Grosse Laurent, Chouinard Sarah, Pâquet Sophie, Verreault Mélanie, Trottier Jocelyn, Bélanger Alain, Barbier Olivier
Centre Hospitalié Universitaire de Québec Research Center, Laboratory of Molecular Pharmacology, Endocrinology and Nephrology Axis, Faculty of Pharmacy, Laval University, Québec, QC G1V 0A6, Canada.
Centre Hospitalié Universitaire de Québec Research Center, Faculty of Medicine, Laval University, Québec, QC G1V 0A6, Canada.
Biology (Basel). 2022 Mar 5;11(3):403. doi: 10.3390/biology11030403.
Glucuronidation, catalyzed by UDP-glucuronosyltransferase UGT2B enzymes, is a major inactivating and elimination pathway for androgen hormones in humans. Whether Ugt2b enzymes from mice are also reactive with these hormones have never been investigated. The present study aimed at evaluating the capability of murine tissues and Ugt2b enzymes to glucuronidated androgens. The 7 murine Ugt2b (Ugt2b1, 2b5, 2b34, 2b35, 2b36, 2b37 and 2b38) enzymes were cloned and stably expressed into HEK293 cells. In vitro glucuronidation assays were performed with microsomal proteins or homogenates from mice tissues (liver, kidney, intestine, adipose, testis, prostate, epididymis, bulbo, seminal vesicle, mammary glands, uterus, and ovary) and from Ugt2b-HEK293 cells. Male and female livers, as well as male kidneys, are the major sites for androgen glucuronidation in mice. The male liver is highly efficient at glucuronidation of dihydrotestosterone (DHT) and testosterone and is enriched in Ugt2b1 and 2b5 enzymes. Androsterone and 3α-Diol are conjugated in the male kidney through an Ugt2b37-dependent process. Interestingly, castration partially abolished hepatic Ugt2b1 expression and activity, while Ugt2b37 was totally repressed. DHT injection partially corrected these changes. In conclusion, these observations revealed the substrate- and tissue-specific manner in which murine Ugt2b enzymes conjugate androgens. They also evidence how androgens modulate their own glucuronide conjugation in mice.
由尿苷二磷酸葡萄糖醛酸基转移酶UGT2B酶催化的葡萄糖醛酸化作用,是人体内雄激素失活和清除的主要途径。小鼠的Ugt2b酶是否也能与这些激素发生反应,此前从未被研究过。本研究旨在评估小鼠组织和Ugt2b酶对雄激素进行葡萄糖醛酸化的能力。将7种小鼠Ugt2b(Ugt2b1、2b5、2b34、2b35、2b36、2b37和2b38)酶克隆并稳定表达于HEK293细胞中。使用来自小鼠组织(肝脏、肾脏、肠道、脂肪、睾丸、前列腺、附睾、球部、精囊、乳腺、子宫和卵巢)以及Ugt2b-HEK293细胞的微粒体蛋白或匀浆进行体外葡萄糖醛酸化试验。雄性和雌性肝脏以及雄性肾脏是小鼠体内雄激素葡萄糖醛酸化的主要部位。雄性肝脏对双氢睾酮(DHT)和睾酮的葡萄糖醛酸化效率很高,并且富含Ugt2b1和2b5酶。雄酮和3α-二醇在雄性肾脏中通过依赖Ugt2b37的过程进行结合。有趣的是,去势部分消除了肝脏中Ugt2b1的表达和活性,而Ugt2b37则被完全抑制。注射DHT可部分纠正这些变化。总之,这些观察结果揭示了小鼠Ugt2b酶结合雄激素的底物特异性和组织特异性方式。它们还证明了雄激素在小鼠体内如何调节自身的葡萄糖醛酸结合作用。