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KMID : 0620920100420050345
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Experimental & Molecular Medicine
2010 Volume.42 No. 5 p.345 ~ p.352
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S-Adenosyl-L-methionine ameliorates TNFα-induced insulin resistance in 3T3-L1 adipocytes
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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
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Abstract
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An association between inflammatory processes and the pathogenesis of insulin resistance has been increasingly suggested. The IκB kinase-β (IKK-β)/ nuclear factor-κB (NF-κB) 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 α (TNFα) in 3T3-L1 adipocytes. SAM partially reversed the basal and insulin stimulated glucose transport, which was impaired by TNFα. The TNFα-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 TNFα-induced degradation of IκB-α and NF-κB activation. Interestingly, SAM directly inhibited the kinase activity of IKK-β in vitro. These results suggest that SAM can alleviate TNFα mediated-insulin resistance by inhibiting the IKK-β/NF-κB pathway and thus can have a beneficial role in the treatment of type 2 diabetes mellitus.
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KEYWORD
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diabetes mellitus, type 2, inflammation, insulin resistance, IκB kinase, NF-κB, S-adenosylmethionine
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