Suppr超能文献

一名尿中排泄3β-羟基-δ5-胆汁酸的儿童成纤维细胞中缺乏3β-羟基-δ5-C27-类固醇脱氢酶/异构酶。一种新的先天性代谢缺陷。

Lack of 3 beta-hydroxy-delta 5-C27-steroid dehydrogenase/isomerase in fibroblasts from a child with urinary excretion of 3 beta-hydroxy-delta 5-bile acids. A new inborn error of metabolism.

作者信息

Buchmann M S, Kvittingen E A, Nazer H, Gunasekaran T, Clayton P T, Sjövall J, Björkhem I

机构信息

Institute of Clinical Biochemistry, Rikshospitalet, University of Oslo, Norway.

出版信息

J Clin Invest. 1990 Dec;86(6):2034-7. doi: 10.1172/JCI114939.

Abstract

Cultured fibroblasts were shown to be capable of catalyzing the conversion of 7 alpha-hydroxy-cholesterol to 7 alpha-hydroxy-4-cholesten-3-one, an important reaction in bile acid synthesis. The apparent Km was approximately 7 mumol/liter and Vmax varied between 3 and 9 nmol/mg protein per h under the assay conditions used. The assay was used to investigate fibroblasts from a patient who presented with a familial giant cell hepatitis and who was found to excrete the monosulfates of 3 beta, 7 alpha-dihydroxy-5-cholenoic acid and 3 beta, 7 alpha, 12 alpha-trihydroxy-5-cholenoic acid in urine (Clayton, P. T., J. V. Leonard, A. M. Lawson, K. D. R. Setchell, S. Andersson, B. Egestad, and J. Sjövall. 1987. J. Clin. Invest. 79:1031-1038). In addition 7 alpha-hydroxy-cholesterol was found to accumulate in the circulation. Cultured fibroblasts from this boy were completely devoid of 3 beta-hydroxy-delta 5-C27-steroid dehydrogenase/isomerase activity. Fibroblasts from his parents had reduced activity, compatible with a heterozygous genotype. The results provide strong evidence for the suggestion that this patient's liver disease was caused by a primary defect in the 3 beta-hydroxy-delta 5-C27-steroid dehydrogenase/isomerase involved in bile acid biosynthesis.

摘要

培养的成纤维细胞被证明能够催化7α-羟基胆固醇转化为7α-羟基-4-胆甾烯-3-酮,这是胆汁酸合成中的一个重要反应。在所使用的测定条件下,表观Km约为7μmol/升,Vmax在每小时3至9nmol/mg蛋白质之间变化。该测定用于研究一名患有家族性巨细胞肝炎的患者的成纤维细胞,发现该患者尿液中排泄3β,7α-二羟基-5-胆烯酸和3β,7α,12α-三羟基-5-胆烯酸的单硫酸盐(克莱顿,P.T.,J.V.伦纳德,A.M.劳森,K.D.R.塞切尔,S.安德森,B.埃格施塔德,和J.舍瓦尔。1987年。《临床研究杂志》79:1031 - 1038)。此外,发现7α-羟基胆固醇在循环中积累。这个男孩的培养成纤维细胞完全缺乏3β-羟基-δ5-C27-类固醇脱氢酶/异构酶活性。他父母的成纤维细胞活性降低,符合杂合子基因型。这些结果为该患者的肝脏疾病是由参与胆汁酸生物合成的3β-羟基-δ5-C27-类固醇脱氢酶/异构酶的原发性缺陷引起的这一观点提供了有力证据。

相似文献

引用本文的文献

5
Disorders of bile acid synthesis.胆汁酸合成障碍。
J Inherit Metab Dis. 2011 Jun;34(3):593-604. doi: 10.1007/s10545-010-9259-3. Epub 2011 Jan 13.
6
Mechanisms of disease: Inborn errors of bile acid synthesis.疾病机制:胆汁酸合成的先天性代谢缺陷
Nat Clin Pract Gastroenterol Hepatol. 2008 Aug;5(8):456-68. doi: 10.1038/ncpgasthep1179. Epub 2008 Jun 24.

本文引用的文献

9
Inborn errors of bile acid synthesis.先天性胆汁酸合成障碍
Semin Liver Dis. 1987 May;7(2):85-99. doi: 10.1055/s-2008-1040568.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验