Calcitonin, zinc, and testicular function

Recent studies demonstrating decreases in transport kinetics of zinc (Zn) in testis in response to calcitonin (CT) and the presence of CT receptors on Leydig cells has suggested a physiological interrelationship between CT and cellular Zn metabolism in the testis. The present studies were undertaken to evaluate the acute effects of human synthetic calcitonin (hCT) on testosterone (T) synthesis and on transmembrane Zn transport as measured in a closed two-compartment model system in Leydig cells isolated from intact and thyroparathyroldectomized (TPTX) rats. Leydig cells acutely exposed to 1 ng/mL equine luteinizing hormone (LH) in vitro had a fivefold increase in medium T concentration. Calcitonin at 42 μg/mL had no effect on the basal T synthesis and did not affect the increase seen after LH administration. Lower doses of LH demonstrated a dose response for T production, but no alteration in the pattern of response. In TPTX rats pretreated with 167 μg/d (25 MRC U/d) hCT subcutaneously (sc) for three days before they were killed, a reduction to 73% of the control value was observed in the in vitro Leydig cell fractional influx coefficient for Zn transport (P < .02). No difference was observed in the fractional efflux coefficient. Fractional flux coefficients from intact rats demonstrated qualitatively similar, but more variable, changes. These data demonstrate that there is no acute effect of CT on T synthesis in the isolated Leydig cell. There does appear, nevertheless, to be a role for CT in the modulation of transmembrane Zn transport. Clinically important Zn-dependent alterations of T synthesis may require long-term changes in Zn metabolism before they become manifest. The differences in transport observed acutely may not be reflected in short-term changes in T synthesis.