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首页> 外文期刊>Journal of Cellular Physiology >TSH/TSHR Signaling Suppresses Fatty Acid Synthase (FASN) Expression in Adipocytes
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TSH/TSHR Signaling Suppresses Fatty Acid Synthase (FASN) Expression in Adipocytes

机译:TSH / TSHR信号抑制脂肪酸合酶(FASN)脂肪细胞中表达

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摘要

TSH/TSHR signaling plays a role in the regulation of lipid metabolism in adipocytes. However, the precise mechanisms are not known. In the present study, we determined the effect of TSH on fatty acid synthase (FASN) expression, and explored the underlying mechanisms. In vitro, TSH reduced FASN expression in both mRNA and protein levels in mature adipocytes and was accompanied by protein kinase A (PKA) activation, cAMP-response element binding protein (CREB) phosphorylation, as well as extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun NH2-terminal kinase (JNK) activation. TSH-induced downregulation of FASN was partially abolished by inhibition of PKA and ERK, but not JNK. TSHR and FASN expression in visceral tissue was significantly increased in C57BL/6 mice with diet-induced obesity compared with control animals, whereas thyroid TSHR expression was normal. These findings suggest that activation of TSHR directly inhibits FASN expression in mature adipocytes, possibly mediated by PKA and ERK. In obese animals, this function of TSHR seems to be counteracted. The precise mechanisms need further investigation. J. Cell. Physiol. 230: 2233-2239, 2015. (c) 2015 Wiley Periodicals, Inc.
机译:TSH / TSHR信号在调节过程中发挥作用脂肪细胞的脂质代谢。精确的机制并不清楚。研究中,我们确定了TSH对脂肪的影响酸合成酶(FASN)表达式,并探讨了底层机制。在mRNA和蛋白表达水平成熟的脂肪细胞,并伴有蛋白质激酶(PKA)激活,cAMP-response元素结合蛋白(分子)磷酸化作为细胞外signal-regulated激酶1/2(ERK1/2), and c-Jun NH2-terminal kinase (JNK)激活。部分被抑制的PKA和兵,但不是物。内脏组织显著增加C57BL / 6小鼠食源性肥胖比较控制动物,而甲状腺TSHR表情是正常的。直接抑制FASN TSHR的激活成熟脂肪细胞的表达,可能由PKA的兵。TSHR的功能似乎抵消。精确的机制需要进一步调查。细胞。威利期刊公司。

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