Cited by 122Heat shock proteins researchExercise and Physiological ResponsesMetabolism, Diabetes, and Cancer

Exercise, heat shock proteins and insulin resistance

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Archer, Ashley E., Von Schulze, Alex T., Geiger, Paige C.·2018·Philosophical Transactions of the Royal Society B: Biological Sciences

Abstract

Best known as chaperones, heat shock proteins (HSPs) also have roles in cell signalling and regulation of metabolism. Rodent studies demonstrate that heat treatment, transgenic overexpression and pharmacological induction of HSP72 prevent high-fat diet-induced glucose intolerance and skeletal muscle insulin resistance. Overexpression of skeletal muscle HSP72 in mice has been shown to increase endurance running capacity nearly twofold and increase mitochondrial content by 50%. A positive correlation between HSP72 mRNA expression and mitochondrial enzyme activity has been observed in human skeletal muscle, and HSP72 expression is markedly decreased in skeletal muscle of insulin resistant and type 2 diabetic patients. In addition, decreased levels of HSP72 correlate with insulin resistance and non-alcoholic fatty liver disease progression in livers from obese patients. These data suggest the targeted induction of HSPs could be a therapeutic approach for preventing metabolic disease by maintaining the body's natural stress response. Exercise elicits a number of metabolic adaptations and is a powerful tool in the prevention and treatment of insulin resistance. Exercise training is also a stimulus for increased HSP expression. Although the underlying mechanism(s) for exercise-induced HSP expression are currently unknown, the HSP response may be critical for the beneficial metabolic effects of exercise. Exercise-induced extracellular HSP release may also contribute to metabolic homeostasis by actively restoring HSP72 content in insulin resistant tissues containing low endogenous levels of HSPs. This article is part of the theme issue ‘Heat shock proteins as modulators and therapeutic targets of chronic disease: an integrated perspective’.

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Crossref · 10.1098/rstb.2016.0529

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  • Hepatokines are a novel class of exercise-inducible soluble factors released by the liver during and after physical activity, including selenoprotein P, FGF21, HSP72, and hepassocin.

    “Hepatokines represent a novel class of exercise-inducible soluble factors released by the liver during and after physical activity, including selenoprotein P (SeP) [93], FGF21 [118], heat shock protein 72 (HSP72) [119], and hepassocin (HPS) (Figure 3) [120].”

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Authors
Archer, A. E., Von Schulze, A. T., & Geiger, P. C.
Affiliations
University of Kansas Medical Center (US)
Venue
Philosophical Transactions of the Royal Society B: Biological Sciences
Published
2017-12-04
Volume
373
Issue
1738
Pages
20160529
ISSN
  • 0962-8436 (ISSN-L)
  • 1471-2970
OpenAlex
W2772015960
Cited by
122
References
141
Citations by year
2026: 6 · 2025: 11 · 2024: 15 · 2023: 20 · 2022: 24 · 2021: 16 · 2020: 16 · 2019: 6 · 2018: 7 · 2017: 1
FWCI
0.77
Type
journal article
Language
en
Open access
Locations
  • Philosophical Transactions of the Royal Society B Biological Sciences (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-002528)
  • Foundation for the National Institutes of Health (AG-031575)
  • National Institute of General Medical Sciences (P20 GM103418)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
  • Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords
heat shock proteins, HSP72, insulin resistance, exercise training, skeletal muscle, type 2 diabetes, non-alcoholic fatty liver disease, mitochondrial function, impaired glucose tolerance, high-fat diet, metabolic adaptation, stress response
MeSH terms
Animals, Heat-Shock Proteins, Humans, Insulin Resistance, Physical Conditioning, Animal, Exercise, Mice, Rats

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