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

Journal Article · Sat May 20 04:00:00 EDT 2017 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/J.BBRC.2017.04.010· OSTI ID:22697017

Kurosaka, Yuka ^[1]; Shiroya, Yoko ^[1]; Yamauchi, Hideki ^[2]; Kitamura, Hiromi ^[3]; Minato, Kumiko ^[1]

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1. Faculty of Human Ecology, Wayo Women's University, 2-3-1, Konodai, Ichikawa, Chiba 272-8533 (Japan)
2. Department of Molecular Physiology, Jikei University School of Medicine, 8-3-1, Kokuryo, Chofu, Tokyo 182-8570 (Japan)
3. Department of Human Health and Wellbeing, University of Marketing and Distribution Sciences, 3-1, Gakuen-Nishimachi, Nishi, Kobe, Hyogo 651-2188 (Japan)

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. - Highlights: • The high-fat, low-carbohydrate diet did not affect body weight or caloric intake. • The high-fat, low-carbohydrate diet caused fatty liver in rats. • De novo lipogenesis was not a crucial factor in fatty liver. • Mitochondria were altered in fatty livers of rats consuming this diet.

• OSTI ID: 22697017
• Journal Information: Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 1 Vol. 487; ISSN BBRCA9; ISSN 0006-291X
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
DIET
FATS
FOOD
INTAKE
LIVER CELLS
METABOLISM
MITOCHONDRIA
RATS