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Effect of Testosterone on Somatomedin-C Concentrations in Prepubertal Boys^*

Departments of Pediatrics, University of Virginia Medical Center Charlottesuille, Virginia 2290
Departments of Medicine, University of Virginia Medical Center Charlottesuille, Virginia 2290
Departments of Pharmacology, University of Virginia Medical Center Charlottesuille, Virginia 2290

Address all correspondence and requests for reprints to: Dr. R. M. Blizzard, Department of Pediatrics, Box 386, University of Virginia School of Medicine, Charlottesville, Virginia 22908.

To investigate the role of testosterone (T) in the pubertal elevation of somatomedin-C (SmC), six prepubertal GH-deficient boys were each given 7-day courses ofGH alone (0.05 U/kgday, im), T alone (T propionate; 25 mg/day, im), and a combination of GH and T at the same dosages. Plasma SmC levels were determined on samples drawn at the start and finish ofeach period, and each course was separated by a 7-day period. SmC was also measured before and after a course of T propionate (25 mg/day, im) in four GH-sufficient boys with delayed adolescence. In the GH-deficient boys, GH and the combination of GH and T resulted in comparable and significantincrements of SmC (mean change, 0.68 U/ml after GH and 0.63 U/ml after the combination of GH and T). T alone caused no change in SmC in the GH-deficient boys (mean change, 0.09 U/ ml), but resulted in increases in all four GH-sufficient subjects (mean change, 1.29 U/ml). In a single subject with constitutionally delayed puberty, the integrated 24-h GH concentration rose from 2.8 ng/ml before to 5.8 ng/ml after T therapy. Both the number and amplitude of GH secretory events were greaterafter therapy.

These data show that T stimulates SmC production in prepubertal boys who can secrete GH, but not in those who are GH deficient. We postulate that the effect of T in this regard is due to its effect on pituitary GH secretion. Although the T levels were within the pharmacological range, physiological levels of T (e.g. at puberty) may be responsible for the adolescent SmC increment in men.

^* This work was supported by USPHS General Clinical Research Grant RR-00847. The opinions and assertions contained herein are those of the authors and do not necessarily represent those of the Department of Defense or the Department of the Air Force.

Received June 10, 1983.

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