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Activation of Wnt/β-catenin pathway causes insulin resistance and increases lipogenesis in HepG2 cells via regulation of endoplasmic reticulum stress.

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资源类型：
Pubmed体系：
作者：
Lei Zili[1] * ; Yang Lanxiang[1,2] * ; Yang Yanhong[3] * ; Yang Jing[1,2] ; Niu Zhenpeng[1,2] ; Zhang Xueying[1,2] ; Song Qi[1] ; Lei Yuting[1] ; Wu Huijuan[1,2] ; Guo Jiao[1] ;
机构： [1]Guangdong Metabolic Disease Research Center of Integrated Chinese and Western Medicine, Guangdong Pharmaceutical University, Guangzhou Higher Education Mega Center, Guangzhou, 510006, PR China [2]School of Traditional Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou Higher Education Mega Center, Guangzhou, 510006, PR China [3]The First Affiliated Hospital (School of Clinical Medicine), Guangdong Pharmaceutical University, Nong-Lin-Xia Road 19#, Yue-Xiu District, Guangzhou, 510080, PR China
出处：
DOI： 10.1016/j.bbrc.2020.03.147
ISSN：

关键词： CP21R7 Endoplasmic reticulum stress Insulin resistance Wnt/b-catenin

摘要：
Wnt/β-catenin signaling is involved in glucose and lipid metabolism, but the mechanism is not clear yet. The objective is to study mechanisms of Wnt/β-catenin signaling on regulating hepatocytes metabolism. Real-time qPCR, Western blot, and Oil-red O staining methods were used. The Wnt/β-catenin signaling was activated in hepatocytes by CP21R7, and the level of phosphorylated IRS-1 (Ser307) and TRB3 were significantly increased, while the levels of phosphorylated IRS-1 (Tyr612) and phosphorylated Akt were decreased. Moreover, the expression of FGF21, FAS, SCD1, PPARγ and ADRP was significantly increased. The expression of ATF4, ATF5, eIF2α, GRP78, CHOP and phosphorylated level of PERK were also increased. The expression of FGF21 and TRB3 was significantly down-regulated, and the lipid droplets were notably reduced after the ER stress was inhibited by TUDCA. The expression of FGF21 was significantly decreased when the IRE1 pathway of the UPR was inhibited by STF-083010. Activation of Wnt/β-catenin signaling pathway could cause insulin resistance and lipogenesis in hepatocytes via regulation of the IRE1 pathway of the ER stress and UPR, providing new targets for the treatment of metabolic disorders. Copyright © 2020 Elsevier Inc. All rights reserved.

基金：
National Natural Science Foundation of China (No. 81830113, No. 81803912, No. 31671520), the Science and Technology Project of Guangdong Province (No. 2017B050504005), the Science and Technology Planning Project of Guangzhou City (No. 201803010069), the Scientific Research Project of the Administration of Traditional Chinese Medicine of Guangdong Province (No. 20182079), the Characteristic Innovation Project (Natural Science) of the Education Department of Guangdong Province and the “Innovation Strong School Project” of Guangdong Pharmaceutical University (No. 2017KTSCX102), and the Science and Technology Project of Yue-Xiu District of Guangzhou (No. 2018-WS-011).
语种：
外文
PubmedID：
中科院(CAS)分区：
出版当年[2019]版：
大类 | 3 区 生物
小类 | 3 区 生物物理 4 区 生化与分子生物学
最新[2025]版：
大类 | 4 区 生物学
小类 | 4 区 生化与分子生物学 4 区 生物物理
第一作者：
第一作者机构： [1]Guangdong Metabolic Disease Research Center of Integrated Chinese and Western Medicine, Guangdong Pharmaceutical University, Guangzhou Higher Education Mega Center, Guangzhou, 510006, PR China
共同第一作者：
通讯作者：
推荐引用方式(GB/T 7714)：
Lei Zili,Yang Lanxiang,Yang Yanhong,et al.Activation of Wnt/β-catenin pathway causes insulin resistance and increases lipogenesis in HepG2 cells via regulation of endoplasmic reticulum stress.[J].Biochemical and biophysical research communications.2020,526(3):764-771.doi:10.1016/j.bbrc.2020.03.147.
APA：
Lei Zili,Yang Lanxiang,Yang Yanhong,Yang Jing,Niu Zhenpeng...&Guo Jiao.(2020).Activation of Wnt/β-catenin pathway causes insulin resistance and increases lipogenesis in HepG2 cells via regulation of endoplasmic reticulum stress..Biochemical and biophysical research communications,526,(3)
MLA：
Lei Zili,et al."Activation of Wnt/β-catenin pathway causes insulin resistance and increases lipogenesis in HepG2 cells via regulation of endoplasmic reticulum stress.".Biochemical and biophysical research communications 526..3(2020):764-771

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