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V Greenwood

Publications and source records attributed to V Greenwood.

4 recordsLinked to original sources

Zinc does not acutely suppress prolactin in normal or hyperprolactinemic women.

In rat pituitary cells in vitro physiological zinc concentrations selectively inhibit basal and stimulated PRL release. This study was done to investigate the serum PRL response to an oral zinc challenge in vivo. Eight hyperprolactinemic [mean serum PRL, 76.0 +/- 43.8 (+/- SD) micrograms/L] and 10 normal (mean serum PRL, 9.6 +/- 2.8 micrograms/L) women were studied. All women had normal thyroid, renal, and hepatic function, and none was taking any medications. Each was studied twice, after both oral zinc (50 mg) and placebo, given in random order. Blood was withdrawn every 15 min from 30 min before to 210 min after zinc or placebo administration; TRH (500 micrograms) was given iv at 180 min. Both hyperprolactinemic and normal women absorbed the zinc well, achieving similar maximal plasma zinc levels [hyperprolactinemic women, 39.5 +/- 6.9 (+/- SD) mumol/L; normal women, 33.3 +/- 7.0; P less than 0.001 vs. placebo]. When 2 women who became symptomatic after zinc administration were excluded, there were no significant differences in basal or TRH-stimulated serum PRL levels after zinc vs. placebo. These findings indicate that zinc is not involved in the acute in vivo regulation of PRL secretion in humans.

Adult↗

Dark adaptation in hyperprolactinemic women.

In a study to test the hypothesis that hyperprolactinemia is caused by subclinical zinc deficiency, dark-adaptation curves of seven women with primary hyperprolactinemia and seven normal women were measured to assess tissue zinc status. Although plasma zinc levels, final dark-adapted thresholds, and the time courses of rod dark-adaptation did not differ significantly between patients and normal subjects, the median cone plateau of the hyperprolactinemic patients was significantly higher (0.66 log units) than that of normal subjects. It appears unlikely that derangements of vitamin A metabolism, for which zinc is a cofactor, explains this unanticipated and subtle abnormality in dark adaptation of the hyperprolactinemic women.

Adult↗