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(Circulation Research. 2005;96:1129.)
© 2005 American Heart Association, Inc.

Editorials

Unraveling the Links Between Diabetes, Obesity, and Cardiovascular Disease

Paul L. Huang

From the Cardiovascular Research Center and Cardiology Division, Massachusetts General Hospital and Harvard Medical School, Charlestown, Mass.

Correspondence to Dr Paul L. Huang, Cardiovascular Research Center and Cardiology Division, Massachusetts General Hospital East, 149 13th St, Charlestown, MA 02129. E-mail phuang1@partners.org

See related article, pages 1178–1184

Key Words: diabetes • obesity • hypercoagulability • hyperlipidemia • hypertension

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Patients with diabetes mellitus are known to be at increased risk for coronary artery disease and myocardial infarction, and have worse outcomes after coronary interventions such as stenting.¹ The mechanisms for this increased risk are not fully known, but are thought to reflect vascular abnormalities of inflammation, hypertension, dyslipidemia, and hypercoagulability.² In turn, these vascular abnormalities may be the result of hyperglycemia, insulin resistance, and advanced glycation products seen in diabetes.^3,4 However, the precise molecular links between the metabolic abnormalities seen in diabetes, and the resulting vascular changes that increase propensity for atherosclerosis are not clearly understood.

One such link is endothelial dysfunction, seen in diabetes, obesity, hypertension, hyperlipidemia, smoking, and aging.^5,6 Endothelial dysfunction is characterized by defects in the normal vascular relaxation response to mediators such as acetylcholine, or to increased blood flow. This can be clinically measured by ultrasound studies of forearm blood flow responses. The basis for endothelial dysfunction may involve a reduction in the amount of bioavailable nitric oxide (NO) in the vasculature. NO is necessary for vascular relaxation and endothelium dependent relaxing factor (EDRF) activity.^7,8 NO also serves to suppress atherosclerosis by reducing endothelial cell activation, smooth muscle proliferation, leukocyte activation and leukocyte-endothelial interactions, and platelet aggregation and adhesion.^9–12 Therefore, reduction in the amount of bioavailable NO would result in a proatherogenic state.

In this issue, Molnar et al describe a mouse model of type 2 diabetes in which they fed C57BL/6 wild-type mice a high- fat diet and sucrose for 9 weeks.¹³ These mice . . . [Full Text of this Article]

Related Article:

Diabetes Induces Endothelial Dysfunction but Does Not Increase Neointimal Formation in High-Fat Diet Fed C57BL/6J Mice

Judit Molnar, Shuiqing Yu, Nino Mzhavia, Clara Pau, Igor Chereshnev, and Hayes M. Dansky
Circ. Res. 2005 96: 1178-1184. [Abstract] [Full Text] [PDF]

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