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Is Potentiated by Growth Hormone and Insulin-Like Growth Factors
Department of Woman and Child Health, Pediatric Endocrinology Unit, Astrid Lindgren Children’s Hospital, Karolinska Institute and University Hospital, S-171 76 Stockholm, Sweden
Address all correspondence and requests for reprints to: Dr. Olle Soder, Department of Woman and Child Health, Pediatric Endocrinology Unit, Q2:08, Karolinska Institute and Hospital, Astrid Lindgren Children’s Hospital, S-171 76 Stockholm, Sweden. E-mail: olle.soder{at}kbh.ki.se.
The cytokine IL-1
is produced constitutively by the intact testis, but its function in this organ remains largely unknown. In this study we examined cooperation between IL-1 and GH and IGFs with regard to stimulation of steroidogenesis by Leydig cells from 40-d-old rats in vitro. IL-1 alone stimulated testosterone (T) and dihydrotestosterone (DHT) production. GH, IGF-I, or IGF-II alone was without effect on T production, but they were found to elevate DHT release, albeit without an obvious dose-response effect. Costimulation with IL-1 and GH or with IL-1 and IGF-I or IGF-II elevated the rate of steroidogenesis (both T and DHT) above that observed with IL-1 alone. GH was found to increase the level of IGF-I in the cultured Leydig cells, an effect that was potentiated by IL-1. The costimulatory effect of GH on steroidogenesis was abolished by treatment with picropodophyllin, a specific inhibitor of the IGF-I receptor, indicating that the action of GH is mediated via IGF-I. Moreover, cells costimulated with IL-1 and GH exhibited a marked decrease in the level of intact IGF-binding protein-3 in the culture medium due to the induction of proteolytic activity toward this binding protein. In contrast, secretion of IGF-binding protein-2 was increased by such costimulation. These findings suggest that the stimulation of steroidogenesis in Leydig cells evoked by GH and IGFs requires cooperation with IL-1. This cooperation may play an important role in connection with postnatal Leydig cell maturation and steroidogenesis.
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