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Postprandial hyperlipidemia, endothelial dysfunction and cardiovascular risk: focus on incretins

Sameer Ansar13, Juraj Koska1 and Peter D Reaven12*

Author Affiliations

1 Department of Endocrinology, Phoenix Veteran Affairs Healthcare System, 650 E Indian School Rd, CS111E, Phoenix, AZ 85012, USA

2 Biodesign Institute, Arizona State University, 727 E. Tyler Street Tempe, AZ 85287, USA

3 Michigan State University, B319 Clinical Center, East Lansing, MI 48824, USA

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Cardiovascular Diabetology 2011, 10:61  doi:10.1186/1475-2840-10-61

Published: 7 July 2011


Cardiovascular disease (CVD) risk in type 2 diabetes (T2DM) is only partially reduced by intensive glycemic control. Diabetic dyslipidemia is suggested to be an additional important contributor to CVD risk in T2DM. Multiple lipid lowering medications effectively reduce fasting LDL cholesterol and triglycerides concentrations and several of them routinely reduce CVD risk. However, in contemporary Western societies the vasculature is commonly exposed to prolonged postprandial hyperlipidemia. Metabolism of these postprandial carbohydrates and lipids yields multiple proatherogenic products. Even a transient increase in these factors may worsen vascular function and induces impaired endothelial dependent vasodilatation, a predictor of atherosclerosis and future cardiovascular events. There is a recent increased appreciation for the role of gut-derived incretin hormones in controlling the postprandial metabolic milieu. Incretin-based medications have been developed and are now used to control postprandial hyperglycemia in T2DM. Recent data indicate that these medications may also have profound effects on postprandial lipid metabolism and may favorably influence several cardiovascular functions. This review discusses (1) the postprandial state with special emphasis on postprandial lipid metabolism and its role in endothelial dysfunction and cardiovascular risk, (2) the ability of incretins to modulate postprandial hyperlipidemia and (3) the potential of incretin-based therapeutic strategies to improve vascular function and reduce CVD risk.