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- Title
Mild Electrical Current and Hyperthermia Ameliorates Insulin Resistance and Beta-Cell Function in Mice Models of Type 2 Diabetes.
- Authors
Kondo, Tatsuya; Sasaki, Kazunari; Adachi, Hironori; Morino, Saori; Kai, Kirofumi; Araki, Eiichi
- Abstract
Both insulin resistance and beta-cell dysfunction are major pathophysiology to develop and deteriorate type 2 diabetes. Here we show new technology to improve these aspects of type 2 diabetes by Mild Electrical stimulation and Thermo (MET) therapy. To investigate the effects of MET (0.175V, 42C, 10 min, twice a week for 10 weeks) on type 2 diabetes, we employed high fat diet (HFD) and db/db mice. In HFD mice, MET treatment significantly decreased fasting blood glucose levels by 20% and fasting serum insulin levels by 38%. Serum adiponectin and UCP1 mRNA expression in BAT were increased by 94% and 45%, respectively. Glucose tolerance upon i.p.GTT was also improved at 15, 30, 60 min of timepoints. Surprisingly, the treated mice showed significantly lower weight of visceral and subcutaneous fat (34% and 44% decrease, respectively), although there was no difference in food intake. Histological examinations showed that fatty liver was markedly improved and the size of adipocytes was also decreased in treated mice. In db/db mice, which exhibited decreased insulin secretion after 10 weeks of age, MET treatment increased insulin secretion and lowered glucose levels upon i.p.GTT. Immunohistochemical analyses showed enhanced insulin and PDX-1 immunoreactivity in pancreatic islets, suggesting that MET ameliorated beta-cell function. Hsp72 is one of the major up-regulated protein by MET and inhibits the activation of JNK (c-jun N-terminal kinase) which is associated with cellular stress signaling. Increased expression of Hsp72 in muscle, liver and pancreas by MET was confirmed both in HFD and db/db mice, which paralleled with decreased JNK activity. We hypothesize that inhibition of JNK activity by Hsp72 is one of the major mechanisms to ameliorate both insulin resistance and beta-cell function. In these animal models of type 2 diabetes, our findings indicate that MET treatment is a novel, non-invasive and promising therapeutic approach for type 2 diabetes.
- Subjects
FEVER; INSULIN resistance; PANCREATIC beta cells; TYPE 2 diabetes; MICE
- Publication
Diabetes, 2007, Vol 56, pA65
- ISSN
0012-1797
- Publication type
Article