tg mice) were generated. |
| 1553 | 18056685 | Subsequently, the effect of human apoA-V expression on plasma triglyceride (TG) concentration and lipoprotein and apolipoprotein distribution was determined and compared with that in mice deficient in apoA-V (apoa5(-/-) mice). |
| 1554 | 18056685 | SDS-PAGE analysis of the d < 1.063 g/ml plasma fraction revealed that the apoB-100/apoB-48 ratio was 14-fold higher in APOA5 Tg versus apoa5(-/-) mice and that the apoE/total apoB ratio was 7-fold greater in APOA5 Tg versus apoa5(-/-) mice. |
| 1555 | 18056685 | It is anticipated that a reduction in apoB-100/apoB-48 ratio as well as that for apoE/apoB would impair the uptake of VLDL and remnants in apoa5(-/-) mice, thereby contributing to increased plasma TG levels. |
| 1556 | 18056685 | Effect of apolipoprotein A-V on plasma triglyceride, lipoprotein size, and composition in genetically engineered mice. |
| 1557 | 18056685 | Transgenic (Tg) mice that overexpress the human apolipoprotein A-V gene (APOA5) yet lack an endogenous mouse apoa5 gene (APOA5 Tg mice) were generated. |
| 1558 | 18056685 | Subsequently, the effect of human apoA-V expression on plasma triglyceride (TG) concentration and lipoprotein and apolipoprotein distribution was determined and compared with that in mice deficient in apoA-V (apoa5(-/-) mice). |
| 1559 | 18056685 | SDS-PAGE analysis of the d < 1.063 g/ml plasma fraction revealed that the apoB-100/apoB-48 ratio was 14-fold higher in APOA5 Tg versus apoa5(-/-) mice and that the apoE/total apoB ratio was 7-fold greater in APOA5 Tg versus apoa5(-/-) mice. |
| 1560 | 18056685 | It is anticipated that a reduction in apoB-100/apoB-48 ratio as well as that for apoE/apoB would impair the uptake of VLDL and remnants in apoa5(-/-) mice, thereby contributing to increased plasma TG levels. |
| 1561 | 18086004 | Genetic susceptibility factors for late-onset Alzheimer's disease remain largely elusive, with the exception of apolipoprotein E4 (APOE e4) as the only confirmed genetic risk factor. |
| 1562 | 18188530 | A large population (n=552) of cardiovascular patients, without diabetes and/or lipid-lowering therapy, with or without metabolic syndrome (MetSyn), was genotyped for epsilon2/epsilon3/epsilon4 polymorphism and their ApoCIII/ApoE ratio was evaluated. |
| 1563 | 18188530 | The ApoCIII/ ApoE ratio showed an opposite trend, gradually increasing from E2/E2 to E4/E4 subjects. |
| 1564 | 18188530 | ApoE epsilon2/epsilon3/epsilon4 gene polymorphism is a determinant of the relative proportion of apolipoprotein C-III to E. |
| 1565 | 18188530 | Carriers of the unfavourable E4 allele present the highest ApoCIII/ApoE ratio and are twofold more frequent among individuals affected by MetSyn. |
| 1566 | 18191050 | Risk of developing an elevated (> or =2 mg/L) CRP was predicted significantly by baseline CRP in both sexes and by apolipoprotein (apo B), current smoking, and family income in men, when adjusted for 5 further variables. |
| 1567 | 18191056 | The specific impact of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors and fibrates on the in vivo metabolism of apolipoprotein (apo) B has not been systematically investigated in patients with type 2 diabetes mellitus with high plasma triglyceride (TG) levels. |
| 1568 | 18201179 | An ABC of apolipoprotein C-III: a clinically useful new cardiovascular risk factor? |
| 1569 | 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)]. |
| 1570 | 18220942 | Dysregulation of lipoprotein metabolism in these circumstances may be caused by a combination of overproduction of VLDL apolipoprotein (apoB) B-100 and VLDL-apoC-III, decreased catabolism of apoB-containing particles, and increased catabolism of HDL apoA-I particles. |
| 1571 | 18220942 | Newer agents, including insulin sensitizers, cholesterol absorption inhibitors, CETP inhibitors, peroxisome proliferator-activated receptor-delta agonists and endocannabinoid-1 receptor blockers, have also been shown to improve plasma lipid and lipoprotein abnormalities in insulin resistant states; their mechanisms of action are at present being investigated. |
| 1572 | 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). |
| 1573 | 18314464 | HDL subfractions were defined by the presence (LpA-I,A-II) or absence (LpA-I) of apolipoprotein A-II (apoA-II). |
| 1574 | 18332268 | Human apolipoprotein A-I gene transfer reduces the development of experimental diabetic cardiomyopathy. |
| 1575 | 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. |
| 1576 | 18418429 | In all subjects, basal glucose, cholesterol (total, HDL, and LDL), oxidized LDL (OxLDL), triglycerides, apolipoprotein (apo)A1, apoB, and apoE, nonesterified fatty acids, insulin, testosterone, sex hormone-binding globulin, homeostasis model assessment (HOMA) index, and free androgen index were determined in the follicular phase of the cycle. |
| 1577 | 18418429 | Elevated OxLDL and the relation of apoE and nonesterified fatty acids with insulin resistance suggest that women with PCOS are at increased risk for premature atherosclerosis. |
| 1578 | 18421072 | The aim of this study was to evaluate the impact of adipocyte fatty acid binding protein 4 (FABP4) on the lipid profile in type 2 diabetic subjects. |
| 1579 | 18421072 | Plasma levels of FABP4 and adiponectin and an extensive lipid profile were analyzed in 169 type 2 diabetic subjects and 105 controls. |
| 1580 | 18421072 | In type 2 diabetic subjects, FABP4 was positively correlated with plasma triglycerides (P = 0.007), apolipoprotein C-III (apoC-III) (P = 0.009), and all the components of triglyceride-rich lipoproteins, including VLDL triglycerides (P = 0.002), VLDL-cholesterol (P = 0.001), and VLDL apoB (P = 0.001). |
| 1581 | 18421072 | These correlations are not significantly affected by age, gender, body mass index, adiponectin, insulin, or any pharmacological treatment. |
| 1582 | 18421072 | The associations are even stronger when the FABP4/adiponectin ratio is considered. |
| 1583 | 18421072 | High FABP4 and low adiponectin levels are independent predictors of atherogenic dyslipidemia. |
| 1584 | 18421072 | In conclusion, FABP4 plasma concentrations hold strong potential for development as a clinical biomarker for atherogenic dyslipidemia, independent of obesity and insulin resistance, in type 2 diabetic subjects. |
| 1585 | 18437350 | Effects of cross-link breakers, glycation inhibitors and insulin sensitisers on HDL function and the non-enzymatic glycation of apolipoprotein A-I. |
| 1586 | 18450648 | Intracellular lipid droplet targeting by apolipoprotein A-V requires the carboxyl-terminal segment. |
