ISSN 0371-0874, CN 31-1352/Q

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The molecular mechanism of fibroblast growth factor 21-inhibited leptin expression in adipocytes

CHEN Di, ZHAO Yan-Yan, LIANG Xiang-Yan, ZHANG Li-Jun, WEI Lan-Lan, XIE Rong, ZHANG Xiao-Chun, SU Xing-Li, ZHAO Yu-Feng*

Institute of Basic Medical Sciences, Department of Basic Medical Sciences, Xi’an Medical University, Xi’an 710021, China

Abstract

The present study was aimed to clarify the signaling molecular mechanism by which fibroblast growth factor 21 (FGF21) regulates leptin gene expression in adipocytes. Differentiated 3T3-F442A adipocytes were used as study object. The mRNA expression level of leptin was detected by fluorescence quantitative RT-PCR. The phosphorylation levels of proteins of signal transduction pathways were detected by Western blot. The results showed that FGF21 significantly down-regulated the mRNA expression level of leptin in adipocytes, and FGF21 receptor inhibitor BGJ-398 could completely block this effect. FGF21 up-regulated the phosphorylation levels of ERK1/2 and AMPK in adipocytes. Either ERK1/2 inhibitor SCH772984 or AMPK inhibitor Compound C could partially block the inhibitory effect of FGF21, and the combined application of these two inhibitors completely blocked the effect of FGF21. Neither PI3K inhibitor LY294002 nor Akt inhibitor AZD5363 affected the inhibitory effect of FGF21 on leptin gene expression. These results suggest that FGF21 may inhibit leptin gene expression by activating ERK1/2 and AMPK signaling pathways in adipocytes.


Key words: fibroblast growth factor 21; leptin; ERK1/2; AMPK; adipocytes

Received: 2019-09-06  Accepted: 2020-01-20

Corresponding author: 赵玉峰  E-mail: yufeng.zhao@xiyi.edu.cn

DOI: 10.13294/j.aps.2020.0022

Citing This Article:

CHEN Di, ZHAO Yan-Yan, LIANG Xiang-Yan, ZHANG Li-Jun, WEI Lan-Lan, XIE Rong, ZHANG Xiao-Chun, SU Xing-Li, ZHAO Yu-Feng. The molecular mechanism of fibroblast growth factor 21-inhibited leptin expression in adipocytes. Acta Physiol Sin 2020; 72 (2): 175-180 (in Chinese with English abstract).