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Calcitonin, zinc, and testicular function.
A B Chausmer1, C Chavez, R M Wain
1Endocrinology and Metabolism Section, Medical Service, VA Medical Center, Bay Pines, FL 33504.
Metabolism: Clinical and Experimental
|August 1, 1989
Summary
Calcitonin (CT) does not acutely affect testosterone synthesis in Leydig cells. However, CT influences zinc transport in the testis, suggesting a role in modulating cellular zinc metabolism.
Area of Science:
- Reproductive Endocrinology
- Cellular Metabolism
- Hormonal Regulation
Background:
- Calcitonin (CT) presence on Leydig cells and its impact on testicular zinc (Zn) transport suggest a physiological link.
- Previous studies indicate CT may decrease Zn transport kinetics in the testis.
Purpose of the Study:
- To investigate the acute effects of human synthetic calcitonin (hCT) on testosterone (T) synthesis.
- To evaluate the impact of hCT on transmembrane Zn transport in isolated Leydig cells.
Main Methods:
- Isolated Leydig cells from intact and thyroparathyroldectomized (TPTX) rats were used.
- A closed two-compartment model system measured transmembrane Zn transport.
- Testosterone synthesis was assessed following stimulation with equine luteinizing hormone (LH).
Main Results:
- Calcitonin (42 µg/mL) did not affect basal or LH-stimulated testosterone synthesis in isolated Leydig cells.
- Subcutaneous hCT pretreatment in TPTX rats significantly reduced the fractional influx coefficient for Zn transport (P < .02).
- No significant changes were observed in the fractional efflux coefficient for Zn transport.
Conclusions:
- Calcitonin (CT) does not exert an acute effect on testosterone synthesis in isolated Leydig cells.
- CT appears to play a role in modulating transmembrane zinc transport in testicular Leydig cells.
- Long-term alterations in zinc metabolism may be necessary for clinically significant Zn-dependent changes in testosterone synthesis.