Abstract
A large and increasing number of people in all over the world suffer from obesity, metabolic syndrome (MS) and type 2 diabetes mellitus (T2DM). Attenuation of the heat shock response (HSR), which was originally identified as a cellular defense mechanism, is one of the key factors involved in the deterioration of metabolic abnormalities. On the other hand, activating the HSR increases heat shock protein 72 (HSP72) expression and improves insulin resistance and glucose homeostasis in rodents and humans, possibly by inhibiting the activation of stress kinases such as c-jun terminal kinase (JNK) and inhibitor of kappa B kinase β (IKKβ). These approaches may also reduce inflammatory cytokine production and prevent the onset of atherogenic complications. This review focuses on the physiological effects of HSR in regulating insulin sensitivity and hyperglycemia, and the potential to target the HSR system for the treatment of MS and T2DM, as well as other cellular stress-related diseases.
Keywords: Chronic inflammation, Endoplasmic reticulum (ER) stress, Heat shock protein (HSP), Insulin resistance, Metabolic syndrome (MS), Type 2 diabetes mellitus (T2DM), Glucose homeostasis, Obesity, Atherogenic complications, Hyperglycemia
Current Diabetes Reviews
Title: Heat Shock Response Regulates Insulin Sensitivity and Glucose Homeostasis: Pathophysiological Impact and Therapeutic Potential
Volume: 7 Issue: 4
Author(s): Tatsuya Kondo, Saori Koga, Rina Matsuyama, Katsutoshi Miyagawa, Rieko Goto, Hirofumi Kai and Eiichi Araki
Affiliation:
Keywords: Chronic inflammation, Endoplasmic reticulum (ER) stress, Heat shock protein (HSP), Insulin resistance, Metabolic syndrome (MS), Type 2 diabetes mellitus (T2DM), Glucose homeostasis, Obesity, Atherogenic complications, Hyperglycemia
Abstract: A large and increasing number of people in all over the world suffer from obesity, metabolic syndrome (MS) and type 2 diabetes mellitus (T2DM). Attenuation of the heat shock response (HSR), which was originally identified as a cellular defense mechanism, is one of the key factors involved in the deterioration of metabolic abnormalities. On the other hand, activating the HSR increases heat shock protein 72 (HSP72) expression and improves insulin resistance and glucose homeostasis in rodents and humans, possibly by inhibiting the activation of stress kinases such as c-jun terminal kinase (JNK) and inhibitor of kappa B kinase β (IKKβ). These approaches may also reduce inflammatory cytokine production and prevent the onset of atherogenic complications. This review focuses on the physiological effects of HSR in regulating insulin sensitivity and hyperglycemia, and the potential to target the HSR system for the treatment of MS and T2DM, as well as other cellular stress-related diseases.
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Cite this article as:
Kondo Tatsuya, Koga Saori, Matsuyama Rina, Miyagawa Katsutoshi, Goto Rieko, Kai Hirofumi and Araki Eiichi, Heat Shock Response Regulates Insulin Sensitivity and Glucose Homeostasis: Pathophysiological Impact and Therapeutic Potential, Current Diabetes Reviews 2011; 7 (4) . https://dx.doi.org/10.2174/157339911796397811
DOI https://dx.doi.org/10.2174/157339911796397811 |
Print ISSN 1573-3998 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6417 |
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