Anti-diabetic effects of benfotiamine on an animal model of type 2 diabetes mellitus
2014
Chung, K.M., Department of Toxicology and Biochemistry, College of Veterinary Medicine, Jeju National University, Jeju, Republic of Korea | Kang, W.Y., Department of Toxicology and Biochemistry, College of Veterinary Medicine, Jeju National University, Jeju, Republic of Korea | Kim, D.G., Department of Toxicology and Biochemistry, College of Veterinary Medicine, Jeju National University, Jeju, Republic of Korea | Hong, H.J., Department of Toxicology and Biochemistry, College of Veterinary Medicine, Jeju National University, Jeju, Republic of Korea | Lee, Y.J., Department of Toxicology and Biochemistry, College of Veterinary Medicine, Jeju National University, Jeju, Republic of Korea | Han, C.H., Department of Toxicology and Biochemistry, College of Veterinary Medicine, Jeju National University, Jeju, Republic of Korea
Although benfotiamine has various beneficial anti-diabetic effects, the detailed mechanisms underlying the impact of this compound on the insulin signaling pathway are still unclear. In the present study, we evaluated the effects of benfotiamine on the hepatic insulin signaling pathway in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which are a type 2 diabetes mellitus model. OLETF rats treated with benfotiamine showed decreased body weight gain and reduced adipose tissue weight. In addition, blood glucose levels were lower in OLETF rats treated with benfotiamine. Following treatment with benfotiamine, the levels of Akt phosphorylation (S473/T308) in the OLETF groups increased significantly compared to the OLETF control group so that they were almost identical to the levels observed in the control group. Moreover, benfotiamine restored the phosphorylation levels of both glycogen synthase kinase (GSK)-3¥�/¥�(S21, S9) and glycogen synthase (GS; S641) in OLETF rats to nearly the same levels observed in the control group. Overall, these results suggest that benfotiamine can potentially attenuate type 2 diabetes mellitus in OLETF rats by restoring insulin sensitivity through upregulation of Akt phosphorylation and activation of two downstream signaling molecules, GSK-3¥�/¥� and GS, thereby reducing blood glucose levels through glycogen synthesis.
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