Circulation. 2005;111:1448-1454
doi: 10.1161/01.CIR.0000158483.13093.9D
doi: 10.1161/01.CIR.0000158483.13093.9D
(Circulation. 2005;111:1448-1454.)
© 2005 American Heart Association, Inc.
Contemporary Reviews in Cardiovascular Medicine |
Metabolic Syndrome
A Comprehensive Perspective Based on Interactions Between Obesity, Diabetes, and Inflammation
From the Division of Endocrinology, Diabetes, and Metabolism, State University of New York at Buffalo, and Kaleida Health, Buffalo, NY.
Correspondence to Paresh Dandona, MD, PhD, Director, Diabetes-Endocrinology Center of Western New York, Professor of Medicine, State University of New York at Buffalo, 3 Gates Circle, Buffalo, NY 14209. E-mail pdandona@kaleidahealth.org
Received June 28, 2004; revision received August 26, 2004; accepted October 15, 2004.
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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The original description of the metabolic syndrome by Reaven1 consisted of obesity, insulin resistance, hypertension, impaired glucose tolerance or diabetes, hyperinsulinemia and dyslipidemia characterized by elevated triglyceride, and low HDL concentrations. All of the features described above are risk factors for atherosclerosis, and thus, metabolic syndrome constituted a significant risk for coronary heart disease2–5 (Table). The features of obesity/overweight and insulin resistance also provided a significant risk for developing type 2 diabetes.5,6 The risks for coronary heart disease and diabetes with metabolic syndrome are greater than those for simple obesity alone, and therefore, an understanding of the pathogenesis and through it, a rational approach to its therapy are of prime importance.
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As our understanding of the action of insulin evolves to comprehensively include the recent discoveries,7 we can better see that insulin resistance is the basis of most if not all of the features of this syndrome. The original conceptualization of this syndrome was on the basis of resistance to the metabolic actions of insulin. Thus, hyperinsulinemia, glucose intolerance, type 2 diabetes, hypertriglyceridemia, and low HDL concentrations could be accounted for by resistance to the actions of insulin on carbohydrate and lipid metabolism. Although the features described above would to some extent explain the atherogenesis, Reaven has maintained that hyperinsulinemia itself contributes to atherogenicity, and thus, insulin is atherogenic, leading to the coronary heart disease and cerebrovascular disease associated with
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