The hepatic circadian clock is preserved in a lipid-induced mouse model of non-alcoholic steatohepatitis |
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Authors: | Hitoshi Ando Toshinari Takamura Naoto Matsuzawa-Nagata Seiji Nakamura Seiichiro Kurita Naoyuki Togawa Akio Fujimura |
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Affiliation: | a Department of Disease Control and Homeostasis, Kanazawa University Graduate School of Medical Science, 13-1 Takara-machi, Kanazawa, Ishikawa 920-8641, Japan b Division of Clinical Pharmacology, Department of Pharmacology, School of Medicine, Jichi Medical University, Shimotsuke, Tochigi 329-0498, Japan c Yokohama Research Laboratories, Mitsubishi Rayon Co., Ltd, Yokohama, Kanagawa 230-0053, Japan |
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Abstract: | Recent studies have correlated metabolic diseases, such as metabolic syndrome and non-alcoholic fatty liver disease, with the circadian clock. However, whether such metabolic changes per se affect the circadian clock remains controversial. To address this, we investigated the daily mRNA expression profiles of clock genes in the liver of a dietary mouse model of non-alcoholic steatohepatitis (NASH) using a custom-made, high-precision DNA chip. C57BL/6J mice fed an atherogenic diet for 5 weeks developed hypercholesterolemia, oxidative stress, and NASH. DNA chip analyses revealed that the atherogenic diet had a great influence on the mRNA expression of a wide range of genes linked to mitochondrial energy production, redox regulation, and carbohydrate and lipid metabolism. However, the rhythmic mRNA expression of the clock genes in the liver remained intact. Most of the circadianly expressed genes also showed 24-h rhythmicity. These findings suggest that the biological clock is protected against such a metabolic derangement as NASH. |
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Keywords: | Atherogenic diet Circadian rhythm Clock gene Non-alcoholic steatohepatitis Oxidative stress |
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