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Research Article Free access | 10.1172/JCI114745

Insulin-like growth factor-I enhances luteinizing hormone binding to rat ovarian theca-interstitial cells.

J F Cara, J Fan, J Azzarello, and R L Rosenfield

Department of Pediatrics, University of Chicago Pritzker School of Medicine, Illinois.

Find articles by Cara, J. in: PubMed | Google Scholar

Department of Pediatrics, University of Chicago Pritzker School of Medicine, Illinois.

Find articles by Fan, J. in: PubMed | Google Scholar

Department of Pediatrics, University of Chicago Pritzker School of Medicine, Illinois.

Find articles by Azzarello, J. in: PubMed | Google Scholar

Department of Pediatrics, University of Chicago Pritzker School of Medicine, Illinois.

Find articles by Rosenfield, R. in: PubMed | Google Scholar

Published August 1, 1990 - More info

Published in Volume 86, Issue 2 on August 1, 1990
J Clin Invest. 1990;86(2):560–565. https://doi.org/10.1172/JCI114745.
© 1990 The American Society for Clinical Investigation
Published August 1, 1990 - Version history
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Abstract

We tested the hypothesis that insulin-like growth factor-I (IGF-I) stimulates ovarian androgen production by increasing theca-interstitial cell luteinizing hormone (LH) binding affinity and/or binding capacity. We then investigated the role of transcriptional and translational events in mediating these actions of IGF-I. LH bound to saturable, high affinity binding sites on rat ovarian theca-interstitial cells. Preincubation with LH produced a decrease in LH binding capacity with no effect on LH binding affinity. Treatment with IGF-I, both in the absence and presence of LH, increased LH binding capacity 1.5- to 2-fold with no change in LH binding affinity. Androgen production was increased progressively by LH, suggesting that LH-stimulated steroidogenesis is not tightly coupled to LH receptor downregulation. IGF-I increased androgen synthesis in proportion to its upregulation of LH binding capacity. Transcriptional inhibition with dichlorobenzimidazole riboside inhibited the IGF-I-mediated increase in LH binding capacity but had no effect on androgen production. Translational inhibition with cycloheximide inhibited both the IGF-I-mediated increase in LH binding and stimulation of androgen synthesis. We conclude that IGF-I increases theca-interstitial cell LH binding capacity and reverses the LH-induced downregulation of LH binding sites. The enhancement of LH binding by IGF-I is compatible with transcriptional mediation whereas the effect of IGF-I on androgen synthesis appears to be mediated by a direct effect of the peptide on the translational process(es) involved in steroidogenesis.

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