In women during early follicular phase (FP), the rise of melatonin at night accounts for 40% of the nocturnal core body temperature (Tc) decline. In seven normal-cycling women, the circadian rhythms of Tc and melatonin of the FP were compared with those of the luteal phase (LP). In addition, in both phases the Tc response to daytime melatonin administration was investigated. Melatonin levels were comparable during the two menstrual phases, but the nocturnal melatonin onset was delayed by 90 min in the LP (P < 0.01). This was accompanied by a delay of the nadir of the Tc circadian rhythm (P < 0.002), a 0.3 degrees C elevation (P < 0.005) of the mean 24-h value, and a 40% blunting (P < 0.002) of the amplitude. This attenuation of circadian Tc in LP women was replicated in two estrogen-treated hypogonadal women by the administration of medroxyprogesterone acetate. The daytime administration of melatonin (2.5 mg) decreased Tc during the FP (P < 0.01) but was ineffective in the LP. Present data indicate that in LP, in association with high progesterone levels, an attenuated and phase-delayed circadian Tc rhythm may, in part, be due to a reduced effect of melatonin.

The physiological role of intraovarian activin (beta/beta) and inhibin (alpha/beta) dimers in humans in unclear. The identification of follistatin as a beta-subunit-specific high affinity binding protein has added complexities for the interpretation of in vitro studies concerning the functionalities of these ovarian peptides. We, therefore, have attempted to define in vivo compartmental distributions of gene expression and protein localization for inhibin and activin subunits (alpha, beta A, and beta B) concurrent with follistatin in ovarian follicles and corpus lutea obtained from a large number of human ovaries. In situ hybridization and immunohistochemistry were used for detecting the expression of genes encoding inhibin/activin subunits and follistatin and their gene products, the proteins. Granulosa cells of small antral follicles (1-8 mm) were found to express mRNA for alpha-, beta A-, and beta B-subunits as well as follistatin, and the strongest signals were localized in the cumulus granulosa cells. In the thecal cell layer, only alpha-subunit mRNA was detected. Proteins were localized in cellular compartments corresponding to their mRNA, but in addition, proteins for beta A-subunit and follistatin were detected in the thecal cell layers in the absence of gene expression, an observation compatible with a paracrine action. Thus, granulosa cells of the small antral follicle have the potential to form all dimers of inhibin and activin, and their autocrine and paracrine actions may be modulated by follistatin in both granulosa cell and thecal cell layers. With the development of a dominant follicle, remarkable switches in subunit gene expressions occurred; beta B-subunit mRNA was no longer detectable in any cell type, and beta A-subunit expression emerged in the thecal cells along with continued abundant expression of beta A-subunit and follistatin in the granulosa cells. Proteins were found only in granulosa cells corresponding to their mRNAs. In the corpus luteum, the inhibin/activin alpha- and beta A-subunits and follistatin mRNA and proteins were expressed exclusively in the luteinized granulosa cells. Luteinized thecal cells were devoid of detectable mRNA message or proteins. Thus, the inhibin-activin-follistatin system in the corpus luteum appears to function in an autocrine fashion.(ABSTRACT TRUNCATED AT 400 WORDS)

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Using a specific antiserum, beta-endorphin was quantitated in 8 human pancreas obtained at autopsy by radioimmunoassay and localized by immunocytochemistry. The mean (+/- SE) concentration of beta-endorphin in pancreatic extracts of 5 non-diabetic adults was 13.5 +/- 9.8 ng/gm with a range of 2.1 to 52.8 ng/gm of tissue. Pancreatic beta-endorphin concentration in two premature infants were within the range found in adults. In one diabetic pancreas, there was no measurable beta-endorphin. Specific beta-endorphin immunofluorescence is localized within the pancreatic islets. This finding suggests that beta-endorphin may participate in intraislet regulation of pancreatic hormone secretion.

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