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Dyslipidemia in Visceral Obesity

Mechanisms, Implications, and Therapy

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Abstract

Visceral obesity is frequently associated with high plasma triglycerides and low plasma high density lipoprotein-cholesterol (HDL-C), and with high plasma concentrations of apolipoprotein B (apoB)-containing lipoproteins. Atherogenic dyslipidemia in these patients may be caused by a combination of overproduction of very low density lipoprotein (VLDL) apoB-100, decreased catabolism of apoB-containing particles, and increased catabolism of HDL-apoA-I particles. These abnormalities may be consequent on a global metabolic effect of insulin resistance. Weight reduction, increased physical activity, and moderate alcohol intake are first-line therapies to improve lipid abnormalities in visceral obesity. These lifestyle changes can effectively reduce plasma triglycerides and low density lipoprotein-cholesterol (LDL-C), and raise HDL-C. Kinetic studies show that in visceral obesity, weight loss reduces VLDL-apoB secretion and reciprocally upregulates LDL-apoB catabolism, probably owing to reduced visceral fat mass, enhanced insulin sensitivity and decreased hepatic lipogenesis. Adjunctive pharmacologic treatments, such as HMG-CoA reductase inhibitors, fibric acid derivatives, niacin (nicotinic acid), or fish oils, may often be required to further correct the dyslipidemia. Therapeutic improvements in lipid and lipoprotein profiles in visceral obesity can be achieved by several mechanisms of action, including decreased secretion and increased catabolism of apoB, as well as increased secretion and decreased catabolism of apoA-I. Clinical trials have provided evidence supporting the use of HMG-CoA reductase inhibitors and fibric acid derivatives to treat dyslipidemia in patients with visceral obesity, insulin resistance and type 2 diabetes mellitus. Since drug monotherapy may not adequately optimize dyslipoproteinemia, dual pharmacotherapy may be required, such as HMG-CoA reductase inhibitor/fibric acid derivative, HMG-CoA reductase inhibitor/niacin and HMG-CoA reductase inhibitor/fish oils combinations. Newer therapies, such as cholesterol absorption inhibitors, cholesteryl ester transfer protein antagonists and insulin sensitizers, could also be employed alone or in combination with other agents to optimize treatment. The basis for a multiple approach to correcting dyslipoproteinemia in visceral obesity and the metabolic syndrome relies on understanding the mechanisms of action of the individual therapeutic components.

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Acknowledgement

This work was supported by grants from the National Health and Medical Research Council, the National Heart Foundation and the National Institutes of Health (NIBIB P41 EB-001975). Support was also provided by the Raine Medical Research Foundation, the Royal Perth Hospital Medical Research Foundation, Pfizer. HPR Barrett is a Career Development Fellow of the National Heart Foundation.

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  1. Lipoprotein Research Unit, School of Medicine and Pharmacology, University of Western Australia and The Western Australian Institute for Medical Research, Level 4, MRF Building, 50 Murray Street, Perth, WA, 6000, Australia

    Dick C. Chan, Hugh P. R. Barrett &  Gerald F. Watts

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Chan, D.C., Barrett, H.P.R. & Watts, G.F. Dyslipidemia in Visceral Obesity. Am J Cardiovasc Drugs 4, 227–246 (2004). https://doi.org/10.2165/00129784-200404040-00004

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