The Effect of FSH on LH Induced Testosterone Secretion in the Immature Hypophysectomized Male Rat

Selin, Liisa K.; Moger, William H.

doi:10.1080/07435807709052938

Cited by 26 publications

(12 citation statements)

References 14 publications

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“…Because this same human FSH preparation was highly active in FSH receptortransfected cells investigated during another study [15], there could be no doubt regarding its biological activity. Thus, our observations noting a lack of direct effect on the mouse testis (Leydig cells) is contradictory to those of several earlier studies in which investigators noted that FSH stimulated testosterone production both in vivo [2,19] and in vitro [3,20]. However, such effects may be due to the LH contamination in the FSH preparations, because these studies predate the availability of recombinant FSH [5].…”

Section: Discussioncontrasting

confidence: 99%

Intercellular Communication Between Sertoli Cells and Leydig Cells in the Absence of Follicle-Stimulating Hormone-Receptor Signaling1

Krishnamurthy

Kats

Danilovich

et al. 2001

Biology of Reproduction

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Effective interactions among the various compartments of the testis are necessary to sustain efficiency of the spermatogenic process. To study the intercellular communication between the Sertoli and Leydig cells in the complete absence of FSH receptor signaling, we have examined several indices of Leydig cell function in FSH receptor knockout (FORKO) mice. The serum testosterone levels were reduced in the 3- to 4-mo-old adult FORKO males compared to wild-type mice despite no significant alteration in circulating LH levels. Treatment with ovine LH resulted in a dose-dependent increase in serum testosterone levels in all three genotypes (+/+, +/-, and -/-). However, the response in FORKO males was significantly reduced. Similarly, the total intratesticular testosterone per testis was also lower, but the intratesticular testosterone per milligram of testis was significantly elevated in the FORKO males. Western blot analysis revealed an apparent higher expression of the enzyme 3beta-hydroxysteroid dehydrogenase (3beta-HSD) as well as LH-receptor density in the testis of FORKO males. Immunohistochemistry also showed an increase in the intensity of 3beta-HSD staining in the testicular sections of FORKO males. Although LH receptor binding increased per unit weight in FORKO mice, the total LH binding remained the same in all genotypes. Taken together, the results of the present study suggest that, in the absence of FSH receptor signaling, the testicular milieu is altered to affect Leydig cell response to LH such that circulating testosterone is reduced in the adult mutant. Studies are currently under way to understand the mechanisms underlying this phenomenon.

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Section: Discussioncontrasting

confidence: 99%

Intercellular Communication Between Sertoli Cells and Leydig Cells in the Absence of Follicle-Stimulating Hormone-Receptor Signaling1

Krishnamurthy

Kats

Danilovich

et al. 2001

Biology of Reproduction

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“…Although receptors for FSH on the Sertoli cells are well established (Means and Vaitukaitis, 1972;Means et al, 1976;Orth and Christensen, 1977), the evidence for FSH receptors on Leydig cells is equivocal. It is generally agreed that FSH exerts its effect on Leydig cells by modulating LH receptors (Odell et al, 1973;Chen et al, 1976Chen et al, , 1977Odell and Swerdloff, 1976;Selin and Moger, 1977). Our studies regarding positive staining for FSH on Leydig cells are in agreement with the observation of Yoon et al (1987).…”

Section: Discussionsupporting

confidence: 90%

FSH in testes of marmosets during development: Immunocytochemical localization and de novo biosynthesis

1991

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Immunocytochemical localization of FSH was carried out in various cell types of marmoset testes during development using antisera generated against intact as well as beta-subunit of human FSH. Significant differences in the intensity as well as distribution of FSH in various cell types were observed in neonatal, pubertal, and adult marmosets. Intensity of staining in Leydig cells was maximum at day 1 and in adults (1-3 years), whereas it was minimum at 3 months. In seminiferous tubules (Sertoli cells), FSH was present in trace amount until puberty and subsequently increased at maturity. Further studies demonstrate de novo biosynthesis of FSH-like moiety in vitro by testicular tissue, which was age dependent.

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“…The rats were also hypophysectomized at an earlier age (21-25 days) than the present study; this is a critical period for Leydig cell development and these small differences in age may therefore be important. Selin & Moger (1977) found that 1-5 µg LH/day, a dose comparable to that which we used, resulted in a significant increase in the subsequent testicular response of hypophysectomized rats to LH in vivo. However, the effect was not as great as that with FSH (42-5 µg/day) which contained this quantity of LH as contamination.…”

Section: Discussionsupporting

confidence: 52%

“…This consideration has largely been prompted by the finding that FSH treatment of hypophysectomized rats results in an increase in the maximum quantity of LH-stimulated androgen secretion by Leydig cells, both in vivo (Odell & Swerdloff, 1975;Selin & Moger, 1977) and in vitro (Chen, Payne & Kelch, 1976;van Beurden, Roodnat, de Jong, Mulder & van der Molen, 1976;Chen, Shaw & Payne, 1977). Furthermore, FSH also appears to stimulate the number of LH receptors in testis tissue (Chen et al, 1977).…”

Section: Introductionmentioning

confidence: 99%

LH contamination may explain FSH effects on rat Leydig cells

Purvis¹,

Clausen²,

Hansson³

1979

Reproduction

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Treatment of immature, hypophysectomized male rats with 50 micrograms ovine FSH (NIH-FSH-S12) twice a day for 5 days stimulated the maximum quantity of 17 beta-hydroxyandrogen produced by isolated Leydig cells in response to hCG. Pretreatment of the FSH preparation with an LH antiserum in one study markedly reduced and in another study completely abolished this stimulatory effect of FSH, but only slightly impaired the capacity of the hormone to stimulate the Sertoli cell in vivo (epididymal androgen-binding protein). Administration of another highly potent FSH preparation (LER-1881) had no discernible effects on the dose-response characteristics of the Leydig cells but was superior to the NIH-FSH-S12 in its capacity for stimulating the Sertoli cell. When all hormone preparations were tested for their ability to stimulate steroid secretion from normal Leydig cells in vitro, a close correlation was obtained between their Leydig cell-stimulating activity (a measure of LH contamination) and their capacity to alter Leydig cell responsiveness after in-vivo treatment. FSH treatment had no effects on specific LH binding per 10(6) Leydig cells. It is concluded that the stimulatory influence of FSH on rat Leydig cells may to some extent be a result of the LH contaminating the hormone preparation.

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The Effect of FSH on LH Induced Testosterone Secretion in the Immature Hypophysectomized Male Rat

Cited by 26 publications

References 14 publications

Intercellular Communication Between Sertoli Cells and Leydig Cells in the Absence of Follicle-Stimulating Hormone-Receptor Signaling1

Intercellular Communication Between Sertoli Cells and Leydig Cells in the Absence of Follicle-Stimulating Hormone-Receptor Signaling1

FSH in testes of marmosets during development: Immunocytochemical localization and de novo biosynthesis

LH contamination may explain FSH effects on rat Leydig cells

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