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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Analysis of HSD3B7 knockout mice reveals that a 3α-hydroxyl stereochemistry is required for bile acid function
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Analysis of HSD3B7 knockout mice reveals that a 3α-hydroxyl stereochemistry is required for bile acid function

机译：对HSD3B7基因敲除小鼠的分析表明，胆汁酸功能需要3α-羟基立体化学

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Primary bile acids are synthesized from cholesterol in the liver and thereafter are secreted into the bile and small intestine. Gut flora modify primary bile acids to produce secondary bile acids leading to a chemically diverse bile acid pool that is circulated between the small intestine and liver. A majority of primary and secondary bile acids in higher vertebrates have a 3α-hydroxyl group. Here, we characterize a line of knockout mice that cannot epimerize the 3β-hydroxyl group of cholesterol and as a consequence synthesize a bile acid pool in which 3β-hydroxylated bile acids predominate. This alteration causes death in 90% of newborn mice and decreases the absorption of dietary cholesterol in surviving adults. Negative feedback regulation of bile acid synthesis mediated by the farne-soid X receptor (FXR) is disrupted in the mutant mice. We conclude that the correct stereochemistry of a single hydroxyl group at carbon 3 in bile acids is required to maintain their physiologic and regulatory functions in mammals.
机译：胆汁酸是由肝脏中的胆固醇合成的，然后被分泌到胆汁和小肠中。肠道菌群修饰了初级胆汁酸，产生了次级胆汁酸，导致了化学多样性的胆汁酸池在小肠和肝脏之间循环。高等脊椎动物中的大多数伯和仲胆汁酸具有3α-羟基。在这里，我们表征了一系列不能消除胆固醇的3β-羟基基团的基因敲除小鼠，因此合成了以3β-羟基化胆汁酸为主的胆汁酸库。这种改变导致90％的新生小鼠死亡，并降低了成年小鼠对膳食胆固醇的吸收。法尼-X受体（FXR）介导的胆汁酸合成的负反馈调节在突变小鼠中被破坏。我们得出结论，胆汁酸中第3个碳原子上的单个羟基的正确立体化学是维持哺乳动物的生理和调节功能所必需的。

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