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Mitochondrial Dysfunction in Type 2 Diabetes and Obesity
Abstract
Insulin resistance in skeletal muscle is a major hallmark of type 2 diabetes mellitus (T2D) and obesity that is characterized by impaired insulin-mediated glucose transport and glycogen synthesis and by increased intramyocellular content of lipid metabolites. Several studies have provided evidence for mitochondrial dysfunction in skeletal muscle of type 2 diabetic and prediabetic subjects, primarily due to a lower content of mitochondria (mitochondrial biogenesis) and possibly to a reduced functional capacity per mitochondrion. This article discusses the latest advances in the understanding of the molecular mechanisms underlying insulin resistance in human skeletal muscle in T2D and obesity, with a focus on possible links between insulin resistance and mitochondrial dysfunction.
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“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 [19]
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“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 [19]
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Metadata
- Authors
- Højlund, K., Mogensen, M., Sahlin, K., & Beck-Nielsen, H.
- Affiliations
- Odense University Hospital (DK)
- University of Southern Denmark (DK)
- Corresponding author
- Højlund, Kurt
- ORCID
- Højlund, Kurt
- Venue
- Endocrinology and Metabolism Clinics of North America
- Publisher
- Elsevier BV
- Published
- 2008-09
- Volume
- 37
- Issue
- 3
- Pages
- 713-731
- ISSN
- 0889-8529 (ISSN-L)
- OpenAlex
- W2107088422
- Semantic Scholar
- 31431014b8af686b99bb75eb8c7c784d89c4fca3
- Cited by
- 135
- References
- 102
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 6 · 2023: 12 · 2022: 8 · 2021: 3 · 2020: 8 · 2019: 4 · 2018: 4 · 2017: 10 · 2016: 8 · 2015: 5 · 2014: 9 · 2013: 6 · 2012: 7
- FWCI
- 0.95
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrinology and Metabolism Clinics of North America (publishedVersion)
- PubMed (publishedVersion)
- University of Southern Denmark Research Portal (University of Southern Denmark) (submittedVersion)
- Funders
- Diabetesforeningen
- Sundhed og Sygdom, Det Frie Forskningsråd
- Novo Nordisk UK Research Foundation
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- mitochondrial dysfunction, type 2 diabetes, obesity, insulin resistance, skeletal muscle, mitochondrial biogenesis, glucose transport, glycogen synthesis, intramyocellular lipid, prediabetes
- MeSH terms
- Organelle Biogenesis, Diabetes Mellitus, Type 2, Humans, Insulin Resistance, Mitochondria, Obesity, Oxidation-Reduction, Proteomics
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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