doi: 10.1161/CIRCULATIONAHA.107.741645
(Circulation. 2008;117:3238-3249.)
© 2008 American Heart Association, Inc.
Contemporary Reviews in Cardiovascular Medicine |
Leptin and Cardiovascular Disease
Response to Therapeutic Interventions
From the Division of Cardiology, Gil Heart Center, Gachon University Gil Medical Center, Incheon, Korea (K.K.K., S.M.P.); and Diabetes Unit, Laboratory of Clinical Investigation, National Center for Complementary and Alternative Medicine, National Institutes of Health, Bethesda, Md (M.J.Q.).
Correspondence to Kwang Kon Koh, MD, PhD, Vascular Medicine and Atherosclerosis Unit, Division of Cardiology, Gachon University Gil Medical Center, 1198 Kuwol-dong, Namdong-gu, Incheon, South Korea 405-760. E-mail kwangk@gilhospital.com
Key Words: atherosclerosis • cardiovascular diseases • diabetes mellitus • drugs • hypertension • insulin • obesity
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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Leptin, a 16-kDa hormone identified and cloned in 1994, is synthesized and secreted specifically from white adipose cells.1 Leptin has a variety of important central and peripheral actions to regulate energy balance and metabolism, fertility, and bone metabolism that are mediated by specific cell surface leptin receptors.2,3 Importantly, leptin may also exert actions related to cardiovascular homeostasis that are potentially atherogenic, thrombotic, and angiogenic.4–6 Leptin has peripheral actions to stimulate vascular inflammation, oxidative stress, and vascular smooth muscle hypertrophy that may contribute to pathogenesis of type 2 diabetes mellitus, hypertension, atherosclerosis, and coronary heart disease.3,4,7
Insulin resistance,8 systemic hypertension, and hypercholesterolemia9 all contribute independently to vascular endothelial dysfunction that promotes atherosclerosis and coronary heart disease. Reciprocal relationships between endothelial dysfunction and insulin resistance are characterized by impaired insulin-stimulated nitric oxide (NO) production from endothelium that decreases blood flow to insulin target tissues.10,11 Relationships among obesity, metabolic syndrome, diabetes mellitus, and their cardiovascular complications are well established. However, the mechanisms by which excess adiposity causes both insulin resistance and vascular dysfunction are not well understood. Direct vascular effects of adipokines such as leptin are attractive candidates that may help to explain underlying pathophysiological mechanisms.
Several clinical studies demonstrate that hyperleptinemia predicts acute cardiovascular events, restenosis after coronary injury such as angioplasty, and cerebral stroke independent of traditional risk factors.12–14 Leptin-deficient hyperlipidemic mice (ob/ob; apolipoprotein E [apoE]–/– mice) develop significantly less atherosclerosis than apoE–/– mice on an atherogenic diet. Exogenous leptin significantly increases atherosclerotic areas in apoE–/– mice. Taken together,
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