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]
Citations
Cites
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Dysfunction of Mitochondria in Human Skeletal Muscle in Type 2 Diabetes
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Impaired Mitochondrial Activity in the Insulin-Resistant Offspring of Patients with Type 2 Diabetes
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Mitochondrial dysfunction in the elderly: possible role in insulin resistance
Petersen, K. F., Befroy, D., Dufour, S., Dziura, J., Ariyan, C., Rothman, D. L., DiPietro, L., Cline, G. W., & Shulman, G. I. (2003) · Science · doi:10.1126/science.1082889 · Cited by 2,107
Mitochondrial dysfunction and type 2 diabetes
Lowell, B. B., & Shulman, G. I. (2005) · Science · doi:10.1126/science.1104343 · Cited by 2,070
Adaptations of skeletal muscle to endurance exercise and their metabolic consequences
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Self-citationMetabolic Syndrome and Risk of Incident Cardiovascular Events and Death
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Research works printed but not linked: 3
- Chavez-Velazquez A, Jani R, Abdul-Ghani MA, et al.: Short-term elevation of plasma free fatty acids (FFA) decreases skeletal muscle mitochondrial membrane potential in healthy glucose tolerant subjects. Diabetes 2007, 56(Suppl 1):242A.
- Abdul-Ghani MA, Jani R, Molina M, et al.: Decreased mitochondrial ATP synthesis in obese non-diabetic subjects. Diabetes 2008, 56(Suppl 1):1456A.
- Abdul-Ghani MA, Muller F, Liu Y, et al.: Deleterious effect of elevated fatty acid metabolites concentration on skeletal muscle mitochondrial ATP synthesis. Diabetes 2007, 56(Suppl 1):1303A.
Cited by
Sorted by citations
Bhatti, J. S., Bhatti, G. K., & Reddy, P. H. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2016.11.010 · Cited by 1,655
Pesticides and human chronic diseases: Evidences, mechanisms, and perspectives
Mostafalou, S., & Abdollahi, M. R. (2013) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2013.01.025 · Cited by 1,333
“Abnormal function of the mitochondrial respiratory chain is the primary cause of imbalanced cellular energy homeostasis and has been widely studied in different types of human diseases most of all diabetes (Abdul-Ghani and DeFronzo, 2008; Kim et al., 2008; Lowell and Shulman, 2005; Ma et al., 2012) and neurodegenerati…”
BackgroundDeFronzo, R. A. (2010) · Diabetologia · doi:10.1007/s00125-010-1684-1 · Cited by 908
“In isolated mitochondria from obese and type 2 diabetic individuals, we have demonstrated that ATP synthesis is reduced [179, 180] and correlates closely with decreased insulin-stimulated glucose disposal and increased fasting plasma NEFA.”
BackgroundSelf-citationRonald, C. W., & Chan, J. C. N. (2013) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.12098 · Cited by 841
Sivitz, W. I., & Yorek, M. A. (2010) · Antioxidants & Redox Signaling · doi:10.1089/ars.2009.2531 · Cited by 742
“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).”
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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