mTOR remains unchanged in diet-resistant (DR) rats despite impaired LKB1/AMPK cascade in adipose tissue
mTOR remains unchanged in diet-resistant (DR) rats despite impaired LKB1/AMPK cascade in adipose tissue
复制标题
尽管脂肪组织中的 LKB1/AMPK 级联受损，但饮食抵抗 (DR) 大鼠中的 mTOR 保持不变
DOI：
10.1016/j.bbrc.2016.05.123
复制
发表时间：
2016-08-05
影响因子：
3.1
通讯作者：
Li, Yongmei
中科院分区：
文献类型：
--
作者：
Han, Jie;Liang, Huimin;Li, Yongmei
Liver kinase B1 (LKB1) plays an important role in adipogenesis, but the underlying molecular mechanism is poorly understood. Here, we explored the functional relationship between LKB1 and the mammalian target of rapamycin (mTOR) in regulating adipogenesis in rats and preadipocytes. We found that LKB1 and the adenosine S'-monophosphate (AMP)-activated protein kinase (AMPK) cascade are impaired in the white adipose tissue (WAT) of diet-induced obesity (DIO) and diet-resistant (DR) rats when compared with chow-fed (CF) rats. While DIO activated the mTOR pathway in WAT and led to a more fat mass gain, DR maintained the normal activity of the mTOR pathway and normal weight and percentage of fat mass. We further constructed overexpressed LKB1 (OE) and silenced LKB1 (Si) 3T3-L1 preadipocytes monoclonal cell lines. In the OE cell line, the mTOR pathway was inactivated, and intracellular lipid content was reduced during differentiation. This effect could be reversed by AMPK inhibition. Conversely, in the Si cell line, the mTOR pathway was activated and intracellular lipid content increased. This effect could be reversed by rapamycin, an inhibitor of mTOR. Our results suggest that mTOR mediates the effect of LKB1 on adipogenesis, and normal activity of mTOR in DR rats interferes with the effect of LKB1 in WAT. (C) 2016 Elsevier Inc. All rights reserved.
