The DOI matches its Crossref record; 65 of the 65 references it cites were found in a registry or an index.
Mitochondrial dysfunction, insulin resistance, and type 2 diabetes mellitus
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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In the citing paper
“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]
In the citing paper
“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]
In the citing paper
“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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Metadata
- 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
- Published
- 2008-06
- Volume
- 8
- Issue
- 3
- Pages
- 173-178
- ISSN
- 1534-4827 (ISSN-L)
- 1539-0829
- 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 (medical) › 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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