Single im administration of 1500 IU hCG evoked a biphasic response of 17-hydroxyprogesterone (17-OHP) and testosterone (T) in six eugonadotropic men, with an early peak after 4 h, a nadir at 5 h, and a second peak 24 and 72 h after hCG loading, respectively. Remarkably, in six patients with isolated gonadotropin deficiency, the early rise of both 17-OHP and T was absent, whereas the late peak was attenuated and somewhat delayed. This lack of an immediate response in these hypogonadotropic patients might be accounted for by the lack of gonadotropin-induced enzyme systems capable of rapid steroid synthesis. In the normal men, the 17-OHP rise was more pronounced than the T increase, and thus, from 4 h on, a gradually rising 17-OHP to T ratio was observed, which reached its maximum 24 h after the hCG injection. In contrast, in the hypogonadotropic patients, the 17-OHP to T ratio did not rise but rather decreased to minimal values 72 h after hCG loading. These data suggest that in normal men, but not in hypogonadotropic patients, hCG may rapidly modify steroidogenesis by temporarily depressing the conversion of 17-OHP to T.