Inoue Jun, Satoh Shin-Ichi, Kita Mariko, Nakahara Mayuko, Hachimura Satoshi, Miyata Masaaki, Nishimaki-Mogami Tomoko, Sato Ryuichiro
Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo, Tokyo 113-8657, Japan.
Biochem Biophys Res Commun. 2008 Jul 11;371(4):675-8. doi: 10.1016/j.bbrc.2008.04.100. Epub 2008 Apr 28.
LXR, PXR, and PPARalpha are members of a nuclear receptor family which regulate the expression of genes involved in lipid metabolism. Here, we show the administration of T0901317 stimulates PPARalpha gene expression in the small intestine but not in the liver of both normal and FXR-null mice. The administration of LXR specific ligand GW3965, or PXR specific ligand PCN has the same effect, indicating that ligand-dependent activation of LXR and PXR, but not FXR, is responsible for the increased gene expression of PPARalpha in the mouse small intestine.
肝X受体（LXR）、孕烷X受体（PXR）和过氧化物酶体增殖物激活受体α（PPARα）是核受体家族的成员，它们调节参与脂质代谢的基因的表达。在此，我们发现给予T0901317可刺激正常小鼠和FXR基因敲除小鼠小肠中PPARα基因的表达，但对肝脏无此作用。给予LXR特异性配体GW3965或PXR特异性配体苯巴比妥钠也有相同效果，表明LXR和PXR的配体依赖性激活而非FXR的激活，是小鼠小肠中PPARα基因表达增加的原因。
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