Effect of Short-Term Free Fatty Acids Elevation on Mitochondrial Function in Skeletal Muscle of Healthy Individuals
Open accessAbstract
Context: Mitochondrial dysfunction has been proposed as an underlying mechanism in the pathogenesis of insulin resistance and type 2 diabetes mellitus. Objective: To determine whether mitochondrial dysfunction plays a role in the free fatty acid (FFA)-induced impairment in insulin action in skeletal muscle of healthy subjects. Design: Eleven lean normal glucose tolerant individuals received 8 h lipid and saline infusion on separate days with a euglycemic insulin clamp during the last 2 h. Vastus lateralis muscle biopsies were performed at baseline and after 6 h lipid or saline infusion. Inner mitochondrial membrane potential (Ψm) and mitochondrial mass were determined ex vivo by confocal microscopy. Results: Compared with saline infusion, lipid infusion reduced whole-body glucose uptake by 22% (P < 0.05). Ψm decreased by 33% (P < 0.005) after lipid infusion and the decrement in Ψm correlated with change in plasma FFA after lipid infusion (r = 0.753; P < 0.005). Mitochondrial content and morphology did not change after lipid infusion. No significant changes in genes expression, citrate synthase activity, and total ATP content were observed after either lipid or saline infusion. Conclusions: Short-term physiological increase in plasma FFA concentration in lean normal glucose tolerant subjects induces insulin resistance and impairs mitochondrial membrane potential but has no significant effects on mitochondrial content, gene expression, ATP content, or citrate synthase activity.
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Short-term lipid infusion for 6 to 8 h in healthy individuals does not change mitochondrial content, morphology, and respiration rates in skeletal muscle despite a lower mitochondrial membrane potential.
“Short-term lipid infusion for 6 to 8 h in healthy individuals does not change mitochondrial content, morphology, and respiration rates in skeletal muscle despite a lower mitochondrial membrane potential (4, 10).”
From Mitochondrial Fission Contributes to Mitochondrial Dysfunction and Insulin Resistance in Skeletal Muscle (2012) · cites this paper as [10]
A mitochondrial defect similar to that in insulin-resistant individuals can be produced in young lean healthy subjects by physiologic elevation of plasma FFA concentration.
“a mitochondrial defect similar to that observed in insulin-resistant individuals can be produced in young lean healthy subjects by physiologic elevation of the plasma FFA concentration [110, 131]”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [131]
Acute rises in circulating NEFA in healthy people cause or are linked to insulin resistance.
“Acute elevation in circulating NEFA levels in healthy individuals has been linked to insulin resistance in multiple investigations [10–13].”
From Sleep restriction increases free fatty acids in healthy men (2015) · cites this paper as [12]
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Intermuscular Adipose Tissue in CKD
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Muscle Biopsy to Investigate Mitochondrial Turnover
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Muscle Biopsy To Investigate Mitochondrial Turnover
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synthesis in human skeletal muscle Acute elevation of plasma lipids does not affect ATP
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- Authors
- Chavez, A. O., Kamath, S., Jani, R., Sharma, L. K., Monroy, A., Abdul-Ghani, M. A., Centonze, V. E., Sathyanarayana, P., Coletta, D. K., Jenkinson, C. P., Bai, Y., Folli, F., DeFronzo, R. A., & Tripathy, D.
- Affiliations
- Division of Diabetes (A.O.C., S.K., R.J., A.M., M.A.A.-G., P.S., D.K.C., C.P.J., F.F., R.A.D., D.T.), Department of Medicine, University of Texas Health Science Center at San Antonio, Texas 78229
- The University of Texas at San Antonio Health Science Center (US)
- Corresponding author
- Tripathy, Devjit
- ORCID
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 2010-01-01
- Volume
- 95
- Issue
- 1
- Pages
- 422-429
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- PMC
- PMC2805487
- OpenAlex
- W2170721365
- Cited by
- 52
- References
- 41
- Citations by year
- 2026: 1 · 2025: 2 · 2023: 1 · 2022: 1 · 2021: 3 · 2020: 1 · 2018: 7 · 2017: 3 · 2016: 5 · 2015: 6 · 2014: 3 · 2013: 3 · 2012: 3
- FWCI
- 2.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association
- Deutsches Krebsforschungszentrum
- National Institutes of Health (AG013319, CA54174)
- University of Texas Health Science Center at San Antonio (CA54174)
- National Institute on Aging (P01 AG19316, AG013319, P01AG019316, P30AG013319)
- National Cancer Institute (P30CA 54174, P30CA054174)
- National Institute of Diabetes and Digestive and Kidney Diseases (R56DK024092, DK 24092, R01DK079195, R01DK024092)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- free fatty acids, mitochondrial dysfunction, skeletal muscle, insulin resistance, lipid infusion, mitochondrial membrane potential, glucose uptake, type 2 diabetes, insulin action, mitochondrial content, citrate synthase, ATP levels
- MeSH terms
- Adenosine Triphosphate, Adult, Citrate (si)-Synthase, Fatty Acids, Nonesterified, Female, Glucose, Health, Humans, Infusions, Intravenous, Insulin, Lipids, Male, Mitochondria, Muscle, Glucose Clamp Technique, Up-Regulation, Muscle, Skeletal, Membrane Potential, Mitochondrial
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