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(Circulation Research. 2006;99:1149.)
© 2006 American Heart Association, Inc.

Editorials

C-Peptide in Insulin Resistance and Vascular Complications

Teaching an Old Dog New Tricks

Dennis Bruemmer

From the Division of Endocrinology and Molecular Medicine, University of Kentucky College of Medicine, Lexington.

Correspondence to Dennis Bruemmer, MD, University of Kentucky College of Medicine, Department of Internal Medicine, Division of Endocrinology and Molecular Medicine, Wethington Health Sciences Building Room 575, 900 South Limestone Street, Lexington, KY 40536-0200. E-mail Dennis.Bruemmer@uky.edu

See related article, pages 1181–1187

Key Words: insulin resistance • C-peptide • smooth muscle cell • proliferation

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

	Clinical Evidence Linking Insulin Resistance, Hyperinsulinemia, and Cardiovascular Disease

 
Based on the recent evidence that patients with type 2 diabetes have the same risk of myocardial infarction as nondiabetic subjects with a history of infarction, diabetes has been designated as an atherosclerosis equivalent.¹ Insulin resistance plays a primary role in the development of type 2 diabetes and considerable evidence supports the association between insulin resistance, hyperinsulinemia, and vascular disease.^2,3 Although the molecular mechanisms are incompletely understood, this association is supported by several large clinical studies showing a direct relationship between insulin levels and cardiovascular risk. The Paris Prospective Study⁴ and the Multiple Risk Factor Intervention Trial (MRFIT)⁵ reported positive relationships between insulin levels and atherosclerotic events. In addition, the Veterans Affairs High Density Lipoprotein Intervention Trial (VA-HIT)⁶ demonstrated the highest incidence of cardiovascular events in the subgroups with highest levels of insulin. Finally, the landmark Insulin Resistance Atherosclerosis Study (IRAS) provided further evidence for an inverse relationship between carotid intima-medial thickness and insulin sensitivity.⁷

	Insulin Resistance and Smooth Muscle Cell Proliferation

 
Controversy exists regarding the cellular mechanisms leading to atherosclerosis in insulin resistance and type 2 diabetes. Because of the observed numerical increases and functional abnormalities in intimal smooth muscle cells (SMC) in diabetes, this cell type has received intensive attention. In advanced lesions, SMC and their secreted products are a major component of the lesion comprising up to 70 to 80% of the total content of advanced human lesions.⁸ In particular, diabetes accelerates SMC accumulation in atherosclerotic lesions and SMC proliferation directly correlates with insulin levels.^9,10 SMC proliferation is also the primary mechanism leading to . . . [Full Text of this Article]

Related Article:

C-Peptide Induces Vascular Smooth Muscle Cell Proliferation: Involvement of Src-Kinase, Phosphatidylinositol 3-Kinase, and Extracellular Signal-Regulated Kinase 1/2

Daniel Walcher, Christina Babiak, Paulina Poletek, Stephan Rosenkranz, Helga Bach, Susanne Betz, Renate Durst, Miriam Grüb, Vinzenz Hombach, Jack Strong, and Nikolaus Marx
Circ. Res. 2006 99: 1181-1187. [Abstract] [Full Text] [PDF]