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脂肪组织通过脂联素调节肝脏胆固醇代谢。

Adipose tissue regulates hepatic cholesterol metabolism via adiponectin.

出版信息

Life Sci. 2014 Nov 18;118(1):27-33. doi: 10.1016/j.lfs.2014.10.003.

Abstract

AIMS

Lipid metabolic disorder involves multiple tissues and organs. Hepatic cholesterol metabolism is an important physiological process, which is tightly related to obesity and lipid metabolic disorders. In this study, we examined the direct effects of adipocytes on hepatic cholesterol metabolic factors and investigated the role of potential adipocytokines in it.

MAIN METHODS

Male SD rats were induced by a high-fat diet (HFD) and hepatic cholesterol metabolic factors, 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGR) and ATP-binding cassette transporter A1 (ABCA1) were measured by immunoblotting. Then the effects of adipocytes on the expressions of hepatic cholesterol metabolism proteins were examined in the co-culture system. Finally, the concentrations of several adipocytokines were detected by ELISA and the effect of adiponectin (APN) on hepatic cholesterol metabolism was confirmed by short interference RNA (siRNA) in vitro.

KEY FINDINGS

Our results showed that adipocytes significantly increased ABCA1 and decreased HMGR in hepatocytes after co-culture. Lipopolysaccharide (LPS) treatment in this co-culture system reversed cholesterol metabolism compared with the untreated group. APN, which also decreased in obese rats, had a significant positive correlation with ABCA1 and inversed correlation with HMGR in vitro. Co-culturing with APN-silenced adipocytes partially restored ABCA1 and HMGR levels.

SIGNIFICANCE

The present study demonstrates that adipocytes regulate hepatic cholesterol metabolism partly via APN.

摘要

目的

脂代谢紊乱涉及多个组织和器官。肝胆固醇代谢是一个重要的生理过程,与肥胖和脂代谢紊乱密切相关。本研究旨在探讨脂肪细胞对肝胆固醇代谢因子的直接作用,并研究潜在的脂肪细胞因子在其中的作用。

方法

雄性 SD 大鼠经高脂肪饮食(HFD)诱导,采用免疫印迹法检测肝胆固醇代谢因子 3-羟-3-甲基戊二酰辅酶 A 还原酶(HMGR)和三磷酸腺苷结合盒转运体 A1(ABCA1)的表达。然后,在共培养体系中观察脂肪细胞对肝胆固醇代谢蛋白表达的影响。最后,采用 ELISA 检测几种脂肪细胞因子的浓度,并通过体外短发夹 RNA(siRNA)确认脂联素(APN)对肝胆固醇代谢的影响。

主要发现

我们的结果表明,共培养后脂肪细胞显著增加了肝细胞中 ABCA1 的表达,降低了 HMGR 的表达。与未处理组相比,脂多糖(LPS)处理的共培养系统中胆固醇代谢发生逆转。肥胖大鼠中APN 水平降低,与 ABCA1 呈显著正相关,与 HMGR 呈负相关。与沉默 APN 的脂肪细胞共培养部分恢复了 ABCA1 和 HMGR 的水平。

意义

本研究表明脂肪细胞通过 APN 部分调节肝胆固醇代谢。

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