mAMPK调控线粒体功能参与鹅肥肝的形成

doi:10.11843/j.issn.0366-6964.2025.07.016

摘要/Abstract

摘要：

旨在探究单磷酸腺苷激活蛋白激酶(AMPK)，特别是线粒体AMPK(mAMPK)与鹅肥肝形成的关系。本研究选取了12只70日龄健康朗德鹅公鹅，并随机均分为自由采食对照组(正常肝组)和填饲组(肥肝组)用于活体试验。利用免疫印迹和免疫荧光技术检测鹅肝细胞中AMPKα的主要亚型、亚细胞分布以及鹅肥肝与正常肝全细胞和线粒体中AMPKα1的含量；通过高浓度葡萄糖和棕榈酸处理鹅原代肝细胞，利用免疫印迹技术检测对照组、100 mmol·L^-1葡萄糖组和0.5 mmol·L^-1棕榈酸组细胞中AMPKα1的含量；在AML12细胞中过表达靶向线粒体的AMPK竞争性抑制多肽(mitochondrial AMPK inhibitor peptide, mitoAIP)，利用免疫印迹技术检测空载对照组和mitoAIP过表达组细胞中AMPK下游蛋白的含量；在AML12细胞中过表达mitoAIP并处理2 mmol·L^-1 5-氨基咪唑-4-甲酰胺-1-β-D-呋喃核糖苷(5-aminoimidazole-4-carboxamide 1-β-D-ribofuranoside, AICAR)，利用免疫印迹技术检测空载对照组、AICAR+空载对照组、AICAR+mitoAIP过表达组细胞中AMPK下游蛋白的含量；在AML12细胞中过表达mitoAIP，利用流式细胞术检测空载对照组和mitoAIP过表达组细胞中的线粒体膜电位；在AML12细胞中过表达mitoAIP和MitoTimer，利用流式细胞术检测pMitoTimer+空载对照组和pMitoTimer+mitoAIP过表达组细胞中线粒体的氧化应激水平；在AML12细胞中过表达mitoAIP并进行油酸处理，利用油红O染色分析油酸+空载对照组和油酸+mitoAIP过表达组细胞中的脂肪沉积情况。所有细胞试验中的重复数均不少于3次。研究发现，鹅肝中AMPKα以AMPKα1为主要亚型，主要集中在线粒体组分中且定位于线粒体外膜；鹅肥肝全细胞样和线粒体样中总的AMPKα1(tAMPKα1)与磷酸化的AMPKα1(pAMPKα1)蛋白含量均低于正常肝(P＜0.05，P＜0.01)，但线粒体样中tAMPKα1的减少未达到显著水平；高浓度葡萄糖处理对tAMPKα1和pAMPKα1蛋白丰度无显著影响，而棕榈酸处理降低了线粒体样中pAMPKα1的蛋白丰度(P=0.079)；在AML12细胞中，过表达mitoAIP显著增加了线粒体中pAMPKα1、tAMPKα1、pACC1和tACC1的蛋白丰度(P＜0.05，P＜0.01)，但对全细胞样中AMPK和ACC1蛋白丰度无明显影响；AICAR处理细胞会导致全细胞样中pAMPKα1和pACC1蛋白丰度显著增加(P＜0.05)，线粒体样中pAMPKα1、tAMPKα1、pACC1、tACC1和tULK1蛋白丰度显著减少(P＜0.05)；过表达mitoAIP除了显著抑制AICAR诱导的全细胞样中pACC1蛋白丰度外(P＜0.05)，并不显著影响AICAR处理引起的其他蛋白的丰度变化；mitoAIP过表达可引起线粒体膜电位下降、线粒体氧化应激水平升高以及细胞中脂肪含量的增加(P＜0.05，P＜0.01)。综上所述，mitoAIP在调节全细胞样和线粒体样中AMPK及其底物的蛋白丰度、线粒体的膜电位和线粒体的氧化应激水平方面与已知的全域性AIP的作用有所不同，提示mAMPK在调节线粒体功能上具有独特作用；AML12细胞的mitoAIP过表达试验结果提示，鹅肥肝中磷酸化mAMPK含量的降低可诱导脂肪沉积增加、线粒体膜电位下降和氧化应激水平升高，但这些效应可能还受到其他机制的调控。

关键词: 鹅, 脂肪肝, AMPK, 线粒体

Abstract:

