High-fat diet, muscular lipotoxicity and insulin resistance
Open accessAbstract
A high dietary fat intake and low physical activity characterize the current Western lifestyle. Dietary fatty acids do not stimulate their own oxidation and a surplus of fat is stored in white adipose tissue, liver, heart and muscle. In these organs intracellular lipids serve as a rapidly-available energy source during, for example, physical activity. However, under conditions of elevated plasma fatty acid levels and high dietary fat intake, conditions implicated in the development of modern diseases such as obesity and type 2 diabetes mellitus, fat accumulation in liver and muscle (intramyocellular lipids; IMCL) is associated with the development of insulin resistance. Recent data suggest that IMCL are specifically harmful when combined with reduced mitochondrial function, both conditions that characterize type 2 diabetes. In the (pre)diabetic state reduced expression of the transcription factor PPARγ co-activator-1α (PGC-1α), which is involved in mitochondrial biogenesis, has been suggested to underlie the reduced mitochondrial function. Importantly, the reduction in PGC-1α may be a result of low physical activity, consumption of high-fat diets and high plasma fatty acid levels. Mitochondrial function can also be impaired as a result of enhanced mitochondrial damage by reactive oxygen species. Fatty acids in the vicinity of mitochondria are particularly prone to lipid peroxidation. In turn, lipid peroxides can induce oxidative damage to mitochondrial RNA, DNA and proteins. The mitochondrial protein uncoupling protein 3, which is induced under high-fat conditions, may serve to protect mitochondria against lipid-induced oxidative damage, but is reduced in the prediabetic state. Thus, muscular lipotoxicity may impair mitochondrial function and may be central to insulin resistance and type 2 diabetes mellitus.
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In animals and humans, an increase in body weight is accompanied by an increase in skeletal muscle insulin resistance.
“Studies in experimental animals and in man have demonstrated that the increase in body weight is accompanied with an increase in skeletal muscle insulin resistance [48–52].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [52]
High-fat feeding is associated with insulin resistance and may lead to oversupply of fatty acids to mitochondria.
“High-fat feeding is associated with insulin resistance (286) and may lead to oversupply of fatty acids to mitochondria.”
From Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010) · cites this paper as [286]
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- Authors
- Schrauwen, P.
- Affiliations
- Maastricht University (NL)
- Corresponding author
- Schrauwen, Patrick
- ORCID
- Schrauwen, Patrick
- Venue
- Proceedings of the Nutrition Society
- Publisher
- Cambridge University Press (CUP)
- Published
- 2007-02
- Volume
- 66
- Issue
- 1
- Pages
- 33-41
- ISSN
- 0029-6651 (ISSN-L)
- 1475-2719
- OpenAlex
- W2143488518
- Cited by
- 153
- References
- 65
- Citations by year
- 2026: 1 · 2025: 10 · 2024: 8 · 2023: 6 · 2022: 3 · 2021: 7 · 2020: 6 · 2019: 7 · 2018: 6 · 2017: 7 · 2016: 5 · 2015: 7 · 2014: 5 · 2013: 6 · 2012: 12
- FWCI
- 9.09
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of The Nutrition Society (publishedVersion)
- PubMed (publishedVersion)
- Research Publications (Maastricht University) (submittedVersion, other-oa)
- Funders
- Koninklijke Nederlandse Akademie van Wetenschappen
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- 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
- Keywords
- high-fat diet, insulin resistance, intramyocellular lipid, type 2 diabetes, mitochondrial function, PGC-1α, mitochondrial biogenesis, lipid peroxidation, reactive oxygen species, UCP3, physical inactivity, obesity, plasma fatty acids
- MeSH terms
- Adipose Tissue, Diabetes Mellitus, Type 2, Dietary Fats, Humans, Insulin Resistance, Mitochondria, Muscle, Exercise, Muscle, Skeletal, Lipid Metabolism
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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