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胰岛素对鹅肝细胞脂质沉积的调控通过PI3K-AKT-mTOR信号通路介导。

The Regulation of Lipid Deposition by Insulin in Goose Liver Cells Is Mediated by the PI3K-AKT-mTOR Signaling Pathway.

作者信息

Han Chunchun, Wei Shouhai, He Fang, Liu Dandan, Wan Huofu, Liu Hehe, Li Liang, Xu Hongyong, Du Xiaohui, Xu Feng

机构信息

Institute of Animal Breeding & Genetic, Sichuan Agricultural University, Chengdu, Sichuan 611130, P.R. China.

出版信息

PLoS One. 2015 May 6;10(5):e0098759. doi: 10.1371/journal.pone.0098759. eCollection 2015.

DOI:10.1371/journal.pone.0098759
PMID:25945932
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4422626/
Abstract

BACKGROUND

We previously showed that the fatty liver formations observed in overfed geese are accompanied by the activation of the PI3K-Akt-mTOR pathway and an increase in plasma insulin concentrations. Recent studies have suggested a crucial role for the PI3K-Akt-mTOR pathway in regulating lipid metabolism; therefore, we hypothesized that insulin affects goose hepatocellular lipid metabolism through the PI3K-Akt-mTOR signaling pathway.

METHODS

Goose primary hepatocytes were isolated and treated with serum-free media supplemented with PI3K-Akt-mTOR pathway inhibitors (LY294002, rapamycin, and NVP-BEZ235, respectively) and 50 or 150 nmol/L insulin.

RESULTS

Insulin induced strong effects on lipid accumulation as well as the mRNA and protein levels of genes involved in lipogenesis, fatty acid oxidation, and VLDL-TG assembly and secretion in primary goose hepatocytes. The stimulatory effect of insulin on lipogenesis was significantly decreased by treatment with PI3K-Akt-mTOR inhibitors. These inhibitors also rescued the insulin-induced down-regulation of fatty acid oxidation and VLDL-TG assembly and secretion.

CONCLUSION

These findings suggest that the stimulatory effect of insulin on lipid deposition is mediated by PI3K-Akt-mTOR regulation of lipogenesis, fatty acid oxidation, and VLDL-TG assembly and secretion in goose hepatocytes.

摘要

背景

我们之前发现，过度喂养的鹅出现脂肪肝形成时，伴有PI3K-Akt-mTOR信号通路的激活以及血浆胰岛素浓度升高。近期研究表明，PI3K-Akt-mTOR信号通路在调节脂质代谢中起关键作用；因此，我们推测胰岛素通过PI3K-Akt-mTOR信号通路影响鹅肝细胞脂质代谢。

方法

分离鹅原代肝细胞，并用添加了PI3K-Akt-mTOR信号通路抑制剂（分别为LY294002、雷帕霉素和NVP-BEZ235）以及50或150 nmol/L胰岛素的无血清培养基进行处理。

结果

胰岛素对原代鹅肝细胞中的脂质积累以及参与脂肪生成、脂肪酸氧化和极低密度脂蛋白甘油三酯组装与分泌的基因的mRNA和蛋白质水平具有显著影响。用PI3K-Akt-mTOR抑制剂处理后，胰岛素对脂肪生成的刺激作用显著降低。这些抑制剂还挽救了胰岛素诱导的脂肪酸氧化以及极低密度脂蛋白甘油三酯组装与分泌的下调。

结论

这些发现表明，胰岛素对脂质沉积的刺激作用是通过PI3K-Akt-mTOR对鹅肝细胞中脂肪生成、脂肪酸氧化以及极低密度脂蛋白甘油三酯组装与分泌的调节来介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/a1d6880ffe0d/pone.0098759.g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/f8c10c15b660/pone.0098759.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/0cd3be9818d1/pone.0098759.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/aaa520204324/pone.0098759.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/3550f6894105/pone.0098759.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/943c1672ca18/pone.0098759.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/cd229312cbc3/pone.0098759.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/f8a74cb7d264/pone.0098759.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/be04ce73ce47/pone.0098759.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/3ef10a38a114/pone.0098759.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/a1d6880ffe0d/pone.0098759.g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/f8c10c15b660/pone.0098759.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/0cd3be9818d1/pone.0098759.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/aaa520204324/pone.0098759.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/3550f6894105/pone.0098759.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/943c1672ca18/pone.0098759.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/cd229312cbc3/pone.0098759.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/f8a74cb7d264/pone.0098759.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/be04ce73ce47/pone.0098759.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/3ef10a38a114/pone.0098759.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f979/4422626/a1d6880ffe0d/pone.0098759.g010.jpg

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