Mitochondrial capacity in skeletal muscle is not stimulated by weight loss despite increases in insulin action and decreases in intramyocellular lipid content
Open accessAbstract
OBJECTIVE— In obesity and type 2 diabetes, exercise combined with weight loss increases skeletal muscle mitochondrial capacity. It remains unclear whether mitochondrial capacity increases because of weight loss, improvements in insulin resistance, or physical training. In this study, we examined the effects of an intervention of weight loss induced by diet and compared these with those of a similar intervention of weight loss by diet with exercise. Both are known to improve insulin resistance, and we tested the hypothesis that physical activity, rather than improved insulin resistance, is required to increase mitochondrial capacity of muscle. RESEARCH DESIGN AND METHODS— Sixteen sedentary overweight/obese volunteers were randomized to a 16-week intervention of diet (n = 7) or diet plus exercise (n = 9). Insulin sensitivity was measured using euglycemic clamps. Mitochondria were examined in muscle biopsies before and after intervention. We measured mitochondrial content and size by electron microscopy, electron transport chain (ETC) activity, cardiolipin content, and mitochondrial DNA content. Intramyocellular content of lipid (IMCL) and fiber-type distribution were determined by histology. RESULTS— The diet-only and diet plus exercise groups achieved similar weight loss (10.8 and 9.2%, respectively); only the diet plus exercise group improved aerobic capacity. Insulin sensitivity improved similarly in both groups. Mitochondrial content and ETC activity increased following the diet plus exercise intervention but remained unchanged following the diet-only intervention, and mitochondrial size decreased with weight loss despite improvement in insulin resistance. IMCL decreased in the diet-only but not in the diet plus exercise intervention. CONCLUSIONS— Despite similar effects to improve insulin resistance, these interventions had differential effects on mitochondria. Clinically significant weight loss in the absence of increased physical activity ameliorates insulin resistance and IMCL but does not increase muscle mitochondrial capacity in obesity.
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A low-calorie diet substantially enhanced insulin sensitivity (∼30% increase in insulin-stimulated glucose disposal) but failed to increase skeletal muscle mitochondrial function in the absence of exercise.
“a recent report also indicated that while a low-calorie diet substantially enhanced insulin sensitivity (e.g., ∼30% increase in insulin-stimulated glucose disposal), it failed to increase skeletal muscle mitochondrial function in the absence of exercise (19).”
From Age, Obesity, and Sex Effects on Insulin Sensitivity and Skeletal Muscle Mitochondrial Function (2010) · cites this paper as [19]
Mitochondrial content was determined by mitochondrial volume density measured by standard stereological methods.
“Mitochondrial content was determined by the parameter of mitochondrial volume density measured by standard stereological methods (19, 20) as in our previous studies (17, 18, 21).”
Other studies have reported correlations between mitochondria and insulin resistance in the absence of obesity, and mitochondrial content does not improve after clinically significant weight loss.
“Other studies have reported correlations between mitochondria and insulin resistance in the absence of obesity (8, 9), and mitochondrial content does not improve after clinically significant weight loss (21).”
Even in the insulin-resistant state, skeletal muscle mitochondria respond to training.
“In fact, we have shown that even in the insulin-resistant state, skeletal muscle mitochondria respond to training (17, 18, 21).”
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- Authors
- Toledo, F. G. S., Menshikova, E. V., Azuma, K., Radiková, Z., Kelley, C. A., Ritov, V. B., & Kelley, D. E.
- Affiliations
- University of Pittsburgh (US)
- From the Division of Endocrinology and Metabolism, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2008-04-01
- Volume
- 57
- Issue
- 4
- Pages
- 987-994
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2110869852
- Cited by
- 218
- References
- 36
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 4 · 2023: 12 · 2022: 9 · 2021: 7 · 2020: 13 · 2019: 7 · 2018: 12 · 2017: 10 · 2016: 5 · 2015: 14 · 2014: 14 · 2013: 19 · 2012: 14
- FWCI
- 16.07
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association
- University of Pittsburgh
- Slovenská Akadémia Vied
- National Institutes of Health (DK49200)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30-DK-462, DK-49200-08, R01DK049200)
- National Center for Research Resources (M01RR000056, 5 M01 RR00056)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- weight loss, diet-induced weight loss, exercise training, insulin resistance, insulin sensitivity, intramyocellular lipid, mitochondrial size, cardiolipin, mitochondrial DNA content, obesity, type 2 diabetes, cardiorespiratory fitness, fiber type distribution
- MeSH terms
- Cardiolipins, Diet, Reducing, DNA, Mitochondrial, Glucose Tolerance Test, Humans, Insulin, Life Style, Lipids, Microscopy, Electron, Mitochondria, Muscle, Obesity, Oxygen Consumption, Weight Loss, Exercise, Muscle, Skeletal, Overweight
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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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