Insulin resistance and cardiovascular disease (original) (raw)

Journal Article

,

1

Departments of Pharmacology and Medicine, Medical University of South Carolina

,

Charleston, South Carolina

,

USA

Address correspondence and reprint requests to Dr. Brent M. Egan,

Division of Clinical Pharmacology, Medical University of South Carolina

,

96 Jonthan Lucas Street, CSB 826H, Charleston, SC 29425

E-mail: eganbm@musc.edu

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,

2

Division of Nephrology, Department of Medicine, Mayo Clinic

,

Rochester, Minnesota

,

USA

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3

Departments of Medicine and Pharmacology, William S. Middleton VA Hospital, University of Wisconsin

,

Madison, Wisconsin

,

USA

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Received:

26 February 2001

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Abstract

Cardiovascular risk factors cluster in obese individuals. Insulin resistance emerges as a common pathogenetic denominator underlying the risk factor cluster. Defects in nonesterified fatty acids metabolism have been implicated in the abnormal lipid and glucose metabolism which characterize the cluster. Other evidence also leads to the adipocyte as an important contributor to the risk factor cluster and cardiovascular complications through effects not only on fatty acids but also on leptin, plasminogen activator inhibitor-1, and angiotensinogen, to name a few. Fatty acids are elevated among abdominally obese individuals, are more resistant to suppression by insulin, and may contribute to hypertension. Fatty acids may affect blood pressure by inhibiting endothelial nitric oxide synthase activity and impairing endothelium-dependent vasodilation. Fatty acids increase α1-adrenoceptor-mediated vascular reactivity and enhance the proliferation and migration of cultured vascular smooth-muscle cells. Several effects of fatty acids are mediated through oxidative stress. Fatty acids can also interact with other facets of cluster, including increased angiotensin II, to accentuate oxidative stress. Oxidative stress, in turn, is implicated in the pathogenesis of insulin resistance, hypertension, vascular remodeling, and vascular complications. A clearer delineation of the key reactive oxygen signaling pathways and the impact of various interventions on these pathways could facilitate a rationale approach to antioxidant therapy and improved outcomes among the rapidly growing number of high-risk, insulin-resistant, obese individuals. Am J Hypertens 2001;14:116S–125S © 2001 American Journal of Hypertension, Ltd.

© American Journal of Hypertension, Ltd. 2001

Topic:

• angiotensinogen
• antioxidants
• obesity
• oxidative stress
• oxygen
• hypertension
• insulin resistance
• cardiovascular diseases
• fatty acids
• glucose metabolism
• metabolism
• heart disease risk factors
• smooth muscle
• angiotensin ii
• vascular remodeling
• blood pressure
• adipocytes
• endothelium
• leptin
• nitric oxide synthase
• plasminogen activator inhibitor 1
• adrenergic receptor
• nonesterified fatty acids
• insulin
• lipids
• vasodilation
• signal pathway
• signal transduction pathways
• cardiac complications
• vascular complications
• rationale

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