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高脂低碳水化合物饮食所致脂肪肝中脂肪代谢的特征:同等能量条件下的一项研究

Characterization of fat metabolism in the fatty liver caused by a high-fat, low-carbohydrate diet: A study under equal energy conditions.

作者信息

Kurosaka Yuka, Shiroya Yoko, Yamauchi Hideki, Kitamura Hiromi, Minato Kumiko

机构信息

Faculty of Human Ecology, Wayo Women's University, 2-3-1, Konodai, Ichikawa, Chiba 272-8533, Japan.

Faculty of Human Ecology, Wayo Women's University, 2-3-1, Konodai, Ichikawa, Chiba 272-8533, Japan.

出版信息

Biochem Biophys Res Commun. 2017 May 20;487(1):41-46. doi: 10.1016/j.bbrc.2017.04.010. Epub 2017 Apr 4.

Abstract

The pathology of fatty liver due to increased percentage of calories derived from fat without increased overall caloric intake is largely unclear. In this study, we aimed to characterize fat metabolism in rats with fatty liver resulting from consumption of a high-fat, low-carbohydrate (HFLC) diet without increased caloric intake. Four-week-old male Sprague-Dawley rats were randomly assigned to the control (Con) and HFLC groups, and rats were fed the corresponding diets ad libitum. Significant decreases in food intake per gram body weight were observed in the HFLC group compared with that in the Con group. Thus, there were no significant differences in body weights or caloric intake per gram body weight between the two groups. Marked progressive fat accumulation was observed in the livers of rats in the HFLC group, accompanied by suppression of de novo lipogenesis (DNL)-related proteins in the liver and increased leptin concentrations in the blood. In addition, electron microscopic observations revealed that many lipid droplets had accumulated within the hepatocytes, and mitochondrial numbers were reduced in the hepatocytes of rats in the HFLC group. Our findings confirmed that consumption of the HFLC diet induced fatty liver, even without increased caloric intake. Furthermore, DNL was not likely to be a crucial factor inducing fatty liver with standard energy intake. Instead, ultrastructural abnormalities found in mitochondria, which may cause a decline in β-oxidation, could contribute to the development of fatty liver.

摘要

在总热量摄入未增加的情况下,因脂肪来源热量百分比增加而导致的脂肪肝病理情况在很大程度上尚不清楚。在本研究中,我们旨在对因食用高热量、低碳水化合物(HFLC)饮食且热量摄入未增加而导致脂肪肝的大鼠的脂肪代谢特征进行描述。将四周龄雄性斯普拉格-道利大鼠随机分为对照组(Con)和HFLC组,并随意喂食相应的饮食。与Con组相比,HFLC组每克体重的食物摄入量显著降低。因此,两组之间的体重或每克体重的热量摄入没有显著差异。在HFLC组大鼠的肝脏中观察到明显的进行性脂肪积累,同时肝脏中与从头脂肪生成(DNL)相关的蛋白质受到抑制,血液中的瘦素浓度升高。此外,电子显微镜观察显示,肝细胞内积累了许多脂滴,HFLC组大鼠肝细胞中的线粒体数量减少。我们的研究结果证实,即使在热量摄入未增加的情况下,食用HFLC饮食也会诱发脂肪肝。此外,在标准能量摄入情况下,DNL不太可能是诱发脂肪肝的关键因素。相反,线粒体中发现的超微结构异常可能会导致β-氧化下降,这可能有助于脂肪肝的发展。

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