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This Article Full Text Full Text (PDF) All Versions of this Article: 68/4/1199    most recent biolreprod.102.007831v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Caprio, M. Articles by Fabbri, A. Search for Related Content PubMed PubMed Citation Articles by Caprio, M. Articles by Fabbri, A. Agricola Articles by Caprio, M. Articles by Fabbri, A.

Ontogenesis of Leptin Receptor in Rat Leydig Cells¹

^a Cattedra di Endocrinologia, Dipartimento di Medicina Interna, Università "Tor Vergata," 00133 Rome, Italy ^b Cattedra di Andrologia, Dipartimento di Fisiopatologia Medica, Università "La Sapienza," 00161 Rome, Italy ^c Cattedra di Medicina Interna, Dipartimento di Fisiopatologia Medica, Università di Roma "La Sapienza," 00161 Rome, Italy ^d Dipartimento di Medicina Sperimentale, Laboratorio di Istologia ed Embriologia, Seconda Università di Napoli, 80138 Naples, Italy ^e Dipartimento di Tossicologia, Università di Cagliari, 09124 Cagliari, Italy

There are still many controversies about the role of leptin in reproductive function and sexual development. We recently demonstrated that leptin receptors are expressed in rodent Leydig cells and that leptin has inhibitory effects on hCG-stimulated testosterone production by adult rat Leydig cells in culture. In this study, we evaluated the expression of leptin receptor (Ob-R) in rat testes from gestational to adult age in comparison with the pattern of expression of relaxin-like factor (RLF), a specific marker of Leydig cell differentiation status. Immunohistochemical analysis showed that, in prenatal life, Ob-R immunoreactivity was absent at early embryonic ages (E14.5) and appeared at a late embryonic age (E19.5); in postnatal life, immunoreactivity was evident only after sexual maturation (35-, 60-, and 90-days old), whereas it was absent in testes from sexually immature rats (7-, 14-, and 21-days old). Immunoreaction was always confined to Leydig cells and no signal of Ob-R was detected within the tubules. The pattern of expression of Ob-R during testicular development was similar with that of RLF immunoreactivity, which was present in mature fetal as well as adult-type Leydig cells. In contrast with the findings in the testis, in the hypothalamus, the immunohistochemical pattern of Ob-R was very similar between pre- and postpubertal life. Reverse transcription-polymerase chain reaction studies showed that Ob-R expression was present in embryonic, prepubertal, and adult rat testes; semiquantitative analysis showed that mRNA levels were much higher in late versus early embryonic testes, as well as in mature adults versus sexually immature testes, with a gradual increase from younger to older ages. Functional studies showed that, while leptin (150 ng/ml) significantly inhibited hCG-stimulated testosterone production in adult rat Leydig cells (46% reduction; P > 0.01), it did not modify prepubertal rat Leydig cells steroidogenic function in vitro. In conclusion, we showed that, in rat testis, Ob-R expression is characteristic of mature Leydig cells (fetal and adult type) and it is functional in adult but not prepubertal life.

¹ Presented in part at the 84th annual meeting of the Endocrine Society, San Francisco, CA, 2002, P3-59. This work was supported by a grant from the Universities of Rome "La Sapienza" and "Tor Vergata," Department of Medical Pathophysiology, and Department of Internal Medicine (Progetti 60%).

² Correspondence: Andrea Fabbri, Endocrinology Unit, Department of Internal Medicine, University Tor Vergata, Via di Tor Vergata 135, 00133 Rome, Italy. FAX: 39 06 72596663; a_fabbri{at}hotmail.com

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