| 1587 | 18450648 | The expression of apolipoprotein A-V (apoA-V) in hepatoma cells results in homing of this protein to intracellular lipid droplets. |
| 1588 | 18450648 | When hepatoma cells transfected with a full-length apoA-V-green fluorescent protein fusion protein were cultured in medium that was not supplemented with oleic acid (OA), intracellular lipid droplet size and number were reduced compared with those of cells supplemented with OA. |
| 1589 | 18450648 | Intracellular lipid droplet targeting by apolipoprotein A-V requires the carboxyl-terminal segment. |
| 1590 | 18450648 | The expression of apolipoprotein A-V (apoA-V) in hepatoma cells results in homing of this protein to intracellular lipid droplets. |
| 1591 | 18450648 | When hepatoma cells transfected with a full-length apoA-V-green fluorescent protein fusion protein were cultured in medium that was not supplemented with oleic acid (OA), intracellular lipid droplet size and number were reduced compared with those of cells supplemented with OA. |
| 1592 | 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. |
| 1593 | 18509206 | Dose-dependent effect of rosuvastatin on VLDL-apolipoprotein C-III kinetics in the metabolic syndrome. |
| 1594 | 18520050 | The blood glucose, hemoglobin A1c, lipid metabolic parameters and hepatic glycogen and triglyceride were measured, and histopathology and peroxisome proliferator-activated receptors (PPARs) alpha/delta/gamma expression of liver were determined by hematoxylin eosin and immunohistochemical staining. |
| 1595 | 18520050 | Berberine restored the increased blood glucose, hemoglobin A1c, total cholesterol, triglyceride, low density lipoprotein-cholesterol, apolipoprotein B and the decreased high density lipoprotein-cholesterol, apolipoprotein AI levels in diabetic rats to near the control ones. |
| 1596 | 18520050 | Berberine increased PPARalpha/delta expression and reduced PPARgamma expression in liver of diabetic rat to near the control ones. |
| 1597 | 18521458 | Apolipoprotein B/apolipoprotein A-I ratio in relation to various definitions of metabolic syndrome among Saudi patients with type 2 diabetes mellitus. |
| 1598 | 18549334 | Mipomersen (ISIS 301012) inhibits human apolipoprotein (apo)B-100 synthesis and lowers circulating apoB and low-density lipoprotein cholesterol levels. |
| 1599 | 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. |
| 1600 | 18622028 | Enhancing apolipoprotein A-I-dependent cholesterol efflux elevates cholesterol export from macrophages in vivo. |
| 1601 | 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. |
| 1602 | 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. |
| 1603 | 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. |
| 1604 | 18622028 | Enhancing apolipoprotein A-I-dependent cholesterol efflux elevates cholesterol export from macrophages in vivo. |
| 1605 | 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. |
| 1606 | 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. |
| 1607 | 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. |
| 1608 | 18676184 | Impaired clearance has long been invoked to explain this accumulation of intestinal TRLs, but more recent studies have highlighted the fact that the production rate of apolipoprotein (apo) B-48-containing particles is also increased in insulin resistance and Type 2 diabetes. |
| 1609 | 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. |
| 1610 | 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. |
| 1611 | 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. |
| 1612 | 18993152 | Furthermore, niacin significantly increased the large alpha-1 apolipoprotein A-I-containing HDL subspecies (12 to 17 nm). |
| 1613 | 19050314 | The ins (cell) and outs (plasma) of apolipoprotein A-V. |
| 1614 | 19050314 | Apolipoprotein A-V (apoA-V) has a close interrelationship with plasma triglyceride (TG). |
| 1615 | 19050314 | A sequence element with high positive charge character, between residues 185 and 228, functions in binding of apoA-V to heparan sulfate proteoglycans as well as to members of the low-density lipoprotein receptor family and glycosylphosphatidylinositol high-density lipoprotein binding protein1. |
| 1616 | 19050314 | The ins (cell) and outs (plasma) of apolipoprotein A-V. |
| 1617 | 19050314 | Apolipoprotein A-V (apoA-V) has a close interrelationship with plasma triglyceride (TG). |
| 1618 | 19050314 | A sequence element with high positive charge character, between residues 185 and 228, functions in binding of apoA-V to heparan sulfate proteoglycans as well as to members of the low-density lipoprotein receptor family and glycosylphosphatidylinositol high-density lipoprotein binding protein1. |
| 1619 | 19080728 | Apolipoprotein A-I mimetic peptides. |
| 1620 | 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. |
| 1621 | 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. |
| 1622 | 19080728 | Apolipoprotein A-I mimetic peptides. |
| 1623 | 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. |
| 1624 | 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. |
| 1625 | 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. |
| 1626 | 19125585 | The expression of apolipoprotein A-I was reduced by 4.2-fold, and galectin-1 was increased 4.8 times in diabetic samples. |
| 1627 | 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. |
| 1628 | 19252740 | HNF4alpha and HNF1alpha dysfunction as a molecular rational for cyclosporine induced posttransplantation diabetes mellitus. |
| 1629 | 19252740 | Furthermore, cyclosporine treatment of the insulinoma-1E cell line resulted in remarkable reduction in HNF4alpha protein and INS1 as well as INS2 gene expression, while transcript expression of HNF4alpha, apolipoprotein C2, glycerolkinase, pyruvatekinase and aldolase B was repressed in treated Caco-2 cells. |
| 1630 | 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. |
| 1631 | 19273745 | To investigate the effect of HDL on AT1R expression in vivo, apolipoprotein A-I gene transfer was performed 5 days after streptozotocin injection. |
| 1632 | 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. |
| 1633 | 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. |
| 1634 | 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. |
| 1635 | 19273745 | To investigate the effect of HDL on AT1R expression in vivo, apolipoprotein A-I gene transfer was performed 5 days after streptozotocin injection. |
| 1636 | 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. |
| 1637 | 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. |
| 1638 | 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. |
