Decreased Fatty Acid <i>β</i>-Oxidation Is the Main Cause of Fatty Liver Induced by Polyunsaturated Fatty Acid Deficiency in Mice
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- Nakajima Takero
- Department of Metabolic Regulation, Shinshu University Graduate School of Medicine Research Center for Agricultural Food Industry, Shinshu University
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- Yang Yang
- Department of Metabolic Regulation, Shinshu University Graduate School of Medicine Department of Cardiology, The Third Hospital of Hebei Medical University
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- Lu Yu
- Department of Metabolic Regulation, Shinshu University Graduate School of Medicine
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- Kamijo Yuji
- Department of Metabolic Regulation, Shinshu University Graduate School of Medicine Department of Nephrology, Shinshu University School of Medicine
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- Yamada Yosuke
- Department of Metabolic Regulation, Shinshu University Graduate School of Medicine Department of Nephrology, Shinshu University School of Medicine
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- Nakamura Kozo
- Research Center for Agricultural Food Industry, Shinshu University Department of Bioscience and Biotechnology, Faculty of Agriculture, Shinshu University
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- Koyama Masahiro
- Department of Bioscience and Biotechnology, Faculty of Agriculture, Shinshu University
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- Yamaguchi Shohei
- Department of Bioscience and Biotechnology, Faculty of Agriculture, Shinshu University
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- Sugiyama Eiko
- Department of Nutritional Science, Nagano Prefectural College
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- Tanaka Naoki
- Department of Metabolic Regulation, Shinshu University Graduate School of Medicine Research Center for Agricultural Food Industry, Shinshu University
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- Aoyama Toshifumi
- Department of Metabolic Regulation, Shinshu University Graduate School of Medicine
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抄録
<p>Insufficient intake of polyunsaturated fatty acids (PUFA) causes fatty liver. The mechanism responsible is primarily related to increased lipogenesis and decreased FA degradation based on rodent studies. However, these studies were limited by the fact that the typical PUFA-deficient diets contained insufficient amounts of long-chain FA, the PUFA-containing diets were primarily composed of n-3 PUFA-enriched oil, and the intake of PUFA was excessive compared with the physiological requirement. To address these issues, mice were fed a PUFA-deficient diet containing long-chain FA at a standard fed level and then were orally fed a n-3/n-6-balanced PUFA-containing oil [PUFA (+)] or a PUFA-deficient oil [PUFA (−)] at physiological relevant levels (0.1 mL/mouse/2d). We compared these groups and examined whether fatty liver in PUFA deficiency was attributable to both the effects of increased lipogenesis and decreased FA catabolism. Compared with the PUFA (+) group, the PUFA (−) group showed increases in liver triglyceride and serum FA content. Hepatic gene expression of several mitochondrial β-oxidation enzymes, the serum 3-hydroxybutyrate level, and DNA-binding ability of peroxisome proliferator-activated receptor α (PPARα) were increased in the PUFA (+) group, whereas these adaptive responses were significantly attenuated in the PUFA (−) group. The hepatic expression of typical lipogenesis genes did not differ between the groups. Therefore, fatty liver in PUFA deficiency is attributable to suppression of the FA-degrading system probably from decreased PPARα adaptive responsiveness, and PUFA may be an essential factor for PPARα functioning. This finding is helpful for managing clinical situations having a risk of PUFA deficiency.</p>
収録刊行物
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- The Tohoku Journal of Experimental Medicine
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The Tohoku Journal of Experimental Medicine 242 (3), 229-239, 2017
東北ジャーナル刊行会
