Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities

William I Sivitz; Mark A Yorek

doi:10.1089/ars.2009.2531

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Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities

Journal article

Open access

Peer reviewed

Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities

William I Sivitz and Mark A Yorek

Antioxidants & redox signaling, Vol.12(4), pp.537-577

02/15/2010

DOI: 10.1089/ars.2009.2531

PMCID: PMC2824521

PMID: 19650713

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Abstract

Given their essential function in aerobic metabolism, mitochondria are intuitively of interest in regard to the pathophysiology of diabetes. Qualitative, quantitative, and functional perturbations in mitochondria have been identified and affect the cause and complications of diabetes. Moreover, as a consequence of fuel oxidation, mitochondria generate considerable reactive oxygen species (ROS). Evidence is accumulating that these radicals per se are important in the pathophysiology of diabetes and its complications. In this review, we first present basic concepts underlying mitochondrial physiology. We then address mitochondrial function and ROS as related to diabetes. We consider different forms of diabetes and address both insulin secretion and insulin sensitivity. We also address the role of mitochondrial uncoupling and coenzyme Q. Finally, we address the potential for targeting mitochondria in the therapy of diabetes.

Details

Title: Subtitle: Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities
Creators: William I Sivitz - Department of Internal Medicine, Division of Endocrinology and Metabolism, Iowa City Veterans Affairs Medical Center and the University of Iowa, Iowa City, Iowa
Mark A Yorek - Department of Internal Medicine, Division of Endocrinology and Metabolism, Iowa City Veterans Affairs Medical Center and the University of Iowa, Iowa City, Iowa
Resource Type: Journal article
Publication Details: Antioxidants & redox signaling, Vol.12(4), pp.537-577
DOI: 10.1089/ars.2009.2531
PMID: 19650713
PMCID: PMC2824521
NLM abbreviation: Antioxid Redox Signal
ISSN: 1523-0864
eISSN: 1557-7716
Language: English
Date published: 02/15/2010
Academic Unit: Fraternal Order of Eagles Diabetes Research Center; Endocrinology and Metabolism; Internal Medicine
Record Identifier: 9984094646102771

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