Mitochondrial dysfunction, insulin resistance, and type 2 diabetes mellitus

Muhammad A. Abdul-Ghani, Ralph A. DeFronzo

Research output: Contribution to journalReview articlepeer-review

99 Scopus citations

Abstract

Insulin resistance is a characteristic feature of type 2 diabetes mellitus, obesity, and the metabolic syndrome. Increased intracellular fat content in skeletal muscle and liver associated with insulin resistance has led to the hypothesis that a mitochondrial defect in substrate oxidation exists in disorders of insulin resistance. In vivo measurements of metabolic fluxes through the tricarboxylic acid and oxidative phosphorylation with magnetic resonance spectroscopy have demonstrated multiple defects in mitochondrial function in skeletal muscle. A decrease in mitochondrial density and mitochondrial copy number has been reported in insulin-resistant individuals. However, these findings have not been a consistent observation in all studies. Similarly, an intrinsic functional defect in mitochondrial adenosine triphosphate production synthesis has been reported in some but not all studies, This review summarizes evidence that implicates a defect in mitochondrial oxidative phosphorylation and its relation hip to insulin resistance in common metabolic diseases characterized by impaired insulin action.

Original languageEnglish (US)
Pages (from-to)173-178
Number of pages6
JournalCurrent Diabetes Reports
Volume8
Issue number3
DOIs
StatePublished - Jun 1 2008

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

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