| 1639 | 19273745 | To investigate the effect of HDL on AT1R expression in vivo, apolipoprotein A-I gene transfer was performed 5 days after streptozotocin injection. |
| 1640 | 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. |
| 1641 | 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. |
| 1642 | 19292868 | Novel genes in cell cycle control and lipid metabolism with dynamically regulated binding sites for sterol regulatory element-binding protein 1 and RNA polymerase II in HepG2 cells detected by chromatin immunoprecipitation with microarray detection. |
| 1643 | 19292868 | Sterol regulatory element-binding proteins 1 and 2 (SREBP-1 and SREBP-2) are important regulators of genes involved in cholesterol and fatty acid metabolism, but have also been implicated in the regulation of the cell cycle and have been associated with the pathogenesis of type 2 diabetes, atherosclerosis and obesity, among others. |
| 1644 | 19292868 | Our data identified novel binding sites for SREBP-1 in genes directly or indirectly involved in cholesterol metabolism, e.g. apolipoprotein C-III (APOC3). |
| 1645 | 19292868 | The most interesting biological findings were the binding sites for SREBP-1 in genes for host cell factor C1 (HCFC1), involved in cell cycle regulation, and for filamin A (FLNA). |
| 1646 | 19292868 | Furthermore, we found evidence of sterol-regulated binding of SREBP-1 and RNA polymerase II to HCFC1 and FLNA. |
| 1647 | 19332654 | Maturation of apolipoprotein A-I: unrecognized health benefit or a forgotten rudiment? |
| 1648 | 19388968 | Carotid intima-media thickness and apolipoprotein B/apolipoprotein A-I ratio in middle-aged patients with Type 2 diabetes. |
| 1649 | 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. |
| 1650 | 19582722 | PTMs, such as glycosylation and phosphorylation of apolipoprotein B100 (apoB), are known to be involved with modulating the metabolism of apoB-containing lipoproteins. |
| 1651 | 19604523 | The following variables were assessed at baseline; after washout; and at 1, 2, and 3 months of treatment: body mass index, fasting plasma glucose, glycosylated hemoglobin, total cholesterol, LDL cholesterol, LDL subclasses, LDL size, high-density lipoprotein cholesterol, triglycerides, apolipoprotein A-1, and apolipoprotein B-100. |
| 1652 | 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. |
| 1653 | 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. |
| 1654 | 19605528 | SPI did not affect serum total cholesterol, HDL cholesterol, triacylglycerol, apolipoprotein B, or apolipoprotein A-I. |
| 1655 | 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. |
| 1656 | 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. |
| 1657 | 19605528 | SPI did not affect serum total cholesterol, HDL cholesterol, triacylglycerol, apolipoprotein B, or apolipoprotein A-I. |
| 1658 | 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. |
| 1659 | 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. |
| 1660 | 19605528 | SPI did not affect serum total cholesterol, HDL cholesterol, triacylglycerol, apolipoprotein B, or apolipoprotein A-I. |
| 1661 | 19817643 | Impaired anti-inflammatory function of apolipoprotein A-II concentrations predicts metabolic syndrome and diabetes at 4 years follow-up in elderly Turks. |
| 1662 | 19825998 | Apolipoprotein A-V N-terminal domain lipid interaction properties in vitro explain the hypertriglyceridemic phenotype associated with natural truncation mutants. |
| 1663 | 19825998 | Fluorescence spectroscopy of single Trp variant apoA-V(1-146) indicates that lipid interaction is accompanied by a conformational change. |
| 1664 | 19828159 | Compared with subjects with isolated IFG, those with isolated IGT appeared to have a higher age- and sex-adjusted brachial-ankle pulse wave velocity (1543 +/- 22 vs 1566 +/- 17, P = .07) and to be more insulin resistant (2-hour postload insulin: 54.2 +/- 2.13 vs 26.8 +/- 2.99 muU/mL, P < .001), had a worse lipid profile (apolipoprotein [apo] B: 1.07 +/- 0.02 vs 0.97 +/- 0.02 g/L, P < .001; apo B/apo A-1 ratio: 0.80 +/- 0.02 vs 0.69 +/- 0.02, P < .001), but had lower glycosylated hemoglobin levels (6.03% +/- 0.06% vs 5.86% +/- 0.04%, P < .001) (values are mean +/- SE). |
| 1665 | 19922961 | Anthropometric parameters, cardiorespiratory capacity, glycemic and lipid profile, apolipoprotein (apo) A-I, apo B, interleukin (IL)-10, IL-18, insulin resistance, and blood pressure were measured before and after 12 months of intervention (P < .05). |
| 1666 | 19922961 | Both RSG and EX groups significantly reduced glycemic indexes, insulin resistance, blood pressure, and IL-18, whereas they significantly increased high-density lipoprotein, cardiorespiratory capacity, and IL-10, compared with CO group (P < .05). |
| 1667 | 19922961 | Notably, the combined treatment group yielded pronounced beneficial changes in glycemic indexes, lipid profile, insulin resistance, blood pressure, IL-10, IL-18, apo A-I, and apo B (vs CO group, P < .05). |
| 1668 | 19922964 | Increased nonenzymatic glycation of apolipoprotein (apo) B-containing lipoproteins impairs uptake and metabolism by the high-affinity low-density lipoprotein receptor and is one of the postsecretory modifications contributory to accelerated atherosclerosis in diabetes. |
| 1669 | 19965573 | Percentage increase in apolipoprotein A-I was virtually identical to that of HDL-C at all doses of the three statins. |
| 1670 | 20005515 | The effect of PPAR-alpha agonism on apolipoprotein metabolism in humans. |
| 1671 | 20005515 | The potent and specific PPAR-alpha agonist LY518674, reduced VLDL apoB-100 levels through enhanced fractional catabolism similar to what is seen with fibrates. |
| 1672 | 20005515 | The changes in apoB metabolism in response to PPAR-alpha activation with fibrates and specific PPAR-alpha agonists would be expected to reduce the risk of cardiovascular disease. |
| 1673 | 20019460 | The mentioned protective protein dysfunctions, firstly described in a general population to date, are high-density lipoprotein (HDL), apolipoprotein (apo) A-I, A-II, and apoC-III, apart from adiponectin. |
| 1674 | 20019460 | Based on published findings of the TARF study, this review discusses the role of inflammatory mediators such as elevated C-reactive protein (CRP), apoB, apoC-III, fibrinogen, and low adiponectin serum levels in cardiometabolic risk comprising MetS, type 2 diabetes, and CHD, the degree of independence of these mediators from the ATP-III-defined MetS, and the influence of sex. |
