title: Heat shock response regulates insulin sensitivity and glucose homeostasis: pathophysiological impact and therapeutic potential.
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.
authors.affiliation: Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto 860-8556, Japan.
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Kondo
authors.forename: Saori
authors.initials: S
authors.lastname: Koga
authors.forename: Rina
authors.initials: R
authors.lastname: Matsuyama
authors.forename: Katsutoshi
authors.initials: K
authors.lastname: Miyagawa
authors.forename: Rieko
authors.initials: R
authors.lastname: Goto
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Kai
authors.forename: Eiichi
authors.initials: E
authors.lastname: Araki
mesh_terms: D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy*; D005947:Glucose / Q000378:metabolism*; D018869:Heat-Shock Response / Q000502:physiology*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology*; D008954:Models, Biological
chemical_list: D007328:Insulin; D005947:Glucose