The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.
Increased Lipid Availability Impairs Insulin-Stimulated ATP Synthesis in Human Skeletal Muscle
Open accessAbstract
Insulin resistance correlates with intramyocellular lipid content (IMCL) and plasma free fatty acids (FFAs) and was recently linked to mitochondrial dysfunction. We examined the underlying relationships by measuring skeletal muscle ATP synthase flux, glucose transport/phosphorylation, and IMCL in response to different plasma insulin and plasma FFA concentrations. Healthy men were studied twice during hyperinsulinemic-euglycemic clamps with (LIP) or without (CON) lipid infusion (plasma FFA: CON ∼36 vs. LIP ∼1,034 μmol/l, P < 0.001). ATP synthase flux, glucose-6-phosphate (G6P), and IMCL were determined before and during the clamp in calf muscle using 31P and 1H magnetic resonance spectroscopy. Plasma lipid elevation resulted in ∼46% reduced whole-body glucose metabolism (180–360 min; P < 0.0001 vs. CON) and a 70% lower rise of G6P (P < 0.05 vs. CON) without significant changes in IMCL (LIP 117 ± 12% vs. CON 93 ± 3% of basal, P = 0.073). During the clamp, ATP synthase flux increased by ∼60% under control conditions (P = 0.02 vs. baseline) and was 24% lower during lipid infusion (LIP 11.0 ± 0.9 vs. CON 14.6 ± 1.2 μmol · g muscle−1 · min−1, P < 0.05). Physiologically increased plasma FFA concentrations reduce insulin-stimulated muscle ATP synthase flux in parallel with induction of insulin resistance.
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“Lastly, experimental induction of insulin resistance in skeletal muscle, by a physiological increase in plasma FFA concentration in lean healthy insulin-sensitive individuals, is associated with a decrease in oxidative phosphorylation flux in skeletal muscle [110].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [110]
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“High levels of free FA (FFA) were shown to alter ATP synthesis in skeletal muscle (30).”
From TFAM Enhances Fat Oxidation and Attenuates High-Fat Diet–Induced Insulin Resistance in Skeletal Muscle (2019) · cites this paper as [30]
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“Moreover, it was shown in a comparable study that short-term elevation of lipid availability reduces insulin-stimulated increase in ATP synthase flux in skeletal muscle (10), although this may mainly reflect an effect of muscular insulin resistance on ATP flux.”
From Prolonged fasting identifies skeletal muscle mitochondrial dysfunction as consequence rather than cause of human insulin resistance (2010) · cites this paper as [10]
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“PGC-1α expression (9) and the insulin-stimulated increase in skeletal muscle ATP synthesis (10) were reduced upon lipid infusion.”
From Prolonged fasting identifies skeletal muscle mitochondrial dysfunction as consequence rather than cause of human insulin resistance (2010) · cites this paper as [10]
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“one cannot completely exclude the possibility that the mitochondrial defect results secondary to insulin resistance.”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [110]
In the citing paper
“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 [110]
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A short questionnaire for the measurement of habitual physical activity in epidemiological studies
Baecke, J. A. H., BUREMA, J., & Frijters, J. E. R. (1982) · American Journal of Clinical Nutrition · doi:10.1093/ajcn/36.5.936 · Cited by 3,950
Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes
Özcan, U., Cao, Q., Yilmaz, E., Lee, A.-H., Iwakoshi, N. N., Özdelen, E., Tuncman, G., Görgün, C., Glimcher, L. H., & Hotamisligil, G. S. (2004) · Science · doi:10.1126/science.1103160 · Cited by 3,844
Dysfunction of Mitochondria in Human Skeletal Muscle in Type 2 Diabetes
Kelley, D. E., He, J., Menshikova, E. V., & Ritov, V. B. (2002) · Diabetes · doi:10.2337/diabetes.51.10.2944 · Cited by 2,321
Impaired Mitochondrial Activity in the Insulin-Resistant Offspring of Patients with Type 2 Diabetes
Petersen, K. F., Dufour, S., Befroy, D., Garcia, R., & Shulman, G. I. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa031314 · Cited by 2,193
Mitochondrial dysfunction in the elderly: possible role in insulin resistance
Petersen, K. F., Befroy, D., Dufour, S., Dziura, J., Ariyan, C., Rothman, D. L., DiPietro, L., Cline, G. W., & Shulman, G. I. (2003) · Science · doi:10.1126/science.1082889 · Cited by 2,107
Mitochondrial dysfunction and type 2 diabetes
Lowell, B. B., & Shulman, G. I. (2005) · Science · doi:10.1126/science.1104343 · Cited by 2,070
Patti, M. E., Butte, A. J., Crunkhorn, S., Cusi, K., Berria, R., Kashyap, S., Miyazaki, Y., Kohane, I., Costello, M., Saccone, R., et al. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1032913100 · Cited by 1,952
Mechanism of free fatty acid-induced insulin resistance in humans.
Roden, M., Price, T. B., Perseghin, G., Petersen, K. F., Rothman, D. L., Cline, G. W., & Shulman, G. I. (1996) · Journal of Clinical Investigation · doi:10.1172/jci118742 · Cited by 1,539
Self-citationItani, S. I., Ruderman, N. B., Schmieder, F., & Boden, G. (2002) · Diabetes · doi:10.2337/diabetes.51.7.2005 · Cited by 1,390
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Role of Mitochondrial Dysfunction in Insulin Resistance
Kim, J.-A., Wei, Y., & Sowers, J. R. (2008) · Circulation Research · doi:10.1161/circresaha.107.165472 · Cited by 1,103
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Metadata
- Authors
- Brehm, A., Krssak, M., Schmid, A. I., Nowotny, P., Waldhäusl, W., & Roden, M.
- Affiliations
- Medical University of Vienna (AT)
- Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
- Hanusch Hospital (AT)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2006-01-01
- Volume
- 55
- Issue
- 1
- Pages
- 136-140
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2148020672
- Semantic Scholar
- b3a41abeca324733de403ba64f78380ee994679e
- Cited by
- 239
- References
- 47
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 4 · 2023: 2 · 2022: 6 · 2021: 7 · 2020: 7 · 2019: 7 · 2018: 14 · 2017: 13 · 2016: 16 · 2015: 16 · 2014: 19 · 2013: 20 · 2012: 15
- FWCI
- 7.74
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- UCLA - Biblioteca de Ciencias de la Salud (submittedVersion)
- Funders
- European Foundation for the Study of Diabetes
- Austrian Science Fund (P 15656)
- Universität Wien
- Novo Nordisk
- Medizinische Universität Wien
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
- Keywords
- insulin resistance, intramyocellular lipid, plasma free fatty acids, skeletal muscle, mitochondrial dysfunction, glucose transport, glucose-6-phosphate, hyperinsulinemic-euglycemic clamp, lipid infusion, glucose metabolism
- MeSH terms
- Adenosine Triphosphate, Adult, Biological Transport, Glucose, Humans, Insulin, Male, Glucose Clamp Technique, Muscle, Skeletal, Glucose-6-Phosphate, Lipid Metabolism
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