| 1675 | 20019460 | Moreover, it is emphasized that dysfunctions of adiponectin and protective proteins related to HDL particles increase not only cardiometabolic risk significantly but also CHD risk among half of Turkish adults in a magnitude similar to or greater than that associated with traditional risk factors. |
| 1676 | 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. |
| 1677 | 20110571 | Nonenzymatic glycation impairs the antiinflammatory properties of apolipoprotein A-I. |
| 1678 | 20116212 | Apolipoprotein A-I positively associated with diabetes in women independently of apolipoprotein E genotype and apolipoprotein B levels. |
| 1679 | 20125002 | The promise of apolipoprotein A-I mimetics. |
| 1680 | 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. |
| 1681 | 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. |
| 1682 | 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. |
| 1683 | 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. |
| 1684 | 20153840 | Apolipoprotein A-V associates with intrahepatic lipid droplets and influences triglyceride accumulation. |
| 1685 | 20153840 | Apolipoprotein A-V (apoA-V), secreted solely by the liver, is a low abundance protein that strongly influences plasma triglyceride (TG) levels. |
| 1686 | 20153840 | Apolipoprotein A-V associates with intrahepatic lipid droplets and influences triglyceride accumulation. |
| 1687 | 20153840 | Apolipoprotein A-V (apoA-V), secreted solely by the liver, is a low abundance protein that strongly influences plasma triglyceride (TG) levels. |
| 1688 | 20211930 | Lower HDL-C and apolipoprotein A-I are related to higher glomerular filtration rate in subjects without kidney disease. |
| 1689 | 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. |
| 1690 | 20395699 | Apolipoprotein A-I mimetic peptides: a potential new therapy for the prevention of atherosclerosis. |
| 1691 | 20395699 | The beneficial effects of high-density lipoprotein (HDL) on atherosclerosis have largely been attributed to its major protein, apolipoprotein A-I (apoA-I). |
| 1692 | 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. |
| 1693 | 20395699 | Apolipoprotein A-I mimetic peptides: a potential new therapy for the prevention of atherosclerosis. |
| 1694 | 20395699 | The beneficial effects of high-density lipoprotein (HDL) on atherosclerosis have largely been attributed to its major protein, apolipoprotein A-I (apoA-I). |
| 1695 | 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. |
| 1696 | 20469899 | The carboxyl-terminal segment of apolipoprotein A-V undergoes a lipid-induced conformational change. |
| 1697 | 20469899 | A peptide corresponding to the 48-residue segment beyond the tetraproline motif was generated from a recombinant apoA-V precursor wherein Pro295 was replaced by Met. |
| 1698 | 20500116 | In a multiple regression model, these results were independent of gender, site of onset, history of diabetes mellitus and apolipoprotein (ApoE) genotype. |
| 1699 | 20508181 | Structure/function relationships of apolipoprotein a-I mimetic peptides: implications for antiatherogenic activities of high-density lipoprotein. |
| 1700 | 20538481 | Among traditional cardiovascular risk factors, apolipoprotein (apo)B/apoA1 ratio is considered to have the strongest predictive value for ischemic stroke. |
| 1701 | 20538481 | In this case-control study, we evaluated apoB/apoA1 ratio as a predictor of ischemic stroke in a cohort of elderly subjects. |
| 1702 | 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. |
| 1703 | 20538481 | Stroke patients exhibited a higher apoB/apoA1 ratio than controls (1.04±0.33 vs 0.86±0.22; P<.001). |
| 1704 | 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). |
| 1705 | 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). |
| 1706 | 20538481 | Our findings support elevated apoB/apoA1 ratio as an independent predictor of ischemic stroke in individuals over age 70. |
| 1707 | 20655898 | Recent evidence suggests that the forkhead transcription factor Foxo1 plays an important role in the regulation of glucose and triglyceride metabolism at the gene transcription level for glucose-6 phosphatase (G6Pase), phosphoenolpyruvate carboxykinase (PEPCK), and apolipoprotein C-III (apoC-III). |
| 1708 | 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. |
| 1709 | 20683626 | Negative correlation between serum syndecan-1 and apolipoprotein A1 in patients with type 2 diabetes mellitus. |
| 1710 | 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. |
| 1711 | 20683626 | Serum syndecan-1 level correlated negatively with apoA1 (r = -0.46, P = 0.003). |
| 1712 | 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. |
| 1713 | 20826564 | Apolipoprotein A-I mimetic peptides prevent atherosclerosis development and reduce plaque inflammation in a murine model of diabetes. |
| 1714 | 20966404 | Intravenous injection of apolipoprotein A-V reconstituted high-density lipoprotein decreases hypertriglyceridemia in apoav-/- mice and requires glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1. |
| 1715 | 21042216 | Apolipoprotein A-I mimetic peptides. |
| 1716 | 21110784 | Examples discussed are: type IV collagen modification leading to endothelial cell detachment and anoikis, mitochondrial protein modification leading to oxidative stress and apolipoprotein B100 modification in low density lipoprotein leading to vascular retention and atherosclerosis. |
| 1717 | 21128827 | The ratio of apolipoprotein B and apolipoprotein A-1 concentrations (2.5) was significantly reduced in the CH group compared to the initial value (3.0). |
| 1718 | 21185820 | APOC3 -482C>T polymorphism, circulating apolipoprotein C-III and smoking: interrelation and roles in predicting type-2 diabetes and coronary disease. |
| 1719 | 21199528 | Polymorphisms within apolipoprotein C3 (APOC3) gene have been linked to NAFLD in lean Indian men. |
| 1720 | 21257004 | Comparison of high-density lipoprotein cholesterol to apolipoprotein A-I and A-II to predict coronary calcium and the effect of insulin resistance. |
| 1721 | 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. |
| 1722 | 21257004 | Comparison of high-density lipoprotein cholesterol to apolipoprotein A-I and A-II to predict coronary calcium and the effect of insulin resistance. |
| 1723 | 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. |
| 1724 | 21330603 | Lipid-free apolipoprotein A-I and discoidal reconstituted high-density lipoproteins differentially inhibit glucose-induced oxidative stress in human macrophages. |
| 1725 | 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. |
