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      The Role of Heat Shock Response in Insulin Resistance and Diabetes

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          Abstract

          The expansion of life-style related diseases, such as metabolic syndrome (MS) and type 2 diabetes mellitus (T2DM), appears to be unstoppable. It is also difficult to cease their complications in spite of many antidiabetic medications or intervention of public administration. We and our collaborators found that physical medicine using simultaneous stimulation of heat with mild electric current activates heat shock response, thereby reducing visceral adiposity, insulin resistance, chronic inflammation and improving glucose homeostasis in mice models of T2DM, as well as in humans with MS or T2DM. This combination therapy exerts novel action on insulin signaling, β-cell protection and body compositions, and may provide a new therapeutic alternative in diabetic treatment strategy.

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          A new puffing pattern induced by temperature shock and DNP in drosophila

          F Ritossa (1962)
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            Electrical signals control wound healing through phosphatidylinositol-3-OH kinase-gamma and PTEN.

            Min Zhao, Bing Song, Jin Pu … (2006)
            Wound healing is essential for maintaining the integrity of multicellular organisms. In every species studied, disruption of an epithelial layer instantaneously generates endogenous electric fields, which have been proposed to be important in wound healing. The identity of signalling pathways that guide both cell migration to electric cues and electric-field-induced wound healing have not been elucidated at a genetic level. Here we show that electric fields, of a strength equal to those detected endogenously, direct cell migration during wound healing as a prime directional cue. Manipulation of endogenous wound electric fields affects wound healing in vivo. Electric stimulation triggers activation of Src and inositol-phospholipid signalling, which polarizes in the direction of cell migration. Notably, genetic disruption of phosphatidylinositol-3-OH kinase-gamma (PI(3)Kgamma) decreases electric-field-induced signalling and abolishes directed movements of healing epithelium in response to electric signals. Deletion of the tumour suppressor phosphatase and tensin homolog (PTEN) enhances signalling and electrotactic responses. These data identify genes essential for electrical-signal-induced wound healing and show that PI(3)Kgamma and PTEN control electrotaxis.
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              Suppressor of cytokine signaling 1 (SOCS-1) and SOCS-3 cause insulin resistance through inhibition of tyrosine phosphorylation of insulin receptor substrate proteins by discrete mechanisms.

              Kohjiro Ueki, Tatsuya Kondo, Valerie C Kahn (2004)
              Insulin resistance is a pathophysiological component of type 2 diabetes and obesity and also occurs in states of stress, infection, and inflammation associated with an upregulation of cytokines. Here we show that in both obesity and lipopolysaccharide (LPS)-induced endotoxemia there is an increase in suppressor of cytokine signaling (SOCS) proteins, SOCS-1 and SOCS-3, in liver, muscle, and, to a lesser extent, fat. In concordance with these increases by LPS, tyrosine phosphorylation of the insulin receptor (IR) is partially impaired and phosphorylation of the insulin receptor substrate (IRS) proteins is almost completely suppressed. Direct overexpression of SOCS-3 in liver by adenoviral-mediated gene transfer markedly decreases tyrosine phosphorylation of both IRS-1 and IRS-2, while SOCS-1 overexpression preferentially inhibits IRS-2 phosphorylation. Neither affects IR phosphorylation, although both SOCS-1 and SOCS-3 bind to the insulin receptor in vivo in an insulin-dependent fashion. Experiments with cultured cells expressing mutant insulin receptors reveal that SOCS-3 binds to Tyr960 of IR, a key residue for the recognition of IRS-1 and IRS-2, whereas SOCS-1 binds to the domain in the catalytic loop essential for IRS-2 recognition in vitro. Moreover, overexpression of either SOCS-1 or SOCS-3 attenuates insulin-induced glycogen synthesis in L6 myotubes and activation of glucose uptake in 3T3L1 adipocytes. By contrast, a reduction of SOCS-1 or SOCS-3 by antisense treatment partially restores tumor necrosis factor alpha-induced downregulation of tyrosine phosphorylation of IRS proteins in 3T3L1 adipocytes. These data indicate that SOCS-1 and SOCS-3 act as negative regulators in insulin signaling and serve as one of the missing links between insulin resistance and cytokine signaling.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Diabetes Metab J
                Journal ID (iso-abbrev): Diabetes Metab J
                Journal ID (publisher-id): DMJ
                Title: Diabetes & Metabolism Journal
                Publisher: Korean Diabetes Association
                ISSN (Print): 2233-6079
                ISSN (Electronic): 2233-6087
                Publication date (Print): April 2014
                Publication date (Electronic): 18 April 2014
                Volume: 38
                Issue: 2
                Pages: 100-106
                Affiliations
                [1 ]Department of Metabolic Medicine, Kumamoto University Faculty of Life Sciences, Kumamoto, Japan.
                [2 ]Department of Molecular Medicine, Kumamoto University Faculty of Life Sciences, Kumamoto, Japan.
                Author notes
                Corresponding author: Tatsuya Kondo. Department of Metabolic Medicine, Kumamoto University Faculty of Life Sciences, Honjo 1-1-1, Chuo Ward, Kumamoto 860-8556, Japan. t-kondo@ 123456gpo.kumamoto-u.ac.jp
                Article
                DOI: 10.4093/dmj.2014.38.2.100
                PMC ID: 4021296
                SO-VID: c817d568-d1c8-428e-8fce-95df017bb228
                Copyright © Copyright © 2014 Korean Diabetes Association
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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                Categories
                Subject: Review
                Subject: Pathophysiology

                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: chronic inflammation,cytoprotection,diabetes mellitus,heat-shock response
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: chronic inflammation, cytoprotection, diabetes mellitus, heat-shock response

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