S-Adenosyl-L-methionine ameliorates TNFalpha-induced insulin resistance in 3T3-L1 adipocytes.
10.3858/emm.2010.42.5.036
- Author:
Min Kyong MOON
1
;
Min KIM
;
Sung Soo CHUNG
;
Hyun Joo LEE
;
Sung Hee KOH
;
Peter SVOVODA
;
Myung Hee JUNG
;
Young Min CHO
;
Young Joo PARK
;
Sung Hee CHOI
;
Hak Chul JANG
;
Kyong Soo PARK
;
Hong Kyu LEE
Author Information
1. Department of Internal Medicine, Seoul National University College of Medicine, Seoul 110-744, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
diabetes mellitus, type 2;
inflammation;
insulin resistance;
IkappaB kinase;
NF-kappaB;
S-adenosylmethionine
- From:Experimental & Molecular Medicine
2010;42(5):345-352
- CountryRepublic of Korea
- Language:English
-
Abstract:
An association between inflammatory processes and the pathogenesis of insulin resistance has been increasingly suggested. The IkappaB kinase-beta (IKK-beta)/ nuclear factor-kappaB (NF-kappaB) pathway is a molecular mediator of insulin resistance. S-Adenosyl-L-methionine (SAM) has both antioxidative and anti-inflammatory properties. We investigated the effects of SAM on the glucose transport and insulin signaling impaired by the tumor necrosis factor alpha (TNFalpha) in 3T3-L1 adipocytes. SAM partially reversed the basal and insulin stimulated glucose transport, which was impaired by TNFalpha. The TNFalpha-induced suppression of the tyrosine phosphorylation of the insulin receptor substrate-1 (IRS-1) and Akt in 3T3-L1 adipocytes was also reversed by SAM. In addition, SAM significantly attenuated the TNFalpha-induced degradation of IkappaB-alpha and NF-kappaB activation. Interestingly, SAM directly inhibited the kinase activity of IKK-beta in vitro. These results suggest that SAM can alleviate TNFalpha mediated-insulin resistance by inhibiting the IKK-beta/NF-kappaB pathway and thus can have a beneficial role in the treatment of type 2 diabetes mellitus.
