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Comparative Study
. 1983 May;112(5):1696-701.
doi: 10.1210/endo-112-5-1696.

Luteinizing hormone receptors and testosterone production in whole testes and purified Leydig cells from the mouse: differences among inbred strains

Comparative Study

Luteinizing hormone receptors and testosterone production in whole testes and purified Leydig cells from the mouse: differences among inbred strains

J R Stalvey et al. Endocrinology. 1983 May.

Abstract

Testicular and Leydig cell function were studied in four inbred strains of mice. Significant strain-related differences were found in the number of LH receptors and in the production of testosterone in vitro in response to increasing concentrations of human CG (hCG) by both decapsulated testes and isolated Leydig cells. Maximal testicular testosterone production was similar in the C57BL/10J and C57BL/6J strains and considerably less in the DBA/2J (DBA) and C3H/HeJ strains, which were similar. However, the number of testicular LH receptors was less in C57BL/6J mice than in all three other strains. The pattern of maximal testosterone production by isolated Leydig cells among the four strains was similar to that observed for whole testes, whereas the number of LH receptors per 10(6) Leydig cells was least for Leydig cells from the DBA strain. When the number of Leydig cells per testis was estimated by dividing the number of testicular LH receptors by the number of LH receptors in 10(6) Leydig cells, it was apparent that testes from DBA mice contain approximately twice as many Leydig cells as those from the other strains. Differences in maximal testicular testosterone production appear to be reflected in differences in maximal testosterone production by isolated Leydig cells from each strain. However, there were no differences in testicular sensitivity to hCG but there were differences in Leydig cell sensitivity to hCG among the four strains. Furthermore, the existence of strain-related differences in well defined functional characteristics of Leydig cells offers the opportunity to study the genetic as well as physiological mechanisms involved in the regulation of Leydig cell function in normal individuals.

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