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Cited by 146Mitochondrial Function and PathologyAdipose Tissue and MetabolismMetabolism, Diabetes, and Cancer

Mitochondrial dysfunction, insulin resistance, and type 2 diabetes mellitus

Abdul-Ghani, Muhammad A., DeFronzo, Ralph A.·2008·Current Diabetes Reports
DOI 10.1007/s11892-008-0030-1
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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 relationship to insulin resistance in common metabolic diseases characterized by impaired insulin action.

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Crossref · 10.1007/s11892-008-0030-1

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65 of 65 references verified0 citation errors · 0 not checkable

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  • A mitochondrial oxidative phosphorylation defect in skeletal muscle may contribute to increased intramyocellular fat content.

    “suggest that this mitochondrial defect contributes to the increased intramyocellar fat content.”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [18]

  • Recent studies have reported a defect in mitochondrial oxidative phosphorylation in skeletal muscle in several insulin-resistant states.

    “Recent studies have reported a mitochondrial defect in oxidative phosphorylation in skeletal muscle in variety of insulin resistant states.”

    From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [18]

  • Mitochondrial dysfunction leads to impaired fatty acid oxidation, increased fatty acyl-CoA and DAG, activation of PKC, serine phosphorylation of IRS-1, blocking insulin signaling.

    “Mitochondrial dysfunction should lead to impaired fatty acid oxidation, resulting in increased intracellular fatty acyl-CoA and diacylglycerol content, with consequent activation of protein kinase C (1, 204). This, in turn, triggers a serine kinase cascade, ultimately resulting in serine phosphorylation of insulin-receptor substrate type 1 (IRS-1). This has the consequence of blocking the tyrosine”

    From Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010) · cites this paper as [1]

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Authors
Abdul-Ghani, M. A., & DeFronzo, R. A.
Affiliations
The University of Texas at San Antonio Health Science Center (US)
ORCID
DeFronzo, Ralph A.
Venue
Current Diabetes Reports
Publisher
Springer Science and Business Media LLC
Published
2008-06
Volume
8
Issue
3
Pages
173-178
ISSN
  • 1534-4827 (ISSN-L)
  • 1539-0829
DOI
10.1007/s11892-008-0030-1
OpenAlex
W2111504946
Semantic Scholar
40928a1ba7c82d86511874f290fc872cb921a3cb
Cited by
146
References
65
Citations by year
2026: 6 · 2025: 6 · 2024: 6 · 2023: 6 · 2022: 8 · 2021: 8 · 2020: 7 · 2019: 6 · 2018: 10 · 2017: 7 · 2016: 4 · 2015: 7 · 2014: 8 · 2013: 8 · 2012: 10
FWCI
0.98
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Current Diabetes Reports (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords
mitochondrial dysfunction, insulin resistance, type 2 diabetes, oxidative phosphorylation, skeletal muscle, liver, metabolic syndrome, obesity, mitochondrial density, mitochondrial DNA copy number, ATP production, TCA cycle, substrate oxidation
MeSH terms
Animals, Diabetes Mellitus, Type 2, Fatty Acids, Humans, Insulin Resistance, Mitochondria, Muscle, Skeletal

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