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Cold stress regulates lipid metabolism via AMPK signalling in Cherax quadricarinatus

机译:冷应激通过在Cherax Quadricarinatus中通过AMPK信号调节脂质代谢

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摘要

Lipids play an important role in protecting poikilotherms from cold stress, but relatively little is known about the regulation of lipid metabolism under cold stress, especially in crustaceans. In the present study, red-clawed crayfish Cherax quadricarinatus was employed as a model organism. Animals were divided into four temperature groups (25, 20, 15 and 9 degrees C) and treated for 4 weeks, with the 25 degrees C group serving as a control. The total lipid content in the hepatopancreas as well as the triglyceride, cholesterol and free fatty acid levels in the hemolymph were determined. Lipids stored in the hepatopancreas and hemolymph decreased with decreasing temperature, with changes in the 9 degrees C group most pronounced, indicating that lipids are the main energy source for crayfish at low temperatures. Furthermore, enzyme activity of lipase, fatty acid synthase, acetyl-CoA carboxylase, and lipoprotein esterase, and gene expression analysis of fatty acid synthase gene, acetyl-CoA carboxylase gene and carnitine palmitoyltransferase gene showed that the digestion, synthesis and oxidation of lipids in the hepatopancreas were inhibited under low temperature stress, but expression of sphingolipid delta-4 desaturase (DEGS) was increased, indicating an increase in the demand for highly unsaturated fatty acids at low temperatures. Analysis of the expression of genes related to the AMP-activated protein kinase (AMPK) signalling pathway revealed that the adiponectin receptor gene was rapidly upregulated at low temperatures, which may in turn activate the expression of the downstream AMPK alpha gene, thereby inhibiting lipid anabolism.
机译:脂质在保护Poikilotherms免受冷应激中起重要作用,但是关于在冷应激下的脂质代谢调节的情况下,尤其是在甲壳类动物中的调节。在本研究中,红爪小龙虾Cherax Quadricarinatus被用作模型生物体。将动物分成4个温度基团(25,20,15和9℃)并处理4周,用25℃组用作对照。测定肝癌中的总脂质含量以及甘油三酯,胆固醇和游离脂肪酸水平。储存在肝癌和血淋巴中的脂质随着温度降低而降低,9摄氏度最明显的变化,表明脂质是低温下小龙虾的主要能量源。此外,脂肪酶的酶活性,脂肪酸合酶,乙酰-COA羧化酶和脂蛋白酯酶的基因表达分析,乙酰-COA羧化酶基因和肉毒氨基棕榈酰丙烷基因显示,脂质的消化,合成和氧化在低温胁迫下抑制肝癌,但鞘脂醇-4去饱和酶(DEGS)的表达增加,表明在低温下对高度不饱和脂肪酸的需求增加。分析与AMP活化蛋白激酶(AMPK)信号传导途径相关的基因的表达显示,在低温下脂联素受体基因在低温下快速上调,这可能反过来激活下游AMPKα基因的表达,从而抑制脂质合成代谢。

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