Cited by 135Metabolism, Diabetes, and CancerMitochondrial Function and PathologyAdipose Tissue and Metabolism

Mitochondrial Dysfunction in Type 2 Diabetes and Obesity

Højlund, Kurt, Mogensen, Martin, Sahlin, Kent, Beck-Nielsen, Henning·2008·Endocrinology and Metabolism Clinics of North America

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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Registry

Crossref · 10.1016/j.ecl.2008.06.006

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104 of 104 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 [19]

  • 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 [19]

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Authors
Højlund, K., Mogensen, M., Sahlin, K., & Beck-Nielsen, H.
Affiliations
  • Odense University Hospital (DK)
  • University of Southern Denmark (DK)
Corresponding author
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
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 › 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

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