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(HSP) 72 improves metabolic profiles in diabetic model mice.\nHowever, its impact on pancreatic β-cells is not known. The present study investigated whether\nHSP72 induction can reduce β-cell stress signaling and apoptosis, and preserve β-cell mass.\nMIN6 cells and db/db mice were sham-treated or treated with heat shock (HS) + mild electrical\nstimulation (MES) to induce HSP72. Several cellular markers, metabolic parameters and β-cell\nmass were evaluated.\nHS+MES treatment or HSP72 overexpression increased the HSP72 protein levels and decreased\nTNF-β-induced JNK phosphorylation, ER stress and pro-apoptotic signal in MIN6 cells. In db/db\nmice, HS+MES treatment for 12 weeks significantly improved the insulin sensitivity and glucose\nhomeostasis. Upon glucose challenge, a significant increase in insulin secretion was observed in\nvivo. Compared with sham treatment, the HSP72, insulin, PDX-1, GLUT2 and IRS-2 levels were\nupregulated in the pancreatic islets of HS+MES-treated mice, whereas JNK phosphorylation,\nnuclear translocation of FOXO1 and NF-βB p65 were reduced. Apoptotic signals, ER stress and\noxidative stress markers were attenuated.\nThus, HSP72 induction by HS+MES treatment protects β-cells from apoptosis by attenuating\nJNK activation and cell stresses. HS+MES combination therapy may preserve pancreatic β-cell\nvolume to ameliorate glucose homeostasis in diabetes.","subitem_description_type":"Other"}]},"item_16_description_77":{"attribute_name":"URL","attribute_value_mlt":[{"subitem_description":"http://diabetes.diabetesjournals.org/content/61/4/838.abstract","subitem_description_type":"Other"}]},"item_16_publisher_36":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"American Diabetes 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