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Attenuation of exercise-induced heat shock protein 72 expression blunts improvements in whole-body insulin resistance in rats with type 2 diabetes

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Cell Stress and Chaperones Aims and scope

Abstract

Heat shock proteins (HSPs) play an important role in insulin resistance and improve the cellular stress response via HSP induction by exercise to treat type 2 diabetes. In this study, the effects of exercise-induced HSP72 expression levels on whole-body insulin resistance in type 2 diabetic rats were investigated. Male 25-week-old Otsuka Long-Evans Tokushima Fatty rats were divided into three groups: sedentary (Sed), trained in a thermal-neutral environment (NTr: 25 °C), and trained in a cold environment (CTr: 4 °C). Exercise training was conducted 5 days/week for 10 weeks. Rectal temperature was measured following each bout of exercise. An intraperitoneal glucose tolerance test (IPGTT) was performed after the training sessions. The serum, gastrocnemius muscle, and liver were sampled 48 h after the final exercise session. HSP72 and heat shock cognate protein 73 expression levels were analyzed by Western blot, and serum total cholesterol, triglyceride (TG), and free fatty acid (FFA) levels were measured. NTr animals exhibited significantly higher body temperatures following exercise, whereas, CTr animals did not. Exercise training increased HSP72 levels in the gastrocnemius muscle and liver, whereas, HSP72 expression was significantly lower in the CTr group than that in the NTr group (p < 0.05). Glucose tolerance improved equally in both trained animals; however, insulin levels during the IPGTT were higher in CTr animals than those in NTr animals (p < 0.05). In addition, the TG and FFA levels decreased significantly only in NTr animals compared with those in Sed animals. These results suggest that attenuation of exercise-induced HSP72 expression partially blunts improvement in whole-body insulin resistance and lipid metabolism in type 2 diabetic rats.

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Acknowledgements

This study was supported in part by the MEXT-supported program for Juntendo University and a grant-in-aid for JSPS fellows (13J10819, to T.T.). The Juntendo University Institute of Health and Sports Science & Medicine also supported this research.

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Authors and Affiliations

  1. Graduate School of Health and Sports Science, Juntendo University, Chiba, 270-1695, Japan

    Takamasa Tsuzuki, Hiroyuki Kobayashi, Toshinori Yoshihara, Noriko Ichinoseki-Sekine & Hisashi Naito

  2. Research Fellow of the Japan Society for the Promotion of Science, Tokyo, 102-0083, Japan

    Takamasa Tsuzuki

  3. Department of General Medicine, Mito Medical Center, Tsukuba University Hospital, Ibaraki, 310-0015, Japan

    Hiroyuki Kobayashi

  4. Faculty of Medicine, Juntendo University, Tokyo, 113-8421, Japan

    Ryo Kakigi

  5. Faculty of Liveral Arts, The Open University of Japan, Chiba, 261-8586, Japan

    Noriko Ichinoseki-Sekine

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  1. Takamasa Tsuzuki
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  2. Hiroyuki Kobayashi
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  3. Toshinori Yoshihara
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  4. Ryo Kakigi
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  5. Noriko Ichinoseki-Sekine
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  6. Hisashi Naito
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Correspondence to Hisashi Naito.

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The authors declare that they have no conflict of interest.

Ethical Statement

All procedures were approved by the Juntendo University Animal Care and Use Committee (H24-01).

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Tsuzuki, T., Kobayashi, H., Yoshihara, T. et al. Attenuation of exercise-induced heat shock protein 72 expression blunts improvements in whole-body insulin resistance in rats with type 2 diabetes. Cell Stress and Chaperones 22, 263–269 (2017). https://doi.org/10.1007/s12192-017-0767-z

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  • DOI: https://doi.org/10.1007/s12192-017-0767-z

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