Circulating inhibin is detectable throughout the normal menstrual cycle, correlating with estradiol and progesterone, suggesting it is produced by the maturing follicle and corpus luteum and plays a role in the feedback regulation of FSH.
Correlations support inhibin’s role in luteal FSH feedback; leaves open relevance to anovulatory disorders.
Serum inhibin concentrations were measured daily by RIA in six normal women throughout one menstrual cycle. The RIA was specific for inhibin, and inhibin subunits and related proteins cross-reacted minimally in it. In the early to midfollicular phase, inhibin levels changed little, while in the late follicular phase, inhibin levels rose, in parallel with estradiol (r = 0.43; P less than 0.05; n = 22), to a peak level of 714 (407-1267) U/L (geometric mean +/- 67% confidence limits) coincident with the midcycle LH and FSH surges. An inverse relationship was found between serum inhibin and FSH during the mid- to late follicular phase (r = 0.42; P less than 0.01; n = 45). Inhibin levels rose further during the luteal phase to a peak level of 1490 (1086-2028) U/L 7-8 days after the LH surge, and they correlated positively with serum progesterone (r = 0.76; P less than 0.001; n = 49) and inversely with serum FSH (r = 0.43; P less than 0.01; n = 49) throughout the luteal phase. We conclude that 1) circulating inhibin is detectable throughout the normal menstrual cycle; 2) in the late follicular phase, inhibin levels rise in parallel with estradiol, consistent with the concept that both are products of the maturing follicle; 3) in the luteal phase, the profile of inhibin suggests that it is a secretory product of the corpus luteum; and 4) the inverse relationship between inhibin and FSH in the follicular phase is consistent with the inhibin hypothesis, while at midcycle there is loss of the inhibitory effect of inhibin on FSH secretion. The inverse relationship between FSH and inhibin during the luteal phase suggests a hitherto unsuspected role for inhibin in the feedback regulation of FSH secretion.
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McLachlan et al. (1987) studied this question.
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