Jones Ryan D, Lopez Adam M, Tong Ernest Y, Posey Kenneth S, Chuang Jen-Chieh, Repa Joyce J, Turley Stephen D
Department of Physiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, United States.
Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX, United States.
Steroids. 2015 Jan;93:87-95. doi: 10.1016/j.steroids.2014.11.002. Epub 2014 Nov 28.
Mice deficient in cholesterol 7α-hydroxylase (Cyp7a1) have a diminished bile acid pool (BAP) and therefore represent a useful model for investigating the metabolic effects of restoring the pool with a specific BA. Previously we carried out such studies in Cyp7a1(-/-) mice fed physiological levels of cholic acid (CA) and achieved BAP restoration, along with an increased CA enrichment, at a dietary level of just 0.03% (w/w). Here we demonstrate that in Cyp7a1(-/-) mice fed chenodeoxycholic acid (CDCA) at a level of 0.06% (w/w), the BAP was restored to normal size and became substantially enriched with muricholic acid (MCA) (>70%), leaving the combined contribution of CA and CDCA to be <15%. This resulted in a partial to complete reversal of the main changes in cholesterol and BA metabolism associated with Cyp7a1 deficiency such as an elevated rate of intestinal sterol synthesis, an enhanced level of mRNA for Cyp8b1 in the liver, and depressed mRNA levels for Ibabp, Shp and Fgf15 in the distal small intestine. When Cyp7a1(-/-) and matching Cyp7a1(+/+) mice were fed a diet with added cholesterol (0.2%) (w/w), either alone, or also containing CDCA (0.06%) (w/w) or CA (0.03%) (w/w) for 18days, the hepatic total cholesterol concentrations (mg/g) in the Cyp7a1(-/-) mice were 26.9±3.7, 16.4±0.9 and 47.6±1.9, respectively, vs. 4.9±0.4, 5.0±0.7 and 6.4±1.9, respectively in the corresponding Cyp7a1(+/+) controls. These data affirm the importance of using moderate levels of dietary BA supplementation to elicit changes in hepatic cholesterol metabolism through shifts in BAP size and composition.
胆固醇7α-羟化酶(Cyp7a1)缺陷的小鼠胆汁酸池(BAP)减小,因此是研究用特定胆汁酸恢复胆汁酸池的代谢效应的有用模型。此前我们在喂食生理水平胆酸(CA)的Cyp7a1(-/-)小鼠中进行了此类研究,在仅0.03%(w/w)的饮食水平下实现了胆汁酸池的恢复以及胆酸富集增加。在此我们证明,在喂食0.06%(w/w)鹅去氧胆酸(CDCA)的Cyp7a1(-/-)小鼠中,胆汁酸池恢复到正常大小,并大量富集了鼠胆酸(MCA)(>70%),使得CA和CDCA的总贡献<15%。这导致与Cyp7a1缺乏相关的胆固醇和胆汁酸代谢的主要变化部分或完全逆转,如肠道固醇合成速率升高、肝脏中Cyp8b1的mRNA水平增强以及远端小肠中Ibabp、Shp和Fgf15的mRNA水平降低(在远端小肠中)。当Cyp7a1(-/-)和匹配的Cyp7a1(+/ +)小鼠单独或同时喂食添加了胆固醇(0.2%)(w/w)、或还含有CDCA(0.06%)(w/w)或CA(0.)(w/w)的饮食18天时,Cyp7a1(-/-)小鼠肝脏中的总胆固醇浓度(mg/g)分别为26.9±3.7、16.4±0.9和47.6±1.9,而相应的Cyp7a1(+/ +)对照分别为4.9±0.4、5.0±0.7和6.4±1.9。这些数据证实了通过改变胆汁酸池大小和组成,使用适度水平的膳食胆汁酸补充剂来引发肝脏胆固醇代谢变化的重要性。 (注:原文中“CA (0.) (w/w)”这里的0后面疑似遗漏了数字,译文按原文翻译)