Hyperthermia with mild electrical stimulation protects pancreatic β-cells from cell stresses and apoptosis.

Diabetes
Tatsuya KondoEiichi Araki

Abstract

Induction of heat shock protein (HSP) 72 improves metabolic profiles in diabetic model mice. However, its effect on pancreatic β-cells is not known. The current study investigated whether HSP72 induction can reduce β-cell stress signaling and apoptosis and preserve β-cell mass. MIN6 cells and db/db mice were sham-treated or treated with heat shock (HS) and mild electrical stimulation (MES) (HS+MES) to induce HSP72. Several cellular markers, metabolic parameters, and β-cell mass were evaluated. HS+MES treatment or HSP72 overexpression increased HSP72 protein levels and decreased tumor necrosis factor (TNF)-α-induced Jun NH(2)-terminal kinase (JNK) phosphorylation, endoplasmic reticulum (ER) stress, and proapoptotic signal in MIN6 cells. In db/db mice, HS+MES treatment for 12 weeks significantly improved insulin sensitivity and glucose homeostasis. Upon glucose challenge, a significant increase in insulin secretion was observed in vivo. Compared with sham treatment, levels of HSP72, insulin, pancreatic duodenal homeobox-1, GLUT2, and insulin receptor substrate-2 were upregulated in the pancreatic islets of HS+MES-treated mice, whereas JNK phosphorylation, nuclear translocation of forkhead box class O-1, and nuclear factor-κB p65 ...Continue Reading

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Citations

Mar 12, 2009·Endocrine·Tomonobu Ezure, Satoshi Amano
Nov 6, 2013·Cardiovascular Diabetology·Katsutoshi MiyagawaEiichi Araki
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Methods Mentioned

BETA
transgenic
laser capture microdissection
enzyme-linked immunosorbent assay
transfection
nuclear translocation

Software Mentioned

Image J

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