I have been analyzing various factors and my brain is about to explode with the ammount of information I have been trying to process. Finally, it is all starting to make some sense, to some extent. This is just a theory based on some studies I have read and should not be taken too seriously. Some of the stuidies were perfomed on rats which could severely throw this theory off because the results of the studies may be species dependant.
It seems that FSH may enhance the responsiveness of Leydig cells to LH. One study showed that FSH treatment induced Leydig cell hyperplasia, increased the number of testicular LH receptors, and increased the steroidogenic response of Leydig cells to LH. FSH further enhanced the steroidogenic capacity of Leydig cells and induced a significant increase in the number of hCG receptors which would increase the the sensitivity and effectiveness of HCG. If this is all "true", it would make sense to use a combination of HCG and HMG (FSH/LH) to initiate and maintain restoration of normal Testosterone secretion and achieve spermatogenesis in people
I found this study that concluded that FSH + LH did not provide anything above LH on its own. Here is the summary paragraphs:
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In the present study, the increase in mean plasma T levels induced by rhLH was not enhanced by the concomitant administration of rhFSH, despite the effective stimulation of Sertoli cell function, attested by the increase in plasma inhibin B. The same result was observed with a greater increase in plasma T levels after hCG and hCG plus rhFSH administration. These results are in agreement with recent studies performed in primates (30). Indeed, in juvenile rhesus monkeys receiving a pulsatile iv infusion of GnRH, the concomitant infusion of rhFSH did not affect either the mean plasma levels of T or the amplitude of pulsatile testicular T secretion. Therefore, in man as in primates, the physiological relevance of a role of FSH in LH-induced testicular steroidogenesis seems questionable.
In conclusion, complete acquired HH and the use of rhLH and rhFSH enable the functions of Leydig and Sertoli cells to be studied selectively. Apart from peripheral aromatization of testicular T, the increase of plasma E2 induced by rhLH and the absence of an effect of rhFSH is consistent with the view that Leydig cells are the major site of testicular E2 production in man. The secretion of inhibin B, increased by rhFSH and not by rhLH, confirms that Sertoli cells are the main source of inhibin B production. Finally, the increase in plasma T induced by rhLH or hCG was not enhanced by rhFSH. These results suggest that the stimulatory effect of FSH on Leydig cell steroidogenesis by a Sertoli cell paracrine factor does not seem to play a major physiological role in man.
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