Regulation of cholesteryl ester transfer protein (CETP) activity: review of in vitro and in vivo studies

Lagrost, Laurent

doi:10.1016/0005-2760(94)90047-7

Cited by 181 publications

(120 citation statements)

References 261 publications

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“…The role of cholesteryl ester transfer protein (CETP) in intravascular cholesteryl ester (CE) transport has been fully reviewed [2,[10][11][12]. In addition to promoting a bidirectional flux of cholesteryl ester between LP, CETP also mediates the heteromolecular exchange whereby triglyceride (TG)-rich LP gains CE and loses TG [13].…”

mentioning

confidence: 99%

Plasma lipoproteins from patients with poorly controlled diabetes mellitus and "in vitro" glycation of lipoproteins enhance the transfer rate of cholesteryl ester from HDL to apo-B-containing lipoproteins

et al. 1997

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Several factors may be responsible for the high prevalence of premature atherosclerosis in diabetes mellitus [1], including possible alterations in the reverse cholesterol transport system [2][3][4][5][6][7].Plasma lipoproteins (LP) are continually modified intravascularly and in the interstitium due to enzymatic action and interchanges of lipid fractions and apolipoproteins [2,8,9]. The role of cholesteryl ester transfer protein (CETP) in intravascular cholesteryl ester (CE) transport has been fully reviewed [2,[10][11][12]. In addition to promoting a bidirectional flux of cholesteryl ester between LP, CETP also mediates the heteromolecular exchange whereby triglyceride (TG)-rich LP gains CE and loses TG [13]. The direction of this flow is partially determined by the lipid composition of the LP involved [14,15]. Diabetologia (1997Diabetologia ( ) 40: 1085Diabetologia ( -1093 Plasma lipoproteins from patients with poorly controlled diabetes mellitus and "in vitro" glycation of lipoproteins enhance the transfer rate of cholesteryl ester from HDL to apo-B-containing lipoproteins Summary Alterations in the reverse cholesterol transport system have been described in diabetic mellitus patients in several but not all studies. Furthermore, recently published investigations suggest that a faster "in vitro" transfer rate of cholesteryl ester from high density lipoproteins to apoB-containing lipoproteins could be solely ascribed to variation of the plasma lipoprotein composition and concentration in the diabetic state. The present study analysed the influence of lipoprotein glycation on the cholesteryl ester transfer protein-mediated transfer of esterified cholesterol from high density lipoprotein and its subfractions to lighter density lipoproteins. For this purpose two sets of "in vitro" experiments were carried out utilizing:1) plasma lipoproteins drawn from diabetic and from normal subjects and; 2) normal lipoproteins or partially purified cholesteryl ester transfer protein submitted to "in vitro" glycation. The transfer rate of 14 C-cholesteryl ester labelled HDL subfractions to low or very low density lipoproteins was measured in all experiments. After incubations with plasma d > 1.21 g/ml or with purified cholesteryl ester transfer protein, apoB-containing lipoproteins were precipitated with a dextran sulfate/MgCl 2 solution. The "in vitro" glycation of the partially purified cholesteryl ester transfer protein markedly impaired its activity. However, greater transfer rates were observed when lipoproteins from diabetic individuals or the "in vitro" glycated lipoproteins were utilized. This effect was attributed to glycation of the protein component of HDL. In conclusion, lipoprotein glycation elicits an enrichment of the apoB-containing lipoproteins with cholesteryl ester that is likely related to the premature atherosclerosis in patients with poorly controlled diabetes. [Diabetologia (1997[Diabetologia ( ) 40: 1085[Diabetologia ( -1093

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confidence: 99%

Plasma lipoproteins from patients with poorly controlled diabetes mellitus and "in vitro" glycation of lipoproteins enhance the transfer rate of cholesteryl ester from HDL to apo-B-containing lipoproteins

et al. 1997

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“…Regarding HDL metabolism, thyroid hormones increase 22 cholesteryl ester transport protein (CETP) activity. T 3 upregulates LDL receptors by controlling the LDL receptors 23 gene activation.…”

Section: Outmentioning

confidence: 99%

Spectrum of Lipid Abnormality among Thyroid Disorder Patients in Ucms-Th, South Western Region

