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共轭亚油酸的反式-10,顺式-12异构体可降低仓鼠肝脏三酰甘油含量,且不影响其脂肪生成酶。

The trans-10,cis-12 isomer of conjugated linoleic acid reduces hepatic triacylglycerol content without affecting lipogenic enzymes in hamsters.

作者信息

Zabala Amaia, Churruca Itziar, Macarulla M Teresa, Rodríguez Víctor M, Fernández-Quintela Alfredo, Martínez J Alfredo, Portillo María P

机构信息

Department of Nutrition and Food Science, University of País Vasco, Paseo de la Universidad 7, 01006 Vitoria, Spain.

出版信息

Br J Nutr. 2004 Sep;92(3):383-9. doi: 10.1079/bjn20041220.

Abstract

Conjugated linoleic acid (CLA) refers to the positional and geometric dienoic isomers of linoleic acid. The dietary intake of CLA has been associated with changes in lipid metabolism. The aim of the present work was to assess the effects of the two main isomers of CLA on sterol regulatory element binding protein (SREBP)-1a and SREBP-1c mRNA levels, as well as on mRNA levels and the activities of several lipogenic enzymes in liver. For this purpose hamsters were fed an atherogenic diet supplemented with 5 g linoleic acid, cis-9,trans-11 or trans-10,cis-12 CLA/kg diet for 6 weeks. The trans-10,cis-12 isomer intake produced significantly greater liver weight, but also significantly decreased liver fat accumulation. No changes in mRNA levels of SREBP-1a, SREBP-1c and lipogenic enzymes, or in the activities of these enzymes, were observed. There was no effect of feeding cis-9,trans-11 CLA. These results suggest that increased fat accumulation in liver does not occur on the basis of liver enlargement produced by feeding the trans-10,cis-12 isomer of CLA in hamsters. The reduction in hepatic triacylglycerol content induced by this isomer was not attributable to changes in lipogenesis.

摘要

共轭亚油酸(CLA)是指亚油酸的位置异构体和几何二烯异构体。CLA的膳食摄入量与脂质代谢变化有关。本研究的目的是评估CLA的两种主要异构体对肝脏中固醇调节元件结合蛋白(SREBP)-1a和SREBP-1c mRNA水平,以及几种生脂酶的mRNA水平和活性的影响。为此,给仓鼠喂食含5 g亚油酸、顺-9,反-11或反-10,顺-12 CLA/kg日粮的致动脉粥样化日粮,持续6周。摄入反-10,顺-12异构体显著增加了肝脏重量,但也显著降低了肝脏脂肪堆积。未观察到SREBP-1a、SREBP-1c和生脂酶的mRNA水平及其活性有变化。喂食顺-9,反-11 CLA没有效果。这些结果表明,仓鼠喂食CLA的反-10,顺-12异构体所导致的肝脏肿大并非肝脏脂肪堆积增加的原因。该异构体诱导的肝脏三酰甘油含量降低并非归因于脂肪生成的变化。

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