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Table of Contents
Vol. 58, No. 1, 2011
Issue release date: April 2011
Section title: Review
Ann Nutr Metab 2011;58:25–36
(DOI:10.1159/000323395)

Insulin Resistance: Pathophysiology and Rationale for Treatment

Muntoni S.a · Muntoni S.a, b
aCentre for Metabolic Diseases and Atherosclerosis, The ME.DI.CO. Association and bDepartment of Toxicology, Unit of Oncology and Molecular Pathology, University Medical School, Cagliari, Italy

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Article / Publication Details

First-Page Preview
Abstract of Review

Received: December 30, 2009
Accepted: December 06, 2010
Published online: February 08, 2011
Issue release date: April 2011

Number of Print Pages: 12
Number of Figures: 4
Number of Tables: 0

ISSN: 0250-6807 (Print)
eISSN: 1421-9697 (Online)

For additional information: http://www.karger.com/ANM

Abstract

After binding to its receptor and activating the β-subunit, insulin is faced with two divergent pathways: one is phosphatidylinositol 3-kinase (PI 3-K) dependent, while another is dependent upon activation of mitogen-activated protein kinase (MAP-K). The former is absolutely necessary for mediating most metabolic and antiapoptotic effects; the latter is linked to nonmetabolic, proliferative and mitogenic effects. In obese patients, especially with type 2 diabetes mellitus (DM2), only the PI 3-K, but not the MAP-K, is resistant to insulin stimulation: hence insulin resistance is better defined as metabolic insulin resistance. The resulting ‘compensatory hyperinsulinemia’ is an unsuccessful attempt to overcome the inhibition of the metabolic pathway at the price of unopposed stimulation of the MAP-K pathway, and the administration of exogenous insulin might worsen the metabolic dysfunction. As the preferential activation of the MAP-K pathway in insulin-resistant patients has atherogenic and mitogenic properties, this leads to atherosclerosis and cancer. Metformin may carry out direct protective action on human β cells, inasmuch as it improves both primary and secondary endpoints through selective inhibition of fatty acyl oxidation.

© 2011 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Review

Received: December 30, 2009
Accepted: December 06, 2010
Published online: February 08, 2011
Issue release date: April 2011

Number of Print Pages: 12
Number of Figures: 4
Number of Tables: 0

ISSN: 0250-6807 (Print)
eISSN: 1421-9697 (Online)

For additional information: http://www.karger.com/ANM


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