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在喂食致动脉粥样化饮食的成年仓鼠中,反式-10,顺式-12共轭亚油酸诱导的肝肿大与脂肪变性无关。

Hepatomegaly induced by trans-10,cis-12 conjugated linoleic acid in adult hamsters fed an atherogenic diet is not associated with steatosis.

作者信息

Miranda Jonatan, Fernández-Quintela Alfredo, Churruca Itziar, Rodríguez Víctor M, Simón Edurne, Portillo María P

机构信息

Dpt Nutrition and Food Science, Facultad de Farmacia, Paseo de la Universidad, Vitoria, Spain.

出版信息

J Am Coll Nutr. 2009 Feb;28(1):43-9. doi: 10.1080/07315724.2009.10719760.

Abstract

OBJECTIVE

To study the effects of trans-10,cis-12 conjugated linoleic acid (CLA) on liver size and composition, as well as on hepatic lipogenesis and fatty acid oxidation, in adult hamsters.

METHODS

Sixteen male Syrian Golden hamsters (8-month-old; initial body weight 167 +/- 5 g) were divided into two groups and fed on atherogenic diets supplemented either with 0.5% linoleic acid or trans-10,cis-12 CLA, for 6 weeks. Liver lipids, fatty acid profile, protein, water and DNA contents were analysed. The activity and expression of several enzymes involved in liver fatty oxidation and lipogenesis were assessed, as was the expression of transcriptional factors controlling these enzymes.

RESULTS

The addition of CLA to the diet led to significantly greater liver weight due to hyperplasia. No changes were observed in liver composition. CLA did not modify the expression or the activity of analysed oxidative enzymes. With regard to lipogenic enzymes, an increase in the expression and the activity of acetyl-CoA carboxylase was found.

CONCLUSIONS

These results show that the expected body fat-lowering effect of trans-10,cis-12 CLA, observed in young rodents, is not found in adult hamsters. The lack of increase in liver fatty acid oxidation, help to explain why that effect was not found in these animals. Further, the CLA treatment-induced hepatomegaly is a consequence of hyperplasia.

摘要

目的

研究反式-10,顺式-12共轭亚油酸(CLA)对成年仓鼠肝脏大小和组成,以及肝脏脂肪生成和脂肪酸氧化的影响。

方法

将16只雄性叙利亚金仓鼠(8月龄;初始体重167±5g)分为两组,分别喂食添加0.5%亚油酸或反式-10,顺式-12CLA的致动脉粥样化饮食,持续6周。分析肝脏脂质、脂肪酸谱、蛋白质、水和DNA含量。评估参与肝脏脂肪酸氧化和脂肪生成的几种酶的活性和表达,以及控制这些酶的转录因子的表达。

结果

饮食中添加CLA导致肝脏因增生而显著增重。肝脏组成未观察到变化。CLA未改变所分析的氧化酶的表达或活性。关于脂肪生成酶,发现乙酰辅酶A羧化酶的表达和活性增加。

结论

这些结果表明,在幼年啮齿动物中观察到的反式-10,顺式-12CLA预期的降低体脂作用,在成年仓鼠中未发现。肝脏脂肪酸氧化未增加有助于解释在这些动物中未发现该作用的原因。此外,CLA治疗引起的肝肿大是增生的结果。

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