| 1726 | 21443465 | Preclinical studies show that FoxO1 plays a pivotal role in controlling insulin-dependent regulation of microsomal triglyceride transfer protein (MTP) and apolipoprotein C-III (ApoC-III), two key components that catalyze the rate-limiting steps in the production and clearance of triglyceride-rich lipoproteins. |
| 1727 | 21447785 | To address this question, we generated Ins2(+/Akita):apoE(-/-) mouse by cross-breeding Ins2(+/Akita) mouse (which has Ins2 gene mutation, causing pancreatic β-cell apoptosis and insulin deficiency) with apoE(-/-) mouse. |
| 1728 | 21447785 | Diabetic Ins2(+/Akita):apoE(-/-) mice exhibited diminished VLDL secretion by ~50%, which was accompanied by blunted Akt phosphorylation in response to insulin infusion and decreased triglyceride content in the liver. |
| 1729 | 21447785 | Although the expression of hepatic LDL receptor was not affected, there was a significant reduction in the expression of lipolysis-stimulated lipoprotein receptor (LSR) by ~28%. |
| 1730 | 21447785 | In conclusion, exaggerated hypercholesterolemia and atherosclerosis in spontaneously diabetic Ins2(+/Akita):apoE(-/-) mice may be attributable to impaired lipoprotein clearance in the setting of diminished expression of LSR and altered apolipoprotein composition of lipoproteins. |
| 1731 | 21474825 | Neutrophil activation is attenuated by high-density lipoprotein and apolipoprotein A-I in in vitro and in vivo models of inflammation. |
| 1732 | 21499891 | Association of lipoprotein lipase and apolipoprotein C-III genes polymorphism with acute myocardial infarction in diabetic patients. |
| 1733 | 21499891 | Lipoprotein lipase (LPL) and Apolipoprotein C-III (APOC-III) play an important role in lipid metabolism. |
| 1734 | 21499891 | The aim of this study was to explore the possible associations of the gene polymorphisms (LPL HindIII, LPL Ser(447)-Ter and APOC3 SstI), diabetes mellitus, and plasma lipids with myocardial infarction. |
| 1735 | 21499891 | Association of lipoprotein lipase and apolipoprotein C-III genes polymorphism with acute myocardial infarction in diabetic patients. |
| 1736 | 21499891 | Lipoprotein lipase (LPL) and Apolipoprotein C-III (APOC-III) play an important role in lipid metabolism. |
| 1737 | 21499891 | The aim of this study was to explore the possible associations of the gene polymorphisms (LPL HindIII, LPL Ser(447)-Ter and APOC3 SstI), diabetes mellitus, and plasma lipids with myocardial infarction. |
| 1738 | 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. |
| 1739 | 21598304 | Apolipoprotein A-I mimetic peptide L-4F prevents myocardial and coronary dysfunction in diabetic mice. |
| 1740 | 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. |
| 1741 | 21598304 | In obese mice L-4F increases adiponectin levels, improving insulin sensitivity, and reducing visceral adiposity. |
| 1742 | 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. |
| 1743 | 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). |
| 1744 | 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). |
| 1745 | 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. |
| 1746 | 21598304 | Apolipoprotein A-I mimetic peptide L-4F prevents myocardial and coronary dysfunction in diabetic mice. |
| 1747 | 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. |
| 1748 | 21598304 | In obese mice L-4F increases adiponectin levels, improving insulin sensitivity, and reducing visceral adiposity. |
| 1749 | 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. |
| 1750 | 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). |
| 1751 | 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). |
| 1752 | 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. |
| 1753 | 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. |
| 1754 | 21622202 | Following this analysis, a 6631-Da marker was identified as a fragment of the Apolipoprotein C-I precursor. |
| 1755 | 21670290 | Serum levels of apolipoprotein CIII (apoCIII) are increased in type 1 diabetic patients, and when β cells are exposed to these diabetic sera, apoptosis occurs, an effect abolished by an antibody against apoCIII. |
| 1756 | 21670290 | The endogenous levels of apoCIII were reduced by treating prediabetic animals with an antisense against this apolipoprotein, resulting in a significantly delayed onset of diabetes. |
| 1757 | 21670290 | ApoCIII thus serves as a diabetogenic factor, and intervention with this apolipoprotein in the prediabetic state can arrest disease progression. |
| 1758 | 21670290 | Serum levels of apolipoprotein CIII (apoCIII) are increased in type 1 diabetic patients, and when β cells are exposed to these diabetic sera, apoptosis occurs, an effect abolished by an antibody against apoCIII. |
| 1759 | 21670290 | The endogenous levels of apoCIII were reduced by treating prediabetic animals with an antisense against this apolipoprotein, resulting in a significantly delayed onset of diabetes. |
| 1760 | 21670290 | ApoCIII thus serves as a diabetogenic factor, and intervention with this apolipoprotein in the prediabetic state can arrest disease progression. |
| 1761 | 21670290 | Serum levels of apolipoprotein CIII (apoCIII) are increased in type 1 diabetic patients, and when β cells are exposed to these diabetic sera, apoptosis occurs, an effect abolished by an antibody against apoCIII. |
| 1762 | 21670290 | The endogenous levels of apoCIII were reduced by treating prediabetic animals with an antisense against this apolipoprotein, resulting in a significantly delayed onset of diabetes. |
| 1763 | 21670290 | ApoCIII thus serves as a diabetogenic factor, and intervention with this apolipoprotein in the prediabetic state can arrest disease progression. |
| 1764 | 21693679 | Apolipoprotein CIII reduces proinflammatory cytokine-induced apoptosis in rat pancreatic islets via the Akt prosurvival pathway. |
| 1765 | 21693679 | Apolipoprotein CIII (ApoCIII) is mainly synthesized in the liver and is important for triglyceride metabolism. |
| 1766 | 21693679 | In the presence of the islet-cytotoxic cytokines IL-1β + interferon-γ, ApoCIII reduced cytokine-mediated islet cell death and impairment of β-cell function. |
| 1767 | 21693679 | ApoCIII had no effects on mitogen-activated protein kinases (c-Jun N-terminal kinase, p38, and ERK) and had no impact on IL-1β-induced c-Jun N-terminal kinase activation. |
| 1768 | 21693679 | Further, ApoCIII caused degradation of the nuclear factor κB-inhibitor inhibitor of κB and stimulated Ser473-phosphorylation of the survival serine-threonine kinase Akt. |
| 1769 | 21693679 | Inhibition of the Akt signaling pathway by the phosphatidylinositol 3 kinase inhibitor LY294002 counteracted the antiapoptotic effect of ApoCIII on cytokine-induced apoptosis. |