This study aimed to explore the relationship between adenosine monophosphate-activated protein kinase (AMPK), especially mitochondrial AMPK (mAMPK), and the formation of fatty liver in goose. In this study, 12 healthy 70-day-old male Landes goose were randomly divided into a control group (normal liver group) fed ad libitum and a overfed group (fatty liver group) for in vivo experiments. The main isoforms of AMPKα, its subcellular distribution, and the protein content of AMPKα1 in whole-cell and mitochondrial lysates of normal and fatty livers were detected by Western blotting and immunofluorescence techniques. Goose primary hepatocytes were treated with high concentrations of glucose or palmitic acid, and the protein content of AMPKα1 in the control group, 100 mmol·L^-1 glucose group, and 0.5 mmol·L^-1 palmitic acid group was detected by Western blotting. The mitochondrial AMPK competitive inhibitor peptide (mitoAIP) was overexpressed in AML12 cells, and the content of AMPK downstream proteins in the empty vector control group and the mitoAIP overexpression group were detected by Western blotting. mitoAIP was overexpressed in AML12 cells and treated with 2 mmol·L^-1 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR). The content of AMPK downstream proteins in the empty vector control group, the AICAR+empty vector control group, and the AICAR+mitoAIP overexpression group was detected by Western blotting. mitoAIP was overexpressed in AML12 cells, and the mitochondrial membrane potential was measured in the empty vector control group and the mitoAIP overexpression group using flow cytometry. mitoAIP and MitoTimer were overexpressed in AML12 cells, and the oxidative stress level of mitochondria in the pMitoTimer+empty vector control group and the pMitoTimer+mitoAIP overexpression group was measured using flow cytometry. mitoAIP was overexpressed in AML12 cells treated by oleic acid, and the fat deposition in the oleic acid+empty vector control group and the oleic acid+mitoAIP overexpression group was analyzed using Oil Red O staining. All cell experiments were repeated at least 3 times. The study found that AMPKα1 was the predominant isoform in goose hepatocytes, primarily localized in the mitochondrial fraction and specifically on the outer mitochondrial membrane. Both total AMPKα1 (tAMPKα1) and phosphorylated AMPKα1 (pAMPKα1) protein levels in whole-cell and mitochondrial lysates were lower in fatty liver compared to normal liver (P < 0.05, P < 0.01), the reduction in mitochondrial tAMPKα1 did not reach statistical significance. High glucose treatment did not significantly affect tAMPKα1 and pAMPKα1 protein abundance, while palmitic acid treatment reduced pAMPKα1 protein abundance in the mitochondrial fraction (P=0.079). In AML12 cells, overexpression of mitoAIP significantly increased the protein abundance of pAMPKα1, tAMPKα1, pACC1, and tACC1 in mitochondria (P < 0.05, P < 0.01), but had no significant effect on the protein abundance of AMPK and ACC1 in whole-cell lysate. AICAR treatment significantly increased the abundance of pAMPKα1 and pACC1 proteins in whole cell lysates (P < 0.05), but significantly reduced the abundance of pAMPKα1, tAMPKα1, pACC1, tACC1, and tULK1 proteins in the mitochondrial fraction (P < 0.05). Overexpression of mitoAIP significantly inhibited the AICAR-induced reduction in pACC1 abundance in whole cells (P < 0.05), but did not significantly affect the abundance changes of other proteins induced by AICAR treatment. mitoAIP overexpression caused a decrease in mitochondrial membrane potential, an increase in mitochondrial oxidative stress levels, and an increase in cellular fat content (P < 0.05, P < 0.01). In summary, mitoAIP differs from the known global AIP in regulating the abundance of AMPK and its substrate proteins in whole cells and mitochondria, as well as mitochondrial membrane potential and oxidative stress levels, suggesting that mAMPK plays a unique role in regulating mitochondrial function. The results of mitoAIP overexpression in AML12 cells suggest that the reducion of the phosphorylated mAMPK content in goose fatty liver may induce increase of fat deposition, decrease of mitochondrial membrane potential, and increase of oxidative stress level. However, these effects may also be regulated by other mechanisms.

Key words: goose, fatty liver, AMPK, mitochondria

中图分类号:

S835.2

王雨晴, 邢娅, 周小艺, 龚海洲, 赵敏孟, 刘龙, 龚道清, 葛晶, 耿拓宇. mAMPK调控线粒体功能参与鹅肥肝的形成[J]. 畜牧兽医学报, 2025, 56(7): 3210-3225.

WANG Yuqing, XING Ya, ZHOU Xiaoyi, GONG Haizhou, ZHAO Minmeng, LIU Long, GONG Daoqing, GE Jing, GENG Tuoyu. Mitochondrial AMPK (mAMPK) Regulates Mitochondrial Function and Participates in the Formation of Goose Fatty Liver[J]. Acta Veterinaria et Zootechnica Sinica, 2025, 56(7): 3210-3225.

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