Gautam

Jayan

Jha

et al. 2018

J Univ Coll Med Sci

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INTRODUCTION:Hypothyroidism is the most common cause of secondary dyslipidemia. Thus, thyroid function test should be carried out before starting any hypolipidemic drugs. Even among thyroid disorder, hypothyroidism is more associated with cardiovascular and associated problems and if not detected earlier, it leads to severe clinical consequences. Our study assesses the frequency and spectrum of dyslipidemia in various types of thyroidal illness in the population residing in south western part of Nepal. MATERIALS AND METHODS:This is a cross sectional study carried out in suspected thyroid disorder patients (n=276) and categorized as Euthyroidism (n=55), Subclinical Hypothyroidism (n=89), Primary Hypothyroidism (n=122) and Primary Hyperthyroidism (n=10) patients and to see the association with lipid profiles in the Department of Biochemistry, Universal College of Medical Sciences Teaching Hospital, Bhairahawa Nepal. Serum fT / fT4 and TSH estimations were carried out by competitive 3 ELISA method and Sand-wich double antibody ELISA method respectively using commercially supplied reagents (Human, Germany). The criteria for dyslipidemia was obtained by National Cholesterol Education Expert Panel/ Adult Treatment Protocol III (NCEP/ATPIII). RESULTS:Out of 276 cases the dyslipidemia was observed in 183 cases (66.30%).The dyslipidemia was mostly associated with primary hypothyroidism (55.07%) followed by Subclinical Hypothyroidism (38.04%) than Euthyroid (5.79 %) and Primary Hyperthyroidism (3.62 %) respectively. Out of all cases, the spectrum of dyslipidemia was mostly observed for decreased HDL (18.5 %) followed by increased TG (10.1 %). Moreover, it is significantly differ in relation in HDL (p=0.009), TG/HDL (p=0.02) and Non-HDL/HDL (p=0.033) where as non significant as compared to other lipid profile in different groups. CONCLUSION:Our study revealed the close association of thyroidal illness with dyslipidemia with increased TG, low HDL, increased TG/HDL and Non-HDL/HDL. The increased TG/HDL and/or Non-HDL/HDL could be better indicator than single lipid abnormality which needs to be ascertained prospectively in large population.

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“…a profile with low coronary heart disease risk and longevity. High density lipoprotein apolipoprotein may modulate cholesteryl ester transfer protein activity, but the mechanism between them is not clear and remains to be established (Lagrost 1994). Some inducers, either by stimulating plasma lipoprotein lipase, e.g.…”

Section: Microsomal Induction -Gene Activation and Lipids And Proteinsmentioning

confidence: 99%

Gene Activation, Apolipoprotein A‐I/High Density Lipoprotein, Atherosclerosis Prevention and Longevity

Luoma

1997

Pharmacology & Toxicology

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Recent studies in man and human apolipoprotein A-I transgenic animals emphasize the significance of apolipoprotein A-I and high density lipoprotein in antiatherogenesis. Several drugs and other compounds, e.g. phenobarbital, gemfibrozil, fenofibrate, prednisone, estrogen and alcohol, induce apolipoprotein A-I synthesis. They commonly produce serum lipoprotein patterns typical of a low risk of coronary heart disease, and many of them have been found to prevent atherogenesis, reduce coronary heart disease mortality and increase survival. These compounds act against atherosclerosis by using one or several mechanisms that include overexpression of the apolipoprotein A-I gene with an increase in serum apolipoprotein A-1 and high density lipoprotein and promotion of reverse cholesterol transport, upregulation of the low density lipoprotein receptor gene with a decrease in serum apolipoprotein B and low density lipoprotein, maintenance of endothelial cell function and protection against thrombosis. They have been found to raise high density lipoprotein cholesterol and apolipoprotein A-I together with a decrease in cholesterol ester transfer protein activity, and to induce hepatic cholesterol 7a-hydroxylase and cholesterol and bile acid elimination from the body. By raising the activities of apolipoprotein A-I/ high density lipoprotein-associated paraoxonase and other antioxidative enzymes, the inducers have the capacity to prevent atherogenesis in arterial walls through inhibition of the oxidative modification of low density lipoprotein. Other antiatherogenic vascular actions of high density lipoprotein include interference with low density lipoprotein aggregation and uptake by endothelial cells, and competition with low density lipoprotein for endothelial-localized low density lipoprotein receptors. Apolipoprotein A-I/high density lipoprotein beneficially enhances fibrinolysis. decreases platelet aggregation, increases prostacyclin production and stabilization and prevents atherogenic immune and inflammatory responses. This gene activation or microsomal induction can prevent atherosclerosis and is a basis for tailoring effective new agents and optimal non-invasive therapy against atherosclerotic vascular disease, to promote health and enhance longevity.

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Regulation of cholesteryl ester transfer protein (CETP) activity: review of in vitro and in vivo studies

Cited by 181 publications

References 261 publications

Plasma lipoproteins from patients with poorly controlled diabetes mellitus and "in vitro" glycation of lipoproteins enhance the transfer rate of cholesteryl ester from HDL to apo-B-containing lipoproteins

Plasma lipoproteins from patients with poorly controlled diabetes mellitus and "in vitro" glycation of lipoproteins enhance the transfer rate of cholesteryl ester from HDL to apo-B-containing lipoproteins

Spectrum of Lipid Abnormality among Thyroid Disorder Patients in Ucms-Th, South Western Region

Gene Activation, Apolipoprotein A‐I/High Density Lipoprotein, Atherosclerosis Prevention and Longevity

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