KMID : 0620920100420050345
|
|
Experimental & Molecular Medicine 2010 Volume.42 No. 5 p.345 ~ p.352
|
|
S-Adenosyl-L-methionine ameliorates TNF¥á-induced insulin resistance in 3T3-L1 adipocytes
|
|
Moon Min-Kyong
Kim Min Chung Sung-Soo Lee Hyun-Joo Koh Sung-Hee Svovoda Peter Jung Myung-Hee Cho Young-Min Park Young-Joo Choi Sung-Hee Jang Hak-Chul Park Kyong-Soo Lee Hong-Kyu
|
|
Abstract
|
|
|
An association between inflammatory processes and the pathogenesis of insulin resistance has been increasingly suggested. The I¥êB kinase-¥â (IKK-¥â)/ nuclear factor-¥êB (NF-¥êB) 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 ¥á (TNF¥á) in 3T3-L1 adipocytes. SAM partially reversed the basal and insulin stimulated glucose transport, which was impaired by TNF¥á. The TNF¥á-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 TNF¥á-induced degradation of I¥êB-¥á and NF-¥êB activation. Interestingly, SAM directly inhibited the kinase activity of IKK-¥â in vitro. These results suggest that SAM can alleviate TNF¥á mediated-insulin resistance by inhibiting the IKK-¥â/NF-¥êB pathway and thus can have a beneficial role in the treatment of type 2 diabetes mellitus.
|
|
KEYWORD
|
|
diabetes mellitus, type 2, inflammation, insulin resistance, I¥êB kinase, NF-¥êB, S-adenosylmethionine
|
|
FullTexts / Linksout information
|
|
|
|
Listed journal information
|
|
|