| 1770 | 21693679 | We conclude that ApoCIII in the presence of T1D-relevant proinflammatory cytokines reduces rat pancreatic islet cell apoptosis via Akt. |
| 1771 | 21693679 | Apolipoprotein CIII reduces proinflammatory cytokine-induced apoptosis in rat pancreatic islets via the Akt prosurvival pathway. |
| 1772 | 21693679 | Apolipoprotein CIII (ApoCIII) is mainly synthesized in the liver and is important for triglyceride metabolism. |
| 1773 | 21693679 | In the presence of the islet-cytotoxic cytokines IL-1β + interferon-γ, ApoCIII reduced cytokine-mediated islet cell death and impairment of β-cell function. |
| 1774 | 21693679 | ApoCIII had no effects on mitogen-activated protein kinases (c-Jun N-terminal kinase, p38, and ERK) and had no impact on IL-1β-induced c-Jun N-terminal kinase activation. |
| 1775 | 21693679 | Further, ApoCIII caused degradation of the nuclear factor κB-inhibitor inhibitor of κB and stimulated Ser473-phosphorylation of the survival serine-threonine kinase Akt. |
| 1776 | 21693679 | Inhibition of the Akt signaling pathway by the phosphatidylinositol 3 kinase inhibitor LY294002 counteracted the antiapoptotic effect of ApoCIII on cytokine-induced apoptosis. |
| 1777 | 21693679 | We conclude that ApoCIII in the presence of T1D-relevant proinflammatory cytokines reduces rat pancreatic islet cell apoptosis via Akt. |
| 1778 | 21810592 | Apolipoprotein E4 exaggerates diabetic dyslipidemia and atherosclerosis in mice lacking the LDL receptor. |
| 1779 | 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. |
| 1780 | 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. |
| 1781 | 22020260 | Acyl-CoA synthetase 1 is required for oleate and linoleate mediated inhibition of cholesterol efflux through ATP-binding cassette transporter A1 in macrophages. |
| 1782 | 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. |
| 1783 | 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. |
| 1784 | 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. |
| 1785 | 22020260 | Conversely, overexpression of ACSL1 resulted in reduced ABCA1 levels and reduced cholesterol efflux in the presence of unsaturated fatty acids. |
| 1786 | 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. |
| 1787 | 22075273 | Short-term walnut consumption increases circulating total adiponectin and apolipoprotein A concentrations, but does not affect markers of inflammation or vascular injury in obese humans with the metabolic syndrome: data from a double-blinded, randomized, placebo-controlled study. |
| 1788 | 22075273 | Consumption of walnuts was associated with a statistically significant increase in serum apolipoprotein A concentrations (P = .03), but did not affect circulating levels of fetuin A, resistin, C-reactive protein, serum amyloid A, soluble intercellular adhesion molecules 1 and 3, soluble vascular cell adhesion protein 1, interleukins 6 and 8, tumor necrosis factor α, E-selectin, P-selectin, and thrombomodulin. |
| 1789 | 22075273 | Short-term walnut consumption increases circulating total adiponectin and apolipoprotein A concentrations, but does not affect markers of inflammation or vascular injury in obese humans with the metabolic syndrome: data from a double-blinded, randomized, placebo-controlled study. |
| 1790 | 22075273 | Consumption of walnuts was associated with a statistically significant increase in serum apolipoprotein A concentrations (P = .03), but did not affect circulating levels of fetuin A, resistin, C-reactive protein, serum amyloid A, soluble intercellular adhesion molecules 1 and 3, soluble vascular cell adhesion protein 1, interleukins 6 and 8, tumor necrosis factor α, E-selectin, P-selectin, and thrombomodulin. |
| 1791 | 22118750 | The emerging evidence for vitamin D-mediated regulation of apolipoprotein A-I synthesis. |
| 1792 | 22118750 | This process is inhibited by high-density lipoprotein (HDL), the main protein component of which is apolipoprotein A-I (apo A-I). |
| 1793 | 22118750 | The emerging evidence for vitamin D-mediated regulation of apolipoprotein A-I synthesis. |
| 1794 | 22118750 | This process is inhibited by high-density lipoprotein (HDL), the main protein component of which is apolipoprotein A-I (apo A-I). |
| 1795 | 22209939 | Apolipoprotein A-V dependent modulation of plasma triacylglycerol: a puzzlement. |
| 1796 | 22209939 | The discovery of apolipoprotein A-V (apoA-V) in 2001 has raised a number of intriguing questions about its role in lipid transport and triglyceride (TG) homeostasis. |
| 1797 | 22209939 | The interaction of apoA-V with glycosylphosphatidylinositol-anchored high-density lipoprotein binding protein 1 (GPIHBP1) is discussed relative to its postulated role in TG-rich lipoprotein catabolism. |
| 1798 | 22209939 | Apolipoprotein A-V dependent modulation of plasma triacylglycerol: a puzzlement. |
| 1799 | 22209939 | The discovery of apolipoprotein A-V (apoA-V) in 2001 has raised a number of intriguing questions about its role in lipid transport and triglyceride (TG) homeostasis. |
| 1800 | 22209939 | The interaction of apoA-V with glycosylphosphatidylinositol-anchored high-density lipoprotein binding protein 1 (GPIHBP1) is discussed relative to its postulated role in TG-rich lipoprotein catabolism. |
| 1801 | 22212222 | CETP inhibitor torcetrapib promotes reverse cholesterol transport in obese insulin-resistant CETP-ApoB100 transgenic mice. |
| 1802 | 22212222 | We therefore evaluated the effects of CETP inhibitor torcetrapib in CETP-apolipoprotein (apo)B100 mice made obese and insulin resistant with a 60% high-fat diet. |
| 1803 | 22212222 | In conclusion, CETP inhibition by torcetrapib improves RCT in CETP-apoB100 mice. |
| 1804 | 22219194 | Myeloperoxidase targets apolipoprotein A-I, the major high density lipoprotein protein, for site-specific oxidation in human atherosclerotic lesions. |
| 1805 | 22278086 | Apolipoprotein A-I mimetics and high-density lipoprotein function. |
| 1806 | 22363922 | The Association between Apolipoprotein A-II and Metabolic Syndrome in Korean Adults: A Comparison Study of Apolipoprotein A-I and Apolipoprotein B. |
| 1807 | 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. |
| 1808 | 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. |
| 1809 | 22407494 | Long-term RT ameliorated glycemic control, insulin sensitivity and ApoB/ApoA-I ratio in individuals with T2DM. |
| 1810 | 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. |
| 1811 | 22460246 | In the present study, we aim to investigate the effect of -1131T > C, -3A > G, c.56 C > G, and c.553 G > T SNPs in the apolipoprotein A5 (APOA5) gene and 1100C > T and 3238C > G in the apolipoprotein C3 (APOC3) on plasma lipid and lipoprotein levels and risk of coronary artery disease (CAD) in Indians. |
