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Fibroblast growth factor 21 attenuates tacrolimus-induced hepatic lipid accumulation through TFEB-regulated lipophagy
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Zhensheng ZHANG, Li XU, Xun QIU, Xinyu YANG, Zhengxing LIAN, Xuyong WEI, Di LU, Xiao XU. Fibroblast growth factor 21 attenuates tacrolimus-induced hepatic lipid accumulation through TFEB-regulated lipophagy[J]. Journal of Zhejiang University Science B, 1998, -1(-1): .
@article{title="Fibroblast growth factor 21 attenuates tacrolimus-induced hepatic lipid accumulation through TFEB-regulated lipophagy",
author="Zhensheng ZHANG, Li XU, Xun QIU, Xinyu YANG, Zhengxing LIAN, Xuyong WEI, Di LU, Xiao XU",
journal="Journal of Zhejiang University Science B",
volume="-1",
number="-1",
pages="",
year="1998",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.B2200562"
}
%0 Journal Article
%T Fibroblast growth factor 21 attenuates tacrolimus-induced hepatic lipid accumulation through TFEB-regulated lipophagy
%A Zhensheng ZHANG
%A Li XU
%A Xun QIU
%A Xinyu YANG
%A Zhengxing LIAN
%A Xuyong WEI
%A Di LU
%A Xiao XU
%J Journal of Zhejiang University SCIENCE B
%V -1
%N -1
%P
%@ 1673-1581
%D 1998
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B2200562
TY - JOUR
T1 - Fibroblast growth factor 21 attenuates tacrolimus-induced hepatic lipid accumulation through TFEB-regulated lipophagy
A1 - Zhensheng ZHANG
A1 - Li XU
A1 - Xun QIU
A1 - Xinyu YANG
A1 - Zhengxing LIAN
A1 - Xuyong WEI
A1 - Di LU
A1 - Xiao XU
J0 - Journal of Zhejiang University Science B
VL - -1
IS - -1
SP -
EP -
%@ 1673-1581
Y1 - 1998
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B2200562
Abstract: tacrolimus (TAC), also called FK506, is one of the classical immunosuppressants to prevent allograft rejection after liver transplantation. However, it has been proved to be associated with post-transplant hyperlipemia. The mechanism behind this is unknown, and it is urgent to explore preventive strategies for hyperlipemia after transplantation. Therefore, we established a hyperlipemia mouse model to investigate the mechanism, by injecting TAC intraperitoneally for 8 weeks. After TAC treatment, the mice developed hyperlipemia (manifested as elevated TG and LDL-c) as well as decreased HDL-c. Accumulation of lipid droplets was observed in the liver. In addition to lipid accumulation, TAC induced inhibition of the autophagy-lysosome pathway (LC3B II/I and LC3B II/Actin ratio, TFEB, P62 and LAMP1) and downregulation of FGF21 in vivo. Overexpression of FGF21 may reverse TAC-induced TG accumulation. In this mouse model, the recombinant FGF21 protein ameliorated hepatic lipid accumulation and hyperlipemia through repair of the autophagy-lysosome pathway. We conclude that TAC downregulates FGF21 and thus exacerbates lipid accumulation by impairing the autophagy-lysosome pathway. Recombinant FGF21 protein treatment could therefore reverse TAC-caused lipid accumulation and hypertriglyceridemia by enhancing autophagy.
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