| 短链脂肪酸对肝细胞糖脂代谢调节的作用机制研究 |
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| 引用本文： | 孙亚朝,邓邦利,牛文彦. 短链脂肪酸对肝细胞糖脂代谢调节的作用机制研究[J]. 天津医科大学学报, 2023, 0(2): 126-130 |
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| 作者姓名： | 孙亚朝 邓邦利 牛文彦 |
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| 作者单位： | 天津医科大学基础医学院免疫学系，天津300070 |
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| 摘 要： | 目的:探究肠道菌群代谢产物短链脂肪酸对小鼠肝细胞AML12糖脂代谢的影响。方法:将AML12小鼠肝细胞分别在1、2、4、8和16mmol/L浓度的乙酸钠、丙酸钠和丁酸钠中孵育24h，Western印迹检测糖脂代谢信号通路中关键蛋白蛋白激酶B（Akt）、糖原合成酶激酶-3β（GSK-3β）、腺苷酸活化蛋白激酶（AMPK）和乙酰辅酶A羧化酶（ACC）的磷酸化水平以及AMPK总蛋白的表达量。结果:16mmol/L丙酸钠显著升高Akt磷酸化水平，为对照组的（1.56±0.09）倍（F=3.251，P<0.05），丁酸钠在8mmol/L时即可显著增加Akt的磷酸化，为对照组的（1.66±0.18）倍（F=8.249，P<0.05），而乙酸钠不影响Akt的磷酸化。8mmol/L丁酸钠即可显著上调GSK-3β的磷酸化水平，为对照组的（1.61±0.14）倍（F=4.690，P<0.05），而乙酸钠和丙酸钠不影响GSK-3β的磷酸化。乙酸钠、丙酸钠和丁酸钠在不影响AMPK总蛋白表达的情况下，分别在2、1、2mmol/L时即可显著升高AMPK磷酸化水平，分别为对照组的（1.40±0.13）倍（F=4.720，P<0.05）、（1.66±0.18）倍（F=16.54，P<0.05）和（1.70±0.13）倍（F=23.50，P<0.05）。乙酸钠、丙酸钠和丁酸钠分别在16、4、1mmol/L即可显著升高ACC磷酸化水平，分别为对照组的（2.01±0.30）倍（F=4.807，P<0.01）、（1.66±0.18）倍（F=7.507，P<0.05）和（1.79±0.06）倍（F=7.028，P<0.01）。结论:短链脂肪酸可能通过调节肝细胞Akt/GSK-3β和AMPK/ACC通路减少肝脏脂质积聚并降低血糖。
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| 关 键 词： | 肝细胞 短链脂肪酸 Akt GSK-3β AMPK ACC |
Study of the mechanism of short chain fatty acids-regulated glucose and lipid metabolism in hepatocytes |
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| SUN Ya-zhao,DENG Bang-li,NIU Wen-yan. Study of the mechanism of short chain fatty acids-regulated glucose and lipid metabolism in hepatocytes[J]. Journal of Tianjin Medical University, 2023, 0(2): 126-130 |
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| Authors: | SUN Ya-zhao DENG Bang-li NIU Wen-yan |
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| Affiliation: | Department of Immunology，School of Basic Medical Sciences，Tianjin Medical University，Tianjin 300070，China |
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| Abstract: | Objective:To investigate the role of short chain fatty acids produced by intestinal flora on glucose and lipid metabolism in mouse AML12 hepatocytes. Methods:AML12 mouse hepatocytes were incubated in 1，2，4，8 and 16 mmol/L concentrations of sodium acetate，sodium propionate and sodium butyrate for 24 hours，respectively. The level of p-protein kinase B (Akt），p-glycogen synthase kinase-3β （GSK-3β），p-AMP activated protein kinase （AMPK），p-acetyl-CoA carboxylase （ACC）and expression of AMPK were determined by Western blotting. Results:16 mmol/L sodium propionate significantly increased the phosphorylation of Akt [（1.56±0.09）-fold vs. control group]（F=3.251，P<0.05），8 mmol/L sodium butyrate significantly phosphorylated Akt [（1.66±0.18）-fold vs. control group]（F=8.249，P<0.05），while sodium acetate did not affect the level of p-Akt. 8 mmol/L sodium butyrate significantly increased the level of p-GSK-3β [（1.61±0.14）-fold vs. control group]（F=4.690，P<0.05），while sodium acetate and sodium propionate did not affect p-GSK-3β. 2 mmol/L sodium acetate，1 mmol/L sodium propionate and 2 mmol/L sodium butyrate significantly increased the phosphorylation of AMPK[（1.40±0.13）-fold，（1.66±0.18）-fold，（1.70±0.13）-fold vs. control group，respectively）]（all P<0.05；F=4.720，16.54，23.50）without affecting the expression of AMPK. 16 mmol/L sodium acetate，4 mmol/L sodium propionate and 1 mmol/L sodium butyrate significantly increased p-ACC [（2.01±0.30）-fold，（1.66±0.18）-fold，（1.79±0.06）-fold vs. control group，respectively]（P<0.01，P<0.05，P<0.01；F=4.807，7.507，7.028）. Conclusion:Short chain fatty acids have the potential role of regulation glucose and lipid metabolism and blood glucose via Akt/GSK-3β and AMPK/ACC signal pathway. |
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| Keywords: | AML12 Short chain fatty acids Akt GSK-3β AMPK ACC |
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