The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Heat Treatment Improves Glucose Tolerance and Prevents Skeletal Muscle Insulin Resistance in Rats Fed a High-Fat Diet
Open accessAbstract
OBJECTIVE—Heat treatment and overexpression of heat shock protein 72 (HSP72) have been shown to protect against high-fat diet–induced insulin resistance, but little is known about the underlying mechanism or the target tissue of HSP action. The purpose of this study is to determine whether in vivo heat treatment can prevent skeletal muscle insulin resistance. RESEARCH DESIGN AND METHODS—Male Wistar rats were fed a high-fat diet (60% calories from fat) for 12 weeks and received a lower-body heat treatment (41°C for 20 min) once per week. RESULTS—Our results show that heat treatment shifts the metabolic characteristics of rats on a high-fat diet toward those on a standard diet. Heat treatment improved glucose tolerance, restored insulin-stimulated glucose transport, and increased insulin signaling in soleus and extensor digitorum longus (EDL) muscles from rats fed a high-fat diet. Heat treatment resulted in decreased activation of Jun NH2-terminal kinase (JNK) and inhibitor of κB kinase (IKK-β), stress kinases implicated in insulin resistance, and upregulation of HSP72 and HSP25, proteins previously shown to inhibit JNK and IKK-β activation, respectively. Mitochondrial citrate synthase and cytochrome oxidase activity decreased slightly with the high-fat diet, but heat treatment restored these activities. Data from L6 cells suggest that one bout of heat treatment increases mitochondrial oxygen consumption and fatty acid oxidation. CONCLUSIONS—Our results indicate that heat treatment protects skeletal muscle from high-fat diet–induced insulin resistance and provide strong evidence that HSP induction in skeletal muscle could be a potential therapeutic treatment for obesity-induced insulin resistance.
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Cites
Inflammation, stress, and diabetes
Wellen, K. E., & Hotamisligil, G. S. (2005) · Journal of Clinical Investigation · doi:10.1172/jci25102 · Cited by 4,143
Reactive oxygen species have a causal role in multiple forms of insulin resistance
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“Increased oxidative stress has been strongly implicated as a cause of diet-induced insulin resistance (32,33).”
BackgroundImpaired 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
Peroxisome-Proliferator-Activated Receptor δ Activates Fat Metabolism to Prevent Obesity
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Molecular and metabolic mechanisms of insulin resistance and β-cell failure in type 2 diabetes
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High-fat diets cause insulin resistance despite an increase in muscle mitochondria
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“Other studies have demonstrated an increase in mitochondrial function, as measured by oxidative capacity, with a high-fat diet in parallel with increased mitochondrial protein expression (40,41,43).”
BackgroundResultExcess Lipid Availability Increases Mitochondrial Fatty Acid Oxidative Capacity in Muscle
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Cited by
Metabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training
Roberts, C. K., Hevener, A. L., & Barnard, R. J. (2013) · Comprehensive Physiology · doi:10.1002/cphy.c110062 · Cited by 831
Obesity May Accelerate the Aging Process
Salvestrini, V., Sell, C., & Lorenzini, A. (2019) · Frontiers in Endocrinology · doi:10.3389/fendo.2019.00266 · Cited by 260
Nutritional Interventions to Alleviate the Negative Consequences of Heat Stress
Rhoads, R. P., Baumgard, L. H., Suagee, J. K., & Sanders, S. R. (2013) · Advances in Nutrition · doi:10.3945/an.112.003376 · Cited by 256
Skeletal muscle mitochondria as a target to prevent or treat type 2 diabetes mellitus
Hesselink, M. K. C., Schrauwen-Hinderling, V., & Schrauwen, P. (2016) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2016.104 · Cited by 242
Is Alzheimer’s disease a systemic disease?
Morris, J. K., Honea, R. A., Vidoni, E. D., Swerdlow, R. H., & Burns, J. M. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2014.04.012 · Cited by 219
Self-citation
Metadata
- Authors
- Gupte, A. A., Bomhoff, G. L., Swerdlow, R. H., & Geiger, P. C.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2009-03-01
- Volume
- 58
- Issue
- 3
- Pages
- 567-578
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2157386619
- Cited by
- 227
- References
- 13
- FWCI
- 2.73
- Type
- journal article
- Language
- en
- Open access
- hybrid
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