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- Title
Hyperthermia with mild electrical stimulation protects pancreatic β-cells from cell stresses and apoptosis.
- Authors
Kondo T; Sasaki K; Matsuyama R; Morino-Koga S; Adachi H; Suico MA; Kawashima J; Motoshima H; Furukawa N; Kai H; Araki E; Kondo, Tatsuya; Sasaki, Kazunari; Matsuyama, Rina; Morino-Koga, Saori; Adachi, Hironori; Suico, Mary Ann; Kawashima, Junji; Motoshima, Hiroyuki; Furukawa, Noboru
- 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 were reduced. Apoptotic signals, ER stress, and oxidative stress markers were attenuated. Thus, HSP72 induction by HS+MES treatment protects β-cells from apoptosis by attenuating JNK activation and cell stresses. HS+MES combination therapy may preserve pancreatic β-cell volume to ameliorate glucose homeostasis in diabetes.
- Publication
Diabetes, 2012, Vol 61, Issue 4, p838
- ISSN
0012-1797
- Publication type
journal article
- DOI
10.2337/db11-1098