Anti-diabetic effects of benfotiamine on an animal model of type 2 diabetes mellitus.
- Author:
Kang Min CHUNG
1
;
Wonyoung KANG
;
Dong Geon KIM
;
Hyun Ju HONG
;
Youngjae LEE
;
Chang Hoon HAN
Author Information
1. Department of Toxicology and Biochemistry, College of Veterinary Medicine, Jeju National University, Jeju 690-756, Korea. chhan@jejunu.ac.kr
- Publication Type:Original Article
- Keywords:
Akt phosphorylation;
benfotiamine;
insulin signaling pathway;
OLETF rats;
type 2 diabetes mellitus
- MeSH:
Adipose Tissue;
Animals*;
Blood Glucose;
Body Weight;
Diabetes Mellitus, Type 2*;
Glycogen;
Glycogen Synthase;
Glycogen Synthase Kinases;
Insulin;
Insulin Resistance;
Models, Animal*;
Phosphorylation;
Rats;
Rats, Inbred OLETF;
Up-Regulation
- From:Korean Journal of Veterinary Research
2014;54(1):21-26
- CountryRepublic of Korea
- Language:English
-
Abstract:
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)-3alpha/beta (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-3alpha/beta and GS, thereby reducing blood glucose levels through glycogen synthesis.
