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

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

Author information

1
Faculty of Human Ecology, Wayo Women's University, 2-3-1, Konodai, Ichikawa, Chiba 272-8533, Japan. Electronic address: y-kurosaka@wayo.ac.jp.
2
Faculty of Human Ecology, Wayo Women's University, 2-3-1, Konodai, Ichikawa, Chiba 272-8533, Japan.
3
Department of Molecular Physiology, Jikei University School of Medicine, 8-3-1, Kokuryo, Chofu, Tokyo 182-8570, Japan.
4
Department of Human Health and Wellbeing, University of Marketing and Distribution Sciences, 3-1, Gakuen-Nishimachi, Nishi, Kobe, Hyogo 651-2188, Japan.

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.

KEYWORDS:

Caloric intake; De novo lipogenesis; Fatty liver; High-fat diet; Mitochondria

PMID:
28389243
DOI:
10.1016/j.bbrc.2017.04.010
[Indexed for MEDLINE]

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