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肝细胞特异性敲除维持了小鼠肝脏脂质代谢的稳态。

Hepatocyte-Specific Knockout Maintained the Liver Homeostasis of Lipid Metabolism in Mice.

作者信息

Li Caige, Xue Yu, Liu Yiwei, Zheng Kangning, Gao Yuting, Gong Yi, Lu Junlan, Zhang Yuman, Ji Jingmin, Zhang Zhiqin, Shi Xinli

机构信息

Department of Pathobiology and Immunology, Hebei University of Chinese Medicine, Shijiazhuang, Hebei, People's Republic of China.

Department of Endocrinology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, People's Republic of China.

出版信息

Diabetes Metab Syndr Obes. 2024 Aug 27;17:3197-3214. doi: 10.2147/DMSO.S472778. eCollection 2024.

DOI:10.2147/DMSO.S472778
PMID:39220798
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11365535/
Abstract

INTRODUCTION

Yes-associated protein 1 (YAP1) is a crucial molecule in the Hippo pathway. The impact of hepatocyte-specific knockout ( ) on hepatic lipid droplets (LD) and pePLIN2 in metabolic fatty liver has not been reported. This study aims to explore whether could offer a protective effect in a liver injury model.

METHODS

Three-week-old and mice were given aristolochic acid I (AAI) combined carbon tetrachloride (CCL) establish liver injury model. Eight-week-old and mice were fed with a high-fat diet for 18 weeks to establish obesity-related liver injury model. Further biochemical, histomorphological, immunohistochemical, and lipidomic analyses were performed on serum and liver tissues of these mice to elucidate the effects of hepatocyte-specific knockout on hepatic lipid metabolism.

RESULTS

reduced triglyceride (TG) content and PLIN2 expression level in the liver during the intervention of AAI combined CCl. Moreover, improved lipid metabolism homeostasis in the liver by increasing the beneficial lipid molecules and reducing the harmful lipid molecules through lipidomics. Finally, reduced TG content in the serum and liver, hepatic vacuolar degeneration, and hepatic PLIN2 expression level in mice fed with a high-fat diet (HFD).

CONCLUSION

is protective in regulating liver and blood TG when induced with toxic substances AAI combined CCl and a high-fat diet.

摘要

引言

Yes相关蛋白1（YAP1）是Hippo信号通路中的关键分子。肝细胞特异性敲除（ ）对代谢性脂肪肝中肝脂滴（LD）和pePLIN2的影响尚未见报道。本研究旨在探讨 在肝损伤模型中是否能发挥保护作用。

方法

给3周龄的 和 小鼠给予马兜铃酸I（AAI）联合四氯化碳（CCL）建立肝损伤模型。给8周龄的 和 小鼠喂食高脂饮食18周以建立肥胖相关肝损伤模型。对这些小鼠的血清和肝组织进行进一步的生化、组织形态学、免疫组化和脂质组学分析，以阐明肝细胞特异性敲除对肝脏脂质代谢的影响。

结果

在AAI联合CCl干预期间， 降低了肝脏中甘油三酯（TG）含量和PLIN2表达水平。此外， 通过脂质组学增加有益脂质分子并减少有害脂质分子，改善了肝脏脂质代谢稳态。最后， 降低了高脂饮食（HFD）喂养小鼠的血清和肝脏中的TG含量、肝空泡变性以及肝脏PLIN2表达水平。

结论

在由有毒物质AAI联合CCl和高脂饮食诱导时， 对调节肝脏和血液中的TG具有保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ced0/11365535/b8312cd431ab/DMSO-17-3197-g0009.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ced0/11365535/14c4037739e7/DMSO-17-3197-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ced0/11365535/54d56780758e/DMSO-17-3197-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ced0/11365535/31af3d7baf0b/DMSO-17-3197-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ced0/11365535/b8312cd431ab/DMSO-17-3197-g0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ced0/11365535/f9888c141030/DMSO-17-3197-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ced0/11365535/53cce2a1c7f2/DMSO-17-3197-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ced0/11365535/1ec6005e933e/DMSO-17-3197-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ced0/11365535/b8f98b729d25/DMSO-17-3197-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ced0/11365535/8710f26d24c1/DMSO-17-3197-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ced0/11365535/14c4037739e7/DMSO-17-3197-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ced0/11365535/54d56780758e/DMSO-17-3197-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ced0/11365535/31af3d7baf0b/DMSO-17-3197-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ced0/11365535/b8312cd431ab/DMSO-17-3197-g0009.jpg

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