Origin, Development and Regulation of Human Leydig Cells

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Abstract

Sex steroids are crucial regulators of sexual differentiation and the proper development of secondary sex characteristics and patterns of sexual behavior. Since Leydig cells are the primary major producers of these steroid hormones, maintenance of the normal functions of these cells determines the reproductive capacity and fertility of males. The present minireview discusses recent findings concerning endocrine and paracrine regulation of the proliferation, differentiation and involution of human Leydig cells. The physiology and function of the two distinct fetal and adult populations of human Leydig cells are described, with particular focus on the paracrine environment that triggers their differentiation and functional maturation. The roles of established and more recently discovered paracrine regulators of this maturation, including insulin-like factor 3, platelet-derived growth factor-α, desert hedgehog, ghrelin and leptin are considered. A brief description of the origin, ontogenesis and functional markers of human fetal and adult Leydig cells is presented.

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Most cited references 54

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Upregulation of Ghrelin expression in the stomach upon fasting, insulin-induced hypoglycemia, and leptin administration.

M. M. A. Mondal, N Murakami, K. Kangawa … (2001)

Ghrelin is a novel gut-brain peptide that binds to the growth hormone secretagogue receptor (GHS-R), thereby functioning in the regulation of growth hormone (GH) release and food intake. Ghrelin-producing cells are most abundant in the oxyntic glands of the stomach. The regulatory mechanism that governs the biosynthesis and secretion of ghrelin has not been clarified. We report that ghrelin mRNA expression in the gastric fundus was increased, but that ghrelin peptide content decreased after a 48-h fast. Both values returned to control levels after refeeding. The ghrelin plasma concentration in the gastric vein and systemic venous blood increased after 24- and 48-h fasts. Furthermore, des-octanoylated ghrelin and n-octanoylated ghrelin were found in rat stomach, with the ratio of des-octanoylated ghrelin to n-octanoylated ghrelin markedly increased after fasting. The ghrelin mRNA level in the stomach also increased after administration of insulin and leptin. Conversely, db/db mice, which are deficient in the leptin receptor, had lower ghrelin mRNA levels than control mice. These findings suggest that this novel gastrointestinal hormone plays a role in the regulation of energy balance. Copyright 2001 Academic Press.

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Cell biology of Leydig cells in the testis.

Syed Haider (2004)

This article reviews results on differentiation, structure, and regulation of Leydig cells in the testes of rodents and men. Two different populations-fetal and adult Leydig cells-can be recognized in rodents. The cells in these two populations are different in ultrastructure, life span, capacity for androgen synthesis, and mechanisms of regulation. A brief survey on the origin, ontogenesis, characterization of precursors, ultrastructure, and functional markers of fetal and adult Leydig cells is presented, followed by an analysis of genes in Leydig cells and the role of luteinizing hormone and its receptor, steroidogenic acute regulatory protein, hydroxysteroid dehydrogenases, androgen and its receptor, anti-Müllerian hormone, estrogens, and thyroid hormones. Various growth factors modulate Leydig cell differentiation, regeneration, and steroidogenic capacity, for example, interleukin 1alpha, transforming growth factor beta, inhibin, insulin-like growth factors I and II, vascular endothelial growth factor, and relaxin-like growth factor. Retinol and retinoic acid increase basal testosterone secretion in adult Leydig cells, but decrease it in fetal Leydig cells. Resident macrophages in the interstitial tissue of the testis are important for differentiation and function of Leydig cells. Apoptosis of Leydig cells is involved in the regulation of Leydig cell number and can be induced by cytotoxins. Characteristics of aging Leydig cells in rodents seem to be species specific. 11beta-hydroxysteroid dehydrogenase protects testosterone synthesis in the Leydig cells of stressed rats. Last, the following aspects of human Leydig cells are briefly described: origin, differentiation, triphasic development, aging changes, pathological changes, and gene mutations leading to infertility.

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Male pseudohermaphroditism caused by mutations of testicular 17 beta-hydroxysteroid dehydrogenase 3.

W M Geissler, D L Davis, L Wu … (1994)

Defects in the conversion of androstenedione to testosterone in the fetal testes by the enzyme 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) give rise to genetic males with female external genitalia. We have used expression cloning to isolate cDNAs encoding a microsomal 17 beta-HSD type 3 isozyme that shares 23% sequence identity with other 17 beta-HSD enzymes, uses NADPh as a cofactor, and is expressed predominantly in the testes. The 17 beta HSD3 gene on chromosome 9q22 contains 11 exons. Four substitution and two splice junction mutations were identified in the 17 beta HSD3 genes of five unrelated male pseudohermaphrodites. The substitution mutations severely compromised the activity of the 17 beta-HSD type 3 isozyme.

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Author and article information

Journal

Journal ID (publisher-id): HRP

Journal ID (nlm-ta): Horm Res Paediatr

Journal ID (doi): 10.1159/issn.1663-2818

Title: Hormone Research in Paediatrics

Publisher: S. Karger AG

ISSN (Print): 1663-2818

ISSN (Electronic): 1663-2826

Publication date Subscription-year: 2010

Publication date (Print): February 2010

Publication date (Electronic): 09 February 2010

Volume: 73

Issue: 2

Pages: 93-101

Affiliations

Department of Women’s and Children’s Health, Pediatric Endocrinology Unit, Karolinska Institutet and University Hospital, Stockholm, Sweden

Article

Publisher ID: 277141 Other ID: Horm Res Paediatr 2010;73:93–101

DOI: 10.1159/000277141

PubMed ID: 20190545

SO-VID: ec53fa62-a4cd-4e5a-9899-ad9553231b49

License:

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

History

Date received : 21 April 2009

Date accepted : 09 November 2009

Page count

Figures: 2, References: 76, Pages: 9

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