Weight loss increases skeletal muscle mitochondrial energy efficiency in obese mice
Open accessAbstract
Weight loss from an overweight state is associated with a disproportionate decrease in whole-body energy expenditure that may contribute to the heightened risk for weight regain. Evidence suggests that this energetic mismatch originates from lean tissue. Although this phenomenon is well documented, the mechanisms have remained elusive. We hypothesized that increased mitochondrial energy efficiency in skeletal muscle is associated with reduced expenditure under weight loss. Wildtype (WT) male C57BL6/N mice were fed with high-fat diet for 10 weeks, followed by a subset of mice that were maintained on the obesogenic diet (OB) or switched to standard chow to promote weight loss (WL) for additional 6 weeks. Mitochondrial energy efficiency was evaluated using high-resolution respirometry and fluorometry. Mass spectrometric analyses were employed to describe the mitochondrial proteome and lipidome. Weight loss promoted ~50% increase in the efficiency of oxidative phosphorylation (ATP produced per O2 consumed, or P/O) in skeletal muscle. However, Weight loss did not appear to induce significant changes in mitochondrial proteome, nor any changes in respiratory supercomplex formation. Instead, it accelerated the remodeling of mitochondrial cardiolipin (CL) acyl-chains to increase tetralinoleoyl CL (TLCL) content, a species of lipids thought to be functionally critical for the respiratory enzymes. We further show that lowering TLCL by deleting the CL transacylase tafazzin was sufficient to reduce skeletal muscle P/O and protect mice from diet-induced weight gain. These findings implicate skeletal muscle mitochondrial efficiency as a novel mechanism by which weight loss reduces energy expenditure in obesity.
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Weight loss in obese mice did not robustly alter skeletal muscle mitochondrial proteome.
“Notably, weight loss in obese mice did not robustly alter skeletal muscle mitochondrial proteome [78].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [78]
Weight loss itself can enhance OXPHOS efficiency in muscle of obese animals concomitant to a decrease in whole-body energy expenditure.
“Whether the effects of caloric restriction on mitochondria is simply through weight loss is unclear as weight loss itself can enhance OXPHOS efficiency in muscle of obese animals concomitant to a decrease in whole-body energy expenditure [78].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [78]
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- Authors
- Ferrara, P. J., Lang, M. J., Johnson, J. M., Watanabe, S., McLaughlin, K. L., Alan Maschek, J., Verkerke, A. R. P., Siripoksup, P., Chaix, A., Cox, J. E., Fisher-Wellman, K. H., & Funai, K.
- Affiliations
- University of Utah (US)
- East Carolina University (US)
- Diabetes & Metabolism Research Center, University of Utah, Salt Lake City, Utah 84112 , United States
- East Carolina Diabetes & Obesity Institute, East Carolina University , Greenville, North Carolina 27834 , United States
- Corresponding author
- Funai, Katsuhiko
- ORCID
- Venue
- Life Metabolism
- Publisher
- Oxford University Press (OUP)
- Published
- 2023-04-01
- Volume
- 2
- Issue
- 2
- ISSN
- 2755-0230 (ISSN-L)
- PMC
- PMC10195096
- OpenAlex
- W4362552319
- Cited by
- 26
- References
- 52
- Citations by year
- 2026: 7 · 2025: 12 · 2024: 5 · 2023: 2
- FWCI
- 2.32
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Licence
- Locations
- Life Metabolism (publishedVersion, cc-by)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Defense (W81XWH, W81XWH1910213)
- American Heart Association (19PRE34380991, 18PRE33960491, 915674)
- National Institutes of Health (1s10od016232-01, W81XWH, 1s10od021505-01, DK110858)
- National Institute on Aging (R01AG065993, R01AG074535)
- National Institute of General Medical Sciences (R01GM144613)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK127979, R01DK107397, T32DK091317, U54DK110858, P30DK020579)
- 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 › Muscle Physiology and Disorders
- Keywords
- weight loss, skeletal muscle, oxidative phosphorylation, P/O ratio, obesity, energy expenditure, high-fat diet, tafazzin, mitochondrial proteome, respiratory supercomplexes, weight regain
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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