GPR120 promotes adipogenesis through intracellular calcium and extracellular signal-regulated kinase 1/2 signal pathway

MOLECULAR AND CELLULAR ENDOCRINOLOGY

卷:434

Article

Song, Tongxing^1,2  Zhou, Yuanfei^1,2  Peng, Jian^1,2  Tao, Ya-Xiong³  Yang, Yang^1,2  Xu, Tao^1,2  Peng, Jie^1,2  Ren, Jiao^1,2  Xiang, Quanhang^1,2  Wei, Hongkui^1,2 

[1] Huazhong Agr Univ, Coll Anim Sci & Technol, Dept Anim Nutr & Feed Sci, Wuhan 430070, Peoples R China

[2] Cooperat Innovat Ctr Sustainable Pig Prod, Wuhan 430070, Peoples R China

[3] Auburn Univ, Coll Vet Med, Dept Anat Physiol & Pharmacol, Auburn, AL 36849 USA

关键词: GPR120;    3T3-L1;    Adipogenesis;    [Ca2+]i;    ERK1/2;   

DOI  :  10.1016/j.mce.2016.06.009

来源: Elsevier

【 摘 要 】

Numerous researches have demonstrated that GPR120 (also called FFAR4) exerts novel functions in insulin resistance and adipogenesis. However, the molecular mechanism of GPR120-mediated adipogenic differentiation is still unclear. This study was aimed to interpret the relevant function mechanism of GPR120 in the differentiation of 3T3-L1 adipocytes. The results showed that GPR120 expression was dramatically increased along with the adipogenic differentiation of 3T3-L1 adipocytes and the adipogenic ability was significantly inhibited in shGPR120-transfected cells. TUG-891, a selective agonist of GPR120, promoted the intracellular triglyceride accumulation in a dose-dependent manner and did not enhance adipogenesis in shGPR120-transfected cells. Markedly, TUG-891 increased the activation of PPAR gamma in a GPR120-dependent pathway as assessed by luciferase reporter assay. Furthermore, in the adipogenic differentiation process of 3T3-L1 adipocytes, TUG-891 increased the [Ca2+]i and phosphorylation level of ERK1/2. Pretreatment with inhibitors of either ERK1/2 (U0126) or [Ca2+]i (BAPTA-AM) notably attenuated the GPR120-mediated adipogenesis. These results show that GPR120 promotes adipogenesis by increasing PPAR gamma expression via [Ca2+]i and ERK1/2 signal pathway in 3T3-L1 adipocytes. (C) 2016 Published by Elsevier Ireland Ltd.

【 授权许可】

Free