| 1812 | 22460246 | Significant associations between minor alleles and higher TG levels were seen for -1131T > C (P < 0.001), -3A > G (P < 0.001), c.56C > G (P = 0.026), and c.553G > T (P = 0.003) SNPs in the APOA5 gene and 1100C > T (P = 0.001) and 3238C > G (P = 0.009) in the APOC3 gene. |
| 1813 | 22460246 | The APOA5 and APOC3 locus is a strong determinant of plasma TG levels in Indians. |
| 1814 | 22576629 | Synergistic effects of genetic variants of APOA5 and BTN2A1 on dyslipidemia or metabolic syndrome. |
| 1815 | 22576629 | We previously showed that the -1131T→C polymorphism (rs662799) of the apolipoprotein A-V gene (APOA5) and the C→T polymorphism (rs6929846) of the butyrophilin, subfamily 2, member A1 gene (BTN2A1) were significantly associated with an increased serum concentration of triglycerides, a decreased serum concentration of high density lipoprotein (HDL)-cholesterol, and the prevalence of metabolic syndrome (MetS) in Japanese individuals. |
| 1816 | 22576629 | Japanese or Korean individuals with the C allele of APOA5 and the T allele of BTN2A1 had a 2.05- or 1.92-fold increased risk for hypertriglyceridemia and a 1.82- or 1.56-fold increased risk for hypo-HDL-cholesterolemia, respectively, compared to those with the TT genotype of APOA5 and the CC genotype of BTN2A1. |
| 1817 | 22576629 | Similar analysis with adjustment for age and gender revealed that Japanese individuals, but not Korean individuals, with the C allele of APOA5 and the T allele of BTN2A1 had a 2.87-fold increased risk for MetS compared to those with the TT genotype of APOA5 and the CC genotype of BTN2A1. |
| 1818 | 22576629 | Genetic variants of APOA5 and BTN2A1 may synergistically affect the prevalence of dyslipidemia in East Asian populations and of MetS in Japanese individuals. |
| 1819 | 22619326 | Apolipoprotein A-IV improves glucose homeostasis by enhancing insulin secretion. |
| 1820 | 22619326 | Apolipoprotein A-IV (apoA-IV) is secreted by the small intestine in response to fat absorption. |
| 1821 | 22619326 | Apolipoprotein A-IV improves glucose homeostasis by enhancing insulin secretion. |
| 1822 | 22619326 | Apolipoprotein A-IV (apoA-IV) is secreted by the small intestine in response to fat absorption. |
| 1823 | 22648266 | We investigated the association between circulating triglyceride levels, the apolipoprotein A-V (ApoA5) -1131T>C single nucleotide polymorphism and brachial-ankle pulse wave velocity (baPWV) by examining data from 4421 subjects aged 18-74 years who were recruited from the Chinese population. baPWV was significantly associated with the levels of circulating triglycerides after adjusting for age, sex, body mass index (BMI), systolic blood pressure, heart rate, waist-to-hip ratio, antihypertensive treatment and diabetes mellitus status. |
| 1824 | 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. |
| 1825 | 22753665 | Early-onset type 2 diabetes: higher burden of atherogenic apolipoprotein particles during statin treatment. |
| 1826 | 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. |
| 1827 | 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. |
| 1828 | 22903714 | Apolipoprotein C3 (ApoC3) is synthesized in liver so that levels or isoform distributions may constitute indicators of liver pathogenesis. |
| 1829 | 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. |
| 1830 | 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. |
| 1831 | 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). |
| 1832 | 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). |
| 1833 | 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. |
| 1834 | 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. |
| 1835 | 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. |
| 1836 | 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). |
| 1837 | 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). |
| 1838 | 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. |
| 1839 | 22982462 | Regulation of pattern recognition receptors by the apolipoprotein A-I mimetic peptide 4F. |
| 1840 | 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. |
| 1841 | 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. |
| 1842 | 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. |
| 1843 | 23087360 | Retinol-binding protein 4 is an independent factor associated with triglycerides and a determinant of very low-density lipoprotein-apolipoprotein B100 catabolism in type 2 diabetes mellitus. |
| 1844 | 23093701 | These include pyruvate kinase M1/M2, apolipoprotein A-I, albumin, peroxiredoxin 2, annexin A2, α-1-B-glycoprotein, flotillin-1 and haptoglobin. |
| 1845 | 23124103 | We have recently demonstrated that the combination therapy with olmesartan (OLM), an angiotensin II receptor blocker, and azelnidipine (AZL), a dihydroprydine calcium-channel blocker, improves endothelial function in diabetic Apolipoprotein-deficient (ApoE(-/-)) mice. |
| 1846 | 23154241 | Endoplasmic reticulum stress in HepG2 cells inhibits apolipoprotein A-I secretion. |
| 1847 | 23368640 | Apolipoprotein C3 (ApoC3) is one of the many plasma glycoproteins extensively studied for association with disease states. |
| 1848 | 23377670 | Synergistic effect between lipoprotein lipase and apolipoprotein C3 genes in determining the severity of coronary artery disease. |
| 1849 | 23377670 | We aimed to investigate the possible associations between LPL gene and apolipoprotein C3 (APOC3) gene polymorphisms with coronary artery disease (CAD) and its severity, as well as the interaction between these polymorphisms and classical risk factors. |
| 1850 | 23377670 | The HindIII variant of LPL and APOC3 were genotyped in 156 CAD patients and 154 subjects as a control group. |
| 1851 | 23377670 | We found that the odds ratio (OR) estimating the effect of joint exposure to H2H2 genotype of LPL and S2S2 genotype of APOC3 was significantly higher than the OR estimating the effect of each factor in the absence of the other. |
| 1852 | 23377670 | The present study points to a synergistic interaction between H2H2 genotype of LPL gene and S2S2 genotype of APOC3 gene that leads to increased severity of CAD. |
| 1853 | 23377670 | Synergistic effect between lipoprotein lipase and apolipoprotein C3 genes in determining the severity of coronary artery disease. |
| 1854 | 23377670 | We aimed to investigate the possible associations between LPL gene and apolipoprotein C3 (APOC3) gene polymorphisms with coronary artery disease (CAD) and its severity, as well as the interaction between these polymorphisms and classical risk factors. |
