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[Dyslipidemia in visceral obesity: pathophysiological mechanisms, clinical implications and therapy].

Authors
  • Zambon, Alberto1
  • Marchiori, Michela
  • Manzato, Enzo
  • 1 Clinica Medica 1, Dipartimento di Scienze Mediche e Chirurgiche, Università degli Studi, Padova. [email protected]
Type
Published Article
Journal
Giornale italiano di cardiologia (2006)
Publication Date
Apr 01, 2008
Volume
9
Issue
4 Suppl 1
Identifiers
PMID: 18773749
Source
Medline
License
Unknown

Abstract

Visceral (intra-abdominal) obesity is associated with a cluster of cardiovascular risk factors that together promote macrovascular and microvascular disease. An atherogenic dyslipidemia, characterized by an increase in serum triglyceride-rich lipoproteins, a decrease in plasma levels of high-density lipoprotein cholesterol and increased prevalence of small, dense low-density lipoprotein particles (although low-density lipoprotein cholesterol levels are normal or only modestly elevated), as well as chronic inflammation, play key roles in the pathogenesis of visceral obesity-related complication. These abnormalities may be consequent to a global metabolic effect of insulin resistance. Pharmacological treatments, such as 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, fibric acid derivatives, insulin sensitizers and cannabinoid receptor type 1 blockers, are often required to correct the dyslipidemia of visceral obesity. 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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