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Insulin Resistance, Dyslipidemia, and Cardiovascular Disease

Zachary T. Bloomgarden, MD, is a practicing endocrinologist in New York, New York, and is affiliated with the Division of Endocrinology, Mount Sinai School of Medicine, New York, New York

Abbreviations: ADMA, asymmetric dimethyl arginine • ALT, alanine aminotransferase • apo, apolipoprotein • CETP, cholesterol ester transport protein • CVD, cardiovascular disease • DDAH, dimethylarginine dimethylaminohydrolase • HL, hepatic lipase • IGT, impaired glucose tolerance • IRS, insulin resistance syndrome • LPL, lipoprotein lipase • MAPK, mitogen-activated protein kinase • NOS, nitric oxide synthase • PAI, plasminogen inactivator • PI3K, phosphatidylinositol 3-kinase • PPAR, peroxisome proliferetor–activated receptor • RAS, renin-angiotensin system • RXR, retinoid X receptor • SDMA, symmetric dimethyl arginine • TNF, tumor necrosis factor

The first 300 words of the full text of this article appear below.

Perspectives on the News commentaries are now part of a new, free monthly CME activity. The Mount Sinai School of Medicine, New York, New York, is designating this activity for 2.0 AMA PRA Category 1 credits. If you wish to participate, review this article and visit www.diabetes.procampus.net to complete a posttest and receive a certificate. The Mount Sinai School of Medicine is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.

This is the fourth in a series of four articles on presentations at the World Congress on the insulin resistance syndrome (IRS), reviewing aspects of insulin resistance pertaining to dyslipidemia and cardiovascular disease.

Insulin resistance and dyslipidemia
Ronald Krauss (San Francisco, CA) gave insights in the genetics of the more common forms of IRS based on the understanding of the complex topic of dyslipidemia. There is an intimate relationship between diet and dyslipidemia, and dietary manipulations may be used to understand the mechanisms of these abnormalities. LDL particles exist in multiple subclasses, differing in size, density, and lipid content. Large and medium LDL comprise the most abundant species in plasma of the most healthy individuals, but there are two forms of small LDL, exhibiting reduced receptor binding, greater endothelial transport, greater arterial proteoglycan binding, and greater susceptibility to oxidation.

Small LDL is associated with elevations in triglyceride levels. Traditional models describe a pathway from VLDL formation in the liver to formation of IDL and then of LDL particles via lipolysis. Actually, there is heterogeneity in size subspecies of VLDL and IDL (1). With low levels of triglyceride transport from the liver, triglyceride-poor particles are exported as IDL, with lipolysis by lipoprotein lipase (LPL) to form LDL1. Under more typical circumstances of triglyceride formation, VLDL2 is formed. These VLDL particles are substrates for LPL, . . . [Full Text of this Article]

Cardiovascular disease and insulin resistance

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