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testes to respond to endogenous luteinizing hormone. After a long period of inactivity, this ability may have been seriously reduced. In such a state testosterone levels may not reach a normal point, even though the release of endogenous LH has been resumed. Many who have suffered severe testicular shrinkage may be able to relate, as it is often some time before normal testicle size and feelings of virility are restored if ancillary drugs had not been used. The excessive stimulation brought forth by administration of HCG can likewise cause the testicles to rapidly return to their normal size and level of activity. We are not simply looking for it to fix the problem however, as the resulting high testosterone level can itself trigger negative feedback inhibition at the hypothalamus. Estrogen production is also heightened with the use of HCG, due to its ability to increase aromatase activity in the Leydig's cells. This is due to the main action of HCG, namely the increase of cycIicAMP (a secondary messenger that regulates cellular activity). When stimulated by HCG, the ability of the testes to aromati
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