Intramuscular lipid metabolism, insulin action, and obesity
Open accessAbstract
With the increasing prevalence of obesity, research has focused on the molecular mechanism(s) linking obesity and skeletal muscle insulin resistance. Metabolic alterations within muscle, such as changes in the cellular location of fatty acid transporter proteins, decreased mitochondrial enzyme activity, and defects in mitochondrial morphology, likely contribute to obesity and insulin resistance. These defects are thought to play a role in the reduced skeletal muscle fatty acid oxidation and increased intramuscular lipid (IMCL) accumulation that is apparent with obesity and other insulin‐resistant states such as type 2 diabetes. Intramuscular triacylglycerol does not appear to be a ubiquitous marker of insulin resistance, although specific IMCL intermediates such as long‐chain fatty acyl‐CoAs, ceramide, and diacylglycerol may inhibit insulin signal transduction. In this review, we will briefly summarize the defects in skeletal muscle lipid metabolism associated with obesity, and discuss the proposed mechanisms by which these defects may contribute to insulin resistance. © 2008 IUBMB IUBMB Life, 61(1): 47–55, 2009
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Pathological myosteatosis in aging and obesity is associated with decreased insulin sensitivity and muscle mass and strength loss.
“Pathological myosteatosis in aging and obesity is associated with decreased insulin sensitivity and muscle mass and strength loss.”
From The critical role of oxidative stress in sarcopenic obesity (2021) · cites this paper as [35]
Decreased insulin secretion by the pancreas is derived from elevated concentrations of fatty acids, which induce β-cell apoptosis and reduce proliferation of pancreatic cells.
“Together with these events, the decreased insulin secretion by the pancreas is derived from elevated concentrations of fatty acids, which induces β-cell apoptosis and reduces proliferation of pancreatic cells [14, 16, 34–36].”
From The critical role of oxidative stress in sarcopenic obesity (2021) · cites this paper as [35]
The mechanism of myosteatosis-induced insulin resistance involves impaired insulin signaling by lipidic intermediates such as diacylglycerol, long-chain acyl-coenzyme A, and ceramide, which inhibit GLUT-4 translocation to the sarcolemma.
“The mechanism involves the impaired insulin signaling by interacting with lipidic intermediates such as diacylglycerol (DAG), long-chain acyl-coenzyme A, and ceramide. These interactions at various levels inhibit the GLUT-4 translocation to the sarcolemma.”
From The critical role of oxidative stress in sarcopenic obesity (2021) · cites this paper as [35]
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- Authors
- Consitt, L. A., Bell, J. A., & Houmard, J. A.
- Affiliations
- East Carolina University (US)
- Corresponding author
- Consitt, Leslie A.
- Venue
- IUBMB Life
- Publisher
- Wiley
- Published
- 2008-10-06
- Volume
- 61
- Issue
- 1
- Pages
- 47-55
- ISSN
- 1521-6543 (ISSN-L)
- 1521-6551
- PMC
- PMC2612735
- OpenAlex
- W2095780917
- Cited by
- 180
- References
- 100
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 10 · 2023: 5 · 2022: 11 · 2021: 10 · 2020: 9 · 2019: 9 · 2018: 9 · 2017: 13 · 2016: 9 · 2015: 10 · 2014: 16 · 2013: 10 · 2012: 17
- FWCI
- 0.77
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- IUBMB Life (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- The Scholarship East Carolina University's Institutional Repository (East Carolina University) (submittedVersion)
- Funders
- National Institute on Aging (AG025205, R01AG025205)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-56112, R01DK056112)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- obesity, skeletal muscle insulin resistance, fatty acid transporters, mitochondrial dysfunction, fatty acid oxidation, ceramide, diacylglycerol, long-chain fatty acyl-CoA, insulin signaling, type 2 diabetes
- MeSH terms
- Humans, Insulin, Insulin Resistance, Mitochondria, Models, Biological, Obesity, Signal Transduction, 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.
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