Rashid_2003_Clin.Biochem_36_421

Reference

Title : Mechanisms of HDL lowering in insulin resistant, hypertriglyceridemic states: the combined effect of HDL triglyceride enrichment and elevated hepatic lipase activity - Rashid_2003_Clin.Biochem_36_421
Author(s) : Rashid S , Watanabe T , Sakaue T , Lewis GF
Ref : Clinical Biochemistry , 36 :421 , 2003
Abstract : Hypertriglyceridemia, low plasma concentrations of high density lipoproteins (HDL) and qualitative changes in low density lipoproteins (LDL) comprise the typical dyslipidemia of insulin resistant states and type 2 diabetes. 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. We and others have postulated that triglyceride enrichment of HDL particles secondary to enhanced CETP-mediated exchange of triglycerides and cholesteryl ester between HDL and triglyceride-rich lipoproteins, combined with the lipolytic action of hepatic lipase (HL), are driving forces in the reduction of plasma HDL-c and apoA-I plasma concentrations. The present review focuses on these metabolic alterations in insulin resistant states and their important contributions to the reduction of HDL-c and HDL-apoA-I plasma concentrations.
ESTHER : Rashid_2003_Clin.Biochem_36_421
PubMedSearch : Rashid_2003_Clin.Biochem_36_421
PubMedID: 12951168

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Citations formats

Rashid S, Watanabe T, Sakaue T, Lewis GF (2003)
Mechanisms of HDL lowering in insulin resistant, hypertriglyceridemic states: the combined effect of HDL triglyceride enrichment and elevated hepatic lipase activity
Clinical Biochemistry 36 :421

Rashid S, Watanabe T, Sakaue T, Lewis GF (2003)
Clinical Biochemistry 36 :421