S-Adenosyl-L-methionine ameliorates TNFα-induced insulin resistance in 3T3-L1 adipocytes

被引:19
|
作者
Moon, Min Kyong [2 ,3 ]
Kim, Min [2 ]
Chung, Sung Soo [2 ]
Lee, Hyun Joo [3 ]
Koh, Sung Hee [4 ]
Svovoda, Peter [4 ]
Jung, Myung Hee [4 ]
Cho, Young Min [2 ]
Park, Young Joo [2 ,5 ]
Choi, Sung Hee [2 ,5 ]
Jang, Hak Chul [2 ,5 ]
Park, Kyong Soo [2 ]
Lee, Hong Kyu [1 ]
机构
[1] Eulji Univ, Sch Med, Dept Internal Med, Seoul 139872, South Korea
[2] Seoul Natl Univ, Coll Med, Dept Internal Med, Seoul 110744, South Korea
[3] Seoul Natl Univ, Boramae Med Ctr, Seoul 156707, South Korea
[4] Seoul Natl Univ, Coll Med, Dept Pharmacol, Seoul 110744, South Korea
[5] Seoul Natl Univ, Bundang Hosp, Songnam 463707, South Korea
来源
EXPERIMENTAL AND MOLECULAR MEDICINE | 2010年 / 42卷 / 05期
关键词
diabetes mellitus; type; 2; inflammation; insulin resistance; 1 kappa B kinase; NF-kappa B; S-adenosylmethionine; TUMOR-NECROSIS-FACTOR; RECEPTOR SUBSTRATE-1; ADENOSYLMETHIONINE; INFLAMMATION; PHOSPHORYLATION; OSTEOARTHRITIS; TRANSCRIPTION; MODULATION; MECHANISMS; ASPIRIN;
D O I
10.3858/emm.2010.42.5.036
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
An association between inflammatory processes and the pathogenesis of insulin resistance has been increasingly suggested. The I kappa B kinase-beta (IKK-beta)/nuclear factor-kappa B (NF-kappa B) 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 (TNF alpha) in 3T3-L1 adipocytes. SAM partially reversed the basal and insulin stimulated glucose transport, which was impaired by TNF alpha. The TNF alpha-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 alpha-induced degradation of I kappa B-alpha and NF-kappa B activation. Interestingly, SAM directly inhibited the kinase activity of IKK-beta in vitro. These results suggest that SAM can alleviate TNF alpha mediated-insulin resistance by inhibiting the IKK-beta/NF-kappa B pathway and thus can have a beneficial role in the treatment of type 2 diabetes mellitus.
引用
收藏
页码:345 / 352
页数:8
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