Cited by 268Mitochondrial Function and PathologyAdipose Tissue and MetabolismMetabolism, Diabetes, and Cancer

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Mitochondrial dysfunction and lipotoxicity

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Schrauwen, Patrick, Schrauwen-Hinderling, Vera, Hoeks, Joris, Hesselink, Matthijs K.C.·2010·Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids

DOI 10.1016/j.bbalip.2009.09.011

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Abstract

Mitochondrial dysfunction in skeletal muscle has been suggested to underlie the development of insulin resistance and type 2 diabetes mellitus. Reduced mitochondrial capacity will contribute to the accumulation of lipid intermediates, desensitizing insulin signaling and leading to insulin resistance. Why mitochondrial function is reduced in the (pre-)diabetic state is, however, so far unknown. Although it is tempting to suggest that skeletal muscle insulin resistance may result from an inherited or acquired reduction in mitochondrial function in the pre-diabetic state, it cannot be excluded that mitochondrial dysfunction may in fact be the consequence of the insulin-resistant/diabetic state. Lipotoxicity, the deleterious effects of accumulating fatty acids in skeletal muscle cells, may lie at the basis of mitochondrial dysfunction: next to producing energy, mitochondria are also the major source of reactive oxygen species (ROS). Fatty acids accumulating in the vicinity of mitochondria are vulnerable to ROS-induced lipid peroxidation. Subsequently, these lipid peroxides could have lipotoxic effects on mtDNA, RNA and proteins of the mitochondrial machinery, leading to mitochondrial dysfunction. Indeed, increased lipid peroxidation has been reported in insulin resistant skeletal muscle and the mitochondrial uncoupling protein-3, which has been suggested to prevent lipid-induced mitochondrial damage, is reduced in subjects with an impaired glucose tolerance and in type 2 diabetic patients. These findings support the hypothesis that fat accumulation in skeletal muscle may precede the reduction in mitochondrial function that is observed in type 2 diabetes mellitus.

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Authors: Schrauwen, P., Schrauwen-Hinderling, V., Hoeks, J., & Hesselink, M. K. C.
Affiliations: Maastricht University Medical Centre (NL)
Corresponding author: Schrauwen, Patrick
ORCID: Schrauwen, Patrick
Hesselink, Matthijs K.C.
Venue: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
Publisher: Elsevier BV
Published: 2010-03
Volume: 1801
Issue: 3
Pages: 266-271
ISSN: 1388-1981 (ISSN-L)
DOI: 10.1016/j.bbalip.2009.09.011
OpenAlex: W1990194575
Cited by: 268
References: 68
Citations by year: 2026: 11 · 2025: 13 · 2024: 20 · 2023: 11 · 2022: 10 · 2021: 20 · 2020: 21 · 2019: 11 · 2018: 14 · 2017: 12 · 2016: 12 · 2015: 20 · 2014: 19 · 2013: 20 · 2012: 22
FWCI: 1.38
Type: journal article
Language: en
Open access: green
cris.maastrichtuniversity.nl
Licence: other-oa
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids (publishedVersion)
PubMed (publishedVersion)
Research Publications (Maastricht University) (submittedVersion, other-oa)
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, lipotoxicity, skeletal muscle, insulin resistance, type 2 diabetes, lipid peroxidation, reactive oxygen species, fatty acid accumulation, mitochondrial DNA damage, impaired glucose tolerance
MeSH terms: Animals, Diabetes Mellitus, Type 2, Humans, Mitochondria, Models, Biological, Muscle, Skeletal, Mitochondrial Diseases, Lipid Metabolism, Lipid Metabolism Disorders

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