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膳食磷脂酰胆碱可减轻乳清酸诱导的脂肪肝。

Dietary phosphatidylcholine alleviates fatty liver induced by orotic acid.

作者信息

Buang Yohanes, Wang Yu-Ming, Cha Jae-Young, Nagao Koji, Yanagita Teruyoshi

机构信息

Department of Applied Biological Sciences, Saga University, Saga, Japan.

出版信息

Nutrition. 2005 Jul-Aug;21(7-8):867-73. doi: 10.1016/j.nut.2004.11.019.

Abstract

OBJECTIVE

We compared the effect of dietary phosphatidylcholine (PC) with that of triacylglycerol (TG), both with the same fatty acid profiles, on fatty infiltration in orotic acid (OA)-induced fatty liver of Sprague-Dawley rats.

METHODS

Rats were fed an OA-supplemented diets containing TG (TG+OA group) or PC (20% of dietary lipid, PC+OA group) for 10 d. Rats fed the TG diet without OA supplementation served as the basal group.

RESULTS

Administering OA significantly increased the weights and TG accumulation in livers of the TG+OA group compared with the basal group. These changes were attributed to significant increases in the activities of fatty acid synthase, malic enzyme, and glucose-6-phosphate dehydrogenase, which are fatty acid synthetic enzymes, and phosphatidate phosphohydrolase, a rate-limiting enzyme of TG synthesis. However, the PC+OA group did not show TG accumulation and OA-induced increases of these enzyme activities. Further, a significant increase in the activity of carnitine palmitoyl transferase, a rate-limiting enzyme of fatty acid beta-oxidation, was found in the PC+OA group.

CONCLUSIONS

Dietary PC appears to alleviate the OA-induced hepatic steatosis and hepatomegaly, mainly through the attenuation of hepatic TG synthesis and enhancement of fatty acid beta-oxidation in Sprague-Dawley rats.

摘要

目的

我们比较了具有相同脂肪酸谱的膳食磷脂酰胆碱(PC)和三酰甘油(TG)对斯普拉格-道利大鼠乳清酸(OA)诱导的脂肪肝中脂肪浸润的影响。

方法

给大鼠喂食含TG的OA补充饲料(TG+OA组)或PC(占膳食脂质的20%,PC+OA组),持续10天。喂食不含OA补充剂的TG饲料的大鼠作为基础组。

结果

与基础组相比,给予OA显著增加了TG+OA组大鼠肝脏的重量和TG积累。这些变化归因于脂肪酸合成酶、苹果酸酶和葡萄糖-6-磷酸脱氢酶(均为脂肪酸合成酶)以及TG合成的限速酶磷脂酸磷酸水解酶的活性显著增加。然而,PC+OA组未显示TG积累以及OA诱导的这些酶活性增加。此外,在PC+OA组中发现肉碱棕榈酰转移酶(脂肪酸β氧化的限速酶)的活性显著增加。

结论

在斯普拉格-道利大鼠中,膳食PC似乎主要通过减弱肝脏TG合成和增强脂肪酸β氧化来减轻OA诱导的肝脂肪变性和肝肿大。

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