著者
Kazuyuki HIWATASHI Yasuyuki KOSAKA Nao SUZUKI Keishi HATA Toshiyuki MUKAIYAMA Kenji SAKAMOTO Hitoshi SHIRAKAWA Michio KOMAI
出版者
Japan Society for Bioscience, Biotechnology, and Agrochemistry
雑誌
Bioscience, Biotechnology, and Biochemistry (ISSN:09168451)
巻号頁・発行日
pp.1006011996, (Released:2010-07-07)
参考文献数
20
被引用文献数
42

The effects of dietary Yamabushitake mushroom (Hericium erinaceus) on lipid metabolism were examined. C57BL/6J mice were fed a high-fat diet containing hot-water extract (HW-E) and an ethanol extract (EtOH-E) of Yamabushitake mushroom. Administration of HW-E or EtOH-E with a high-fat diet for 28 d resulted in a significant decrease in body weight gain, fat weight, and serum and hepatic triacylglycerol levels. Our in vitro experiments indicated that EtOH-E acts as an agonist of peroxisome proliferator-activated receptor α (PPARα). Quantitative analyses of hepatic mRNA levels revealed that EtOH-E administration resulted in up-regulation of mRNA for a number of PPARα-regulating genes in spite of the fact that the gene expression of PPARα did not change. These results suggest that EtOH-E improves lipid metabolism in mice fed a high-fat diet, and that these effects were mediated by modulation of lipid metabolic gene expression, at least in part via activation of PPARα.
著者
Keishi HATA TOMATSU Sayaka Masaki TAKAHASHI Akira SASAKI Yui UMEKAWA Kazuya MIYASHITA Kazumi OGURA Gen TOSHIMA Masahiro MAEDA Junichiro TAKAHASHI Masakazu KAKUNI
出版者
Biomedical Research Press
雑誌
Biomedical Research (ISSN:03886107)
巻号頁・発行日
vol.41, no.1, pp.33-42, 2020-02-01 (Released:2020-02-22)
参考文献数
24
被引用文献数
5

We investigated lipid metabolism in PXB-cells, which are human primary hepatocytes isolated from liver-humanized mice, and HepG2 and HuH-7 human hepatoma cell lines. Lipoprotein levels were higher in PXB-cells than in the 2 other cell lines, and PXB-cells mainly released triglycerides and cholesterol as very low density lipoprotein (VLDL), similar to actual liver tissue, whereas the major lipoprotein released from the 2 hepatoma cell lines was LDL. RT-PCR analysis demonstrated that the gene expression levels of apolipoprotein B100 (ApoB100), the apolipoprotein of VLDL/LDL, were similar in PXB-cells and HepG2 cells, while the overexpression of ApoC2, ApoC3, and ApoE, which are components of VLDL, but not LDL, was observed in PXBcells. A protein immunoassay revealed that ApoB100 levels secreted from PXB-cells and HuH-7 cells were similar; however, ApoC3 levels were higher in PXB-cells than in the two other cell lines. We also examined the anti-lipidemic activities of fenofibrate using this assay system. Fenofibrate suppressed lipoprotein production from PXB-cells in a dose-dependent manner mainly by activating the β-oxidation pathway. These results suggest that PXB-cells produce high levels of lipoproteins and are suitable for screening anti-lipidemic agents.
著者
Kazuyuki HIWATASHI Yasuyuki KOSAKA Nao SUZUKI Keishi HATA Toshiyuki MUKAIYAMA Kenji SAKAMOTO Hitoshi SHIRAKAWA Michio KOMAI
出版者
Japan Society for Bioscience, Biotechnology, and Agrochemistry
雑誌
Bioscience, Biotechnology, and Biochemistry (ISSN:09168451)
巻号頁・発行日
vol.74, no.7, pp.1447-1451, 2010-07-23 (Released:2010-07-23)
参考文献数
20
被引用文献数
42

The effects of dietary Yamabushitake mushroom (Hericium erinaceus) on lipid metabolism were examined. C57BL/6J mice were fed a high-fat diet containing hot-water extract (HW-E) and an ethanol extract (EtOH-E) of Yamabushitake mushroom. Administration of HW-E or EtOH-E with a high-fat diet for 28 d resulted in a significant decrease in body weight gain, fat weight, and serum and hepatic triacylglycerol levels. Our in vitro experiments indicated that EtOH-E acts as an agonist of peroxisome proliferator-activated receptor α (PPARα). Quantitative analyses of hepatic mRNA levels revealed that EtOH-E administration resulted in up-regulation of mRNA for a number of PPARα-regulating genes in spite of the fact that the gene expression of PPARα did not change. These results suggest that EtOH-E improves lipid metabolism in mice fed a high-fat diet, and that these effects were mediated by modulation of lipid metabolic gene expression, at least in part via activation of PPARα.