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Zinc Does Not Acutely Suppress Prolactin in Normal or Hyperprolactinemic Women^*

Department of Medicine, Division of Endocrinology, Brown University, Miriam Hospital Providence, Rhode Island 02906
The Department of Military Medicine, Uniformed Services University of Health Sciences (P.D.) Bethesda, Maryland 20814

Address all correspondence and requests for reprints to: Dr. Michele C. S. Koppelman, Endocrinology Division, Miriam Hospital, 164 Summit Avenue, Providence, Rhode Island 02906.

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) µg/L] and 10 normal (mean serum PRL, 9.6 ± 2.8 µg/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 Blood was withdrawn every 15 min from 30 min before to 210 min after zinc or placebo administration; TRH (500 µg) was given iv at 180 min.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) µmol/L; normal women, 33.3 ± 7.0; P < 0.001 vs. placebo]. When 2 women who became symptomatic after zinc administration were excluded, there were no significant differences in basal or TRHstimulated 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.

^* This work was supported in part by NIH Grant RR-02038 to the Clinical Research Center of Brown University and in part by a Matrix Grant from Brown University.

Received July 1, 1988.

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