| 1855 | 23377670 | The HindIII variant of LPL and APOC3 were genotyped in 156 CAD patients and 154 subjects as a control group. |
| 1856 | 23377670 | We found that the odds ratio (OR) estimating the effect of joint exposure to H2H2 genotype of LPL and S2S2 genotype of APOC3 was significantly higher than the OR estimating the effect of each factor in the absence of the other. |
| 1857 | 23377670 | The present study points to a synergistic interaction between H2H2 genotype of LPL gene and S2S2 genotype of APOC3 gene that leads to increased severity of CAD. |
| 1858 | 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. |
| 1859 | 23440769 | Semiquantitative analysis of apolipoprotein A-I modified by advanced glycation end products in diabetes mellitus. |
| 1860 | 23450048 | Impaired fasting glucose and impaired glucose tolerance have distinct lipoprotein and apolipoprotein changes: the insulin resistance atherosclerosis study. |
| 1861 | 23470567 | Apolipoprotein C-II deficiency with no rare variant in the APOC2 gene. |
| 1862 | 23542898 | Antisense oligonucleotide inhibition of apolipoprotein C-III reduces plasma triglycerides in rodents, nonhuman primates, and humans. |
| 1863 | 23591583 | Increased apolipoprotein A-I levels mediate the development of prehypertension among Turks. |
| 1864 | 23616933 | Activation of peroxisome proliferator activated receptor-gamma results in an atheroprotective apolipoprotein profile in HepG2 cells. |
| 1865 | 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. |
| 1866 | 23726972 | Apolipoprotein(a) acts as a chemorepellent to human vascular smooth muscle cells via integrin αVβ3 and RhoA/ROCK-mediated mechanisms. |
| 1867 | 23726972 | Exposure of SMC to apo(a) in migration assays induced a potent, concentration-dependent chemorepulsion that was RhoA and integrin αVβ3-dependent, but transforming growth factor β-independent. |
| 1868 | 23726972 | SMC manipulation through RhoA gene silencing, Rho kinase inhibition, statin pre-treatment, αVβ3 neutralising antibody and tyrosine kinase inhibition all markedly inhibited apo(a)-mediated SMC migration. |
| 1869 | 23741493 | Apolipoprotein A-I glycation by glucose and reactive aldehydes alters phospholipid affinity but not cholesterol export from lipid-laden macrophages. |
| 1870 | 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). |
| 1871 | 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. |
| 1872 | 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. |
| 1873 | 23791845 | Diabetic patients showed increased VAT abundance of glutathione S-transferase Mu 2, peroxiredoxin-2, antithrombin-III, apolipoprotein A-IV, Ig κ chain C region, mitochondrial aldehyde dehydrogenase and actin, and decreased abundance of annexin-A1, retinaldehyde dehydrogenase-1, and vinculin, compared with their non-diabetic counterparts. |
| 1874 | 23819752 | Compared with other statins, pitavastatin has distinct pharmacological features that translate into a broad range of actions on both apolipoprotein-B-containing and apolipoprotein-A-containing lipoproteins. |
| 1875 | 23835332 | Proteomic analysis revealed changes in 7 of 45 identified proteins in the T2D group, including apolipoprotein (apo) A-II, apoE, and paraoxonase-1 (P < 0.05). |
| 1876 | 23874769 | An apolipoprotein A-I mimetic peptide designed with a reductionist approach stimulates reverse cholesterol transport and reduces atherosclerosis in mice. |
| 1877 | 23874769 | Apolipoprotein A-I (apoA-I) mimetic peptides are considered a promising novel therapeutic approach to prevent and/or treat atherosclerosis. |
| 1878 | 23874769 | An apolipoprotein A-I mimetic peptide designed with a reductionist approach stimulates reverse cholesterol transport and reduces atherosclerosis in mice. |
| 1879 | 23874769 | Apolipoprotein A-I (apoA-I) mimetic peptides are considered a promising novel therapeutic approach to prevent and/or treat atherosclerosis. |
| 1880 | 23913404 | Other observed effects of colesevelam in combination with other lipid-lowering drugs include reductions in apolipoprotein (apo) B (with statins, fibrates, ezetimibe, statin plus niacin, or statin plus ezetimibe) and high-sensitivity C-reactive protein (with statins), and increases in apo A-I (with statins, ezetimibe, or statins plus niacin). |
| 1881 | 23949443 | Apolipoprotein CIII hyperactivates β cell CaV1 channels through SR-BI/β1 integrin-dependent coactivation of PKA and Src. |
| 1882 | 23949443 | Apolipoprotein CIII (ApoCIII) not only serves as an inhibitor of triglyceride hydrolysis but also participates in diabetes-related pathological events such as hyperactivation of voltage-gated Ca(2+) (CaV) channels in the pancreatic β cell. |
| 1883 | 23949443 | We now demonstrate that ApoCIII increased CaV1 channel open probability and density. |
| 1884 | 23949443 | Moreover, knockdown of β1 integrin or scavenger receptor class B type I (SR-BI) prevented ApoCIII from hyperactivating β cell CaV channels. |
| 1885 | 23949443 | These data reveal that ApoCIII hyperactivates β cell CaV1 channels through SR-BI/β1 integrin-dependent coactivation of PKA and Src. |
| 1886 | 23949443 | Apolipoprotein CIII hyperactivates β cell CaV1 channels through SR-BI/β1 integrin-dependent coactivation of PKA and Src. |
| 1887 | 23949443 | Apolipoprotein CIII (ApoCIII) not only serves as an inhibitor of triglyceride hydrolysis but also participates in diabetes-related pathological events such as hyperactivation of voltage-gated Ca(2+) (CaV) channels in the pancreatic β cell. |
| 1888 | 23949443 | We now demonstrate that ApoCIII increased CaV1 channel open probability and density. |
| 1889 | 23949443 | Moreover, knockdown of β1 integrin or scavenger receptor class B type I (SR-BI) prevented ApoCIII from hyperactivating β cell CaV channels. |
| 1890 | 23949443 | These data reveal that ApoCIII hyperactivates β cell CaV1 channels through SR-BI/β1 integrin-dependent coactivation of PKA and Src. |
| 1891 | 23981600 | In a cohort of patients aged 60 years or older with excellent antiretroviral therapy adherence, correlates to cognitive impairment were apolipoprotein (Apo) E4 genotype and a novel measure of the effectiveness of antiretroviral drugs in monocytes, the monocyte efficacy (ME) score, with trend associations for diabetes and nadir CD4+ cell count. |
| 1892 | 23994331 | Serum amyloid A is independently related to apolipoprotein A-I but not to HDL-cholesterol in patients with angina pectoris. |
| 1893 | 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. |