Differentiation of Adult Leydig Cells in the Neonatal Rat Testis Is Arrested by Hypothyroidism¹

^a Department of Animal Science, College of Veterinary Medicine, The University of Tennessee, Knoxville, Tennessee 37996

The effects of propyl thiouracil (PTU)-induced hypothyroidism on testicular interstitial cells and androgen secretion in vitro in the neonatal rat were investigated using Sprague Dawley rats of 1, 7, 14, and 21 days. The results revealed that the fetal Leydig cell (FLC) number per testis was unchanged between and within treatment groups at all ages tested. FLC size was 50% smaller in 21-day controls than in all other groups. Adult Leydig cells (ALCs) were present at Days 14 and 21 in controls but were absent in PTU rats. ALCs approximated FLCs of 21-day controls in size. ALC number per testis showed a sharp increase at Day 21. 11ß-HSD1-positive cells were absent in 21-day PTU testes, but a few were present in 21-day control testes. Testosterone secretion per testis was unchanged in 1- to 21-day controls and 7- to 21-day PTU rats. However, at Day 21, a significantly lower value was seen in controls compared to PTU rats. Testicular androstenedione secretion was not significantly different between control and PTU rats up to 14 days, but a sharp rise was observed in controls at Day 21. At this age, androstenedione levels in PTU rats were similar to those at younger ages. In summary, histological studies showed that hypothyroidism prevented the hypotrophy of FLC and the emergence of ALC in the neonatal rat testis, and agreed favorably with results concerning testicular androgen secretion in vitro. These findings suggest that thyroid hormones have a regulatory role in precursor cell differentiation into Leydig cells in the neonatal rat testis to establish the ALC population.

¹ Supported in part by grants R180101–08 from the College of Veterinary Medicine Center of Excellence for Livestock Diseases and Human Health, and Minkel Grant, The University of Tennessee, IBN 94–09288 from the National Science Foundation.

² Correspondence. FAX: (423) 974–8222; mendisc{at}utk.edu

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