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Submitted on September 19, 2005
Accepted on December 9, 2005
Division of Cellular Endocrinology, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi-110 067, India
* To whom correspondence should be addressed. E-mail: subeer{at}nii.res.in.
Context: Follicle stimulating hormone (FSH) is known to augment the production of essential germ cell (Gc) survival factors, lactate and estradiol, by Sertoli cells (Sc) of 18-day-old pubertal rats. However, the failure of gonadotropin and androgen treatment to initiate spermatogenesis in testis of some infertile men bearing Sc and Gc is intriguing. The role of FSH in regulation of lactate and estradiol production by primate Sc is currently unknown.
Objective: To determine the role of FSH in regulating lactate and estradiol production by primate Sc.
Methods: Germ cell differentiation was initiated in male juvenile rhesus monkeys by pulsatile administration of GnRH for 4-5 weeks. Sertoli cells from these pseudopubertal monkeys and pubertal rats were cultured. Production of lactate and estradiol in response to FSH and 8-Br-cAMP was evaluated. Inhibin-
B expression, cAMP production and cell proliferation were also assayed.
Results: Unlike Sc from pubertal rats, Sc from pseudopubertal monkeys constitutively aromatized testosterone to estradiol and produced large amounts of lactate without FSH stimulation. Increasing doses of recombinant monkey (rm) FSH or 8-Br-cAMP failed to augment lactate production, although they significantly augmented proliferation of Sc. Production of cAMP and expression of inhibin-
B mRNA was also remarkably augmented by rmFSH.
Conclusions: These results suggest that lactate and estradiol production by monkey Sc is not governed by FSH, as previously thought based on studies of rat Sc. Thus, in a clinical situation, assessment of such gonadotropin-independent functions of Sc may be obligatory for the diagnosis and management of certain forms of idiopathic male infertility.
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