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Journal of Clinical Endocrinology & Metabolism Vol. 72, No. 3 711-717
doi:10.1210/jcem-72-3-711
Copyright © 1991 by the Endocrine Society.
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Altered Patterns of Pituitary Secretion and Renal Excretion of Free {alpha}-Subunit during Gonadotropin-Releasing Hormone Agonist-Induced Pituitary Desensitization*

HAL LANDY, PAUL A. BOEPPLE, M. JOAN MANSFIELD, RANDALL W. WHITCOMB, ALAN L. SCHNEYER, JOHN D. CRAWFORD, JOHN F. CRIGLER, JR and WILLIAM F. CROWLEY, JR

Reproductive Endocrine Unit and the Vincent Memorial Research Laboratories, Department of Medicine, and the Pediatric Endocrinology Unit of the Children’s Service, Massachusetts General Hospital Boston, Massachusetts 02114
the Divisions of Endocrinology and Adolescent and Young Adult Medicine, Department of Medicine, Children’s Hospital Medical Center Boston, Massachusetts 02115

Address all correspondence and requests for reprints to: Dr. Hal Landy, Reproductive Endocrine Unit, Massachusetts General Hospital, Boston, Massachusetts 02114.

Intact LH and free {alpha}-subunit (FAS) are differentially regulated during GnRH agonist (GnRHa)-induced pituitary desensitization; circulating levels of FAS rise, while LH levels decline. Increased steady state {alpha} and decreased LHβ mRNA levels in desensitized rat pituitaries suggest that differential regulation occurs at the level of subunit transcription. We assessed a renal contribution to these changes in serum hormone concentrations by studying LH and FAS levels in serum and urine in 15 pubertal children before and during long term GnRHa administration. Before GnRHa, serum LH and FAS were secreted in concordant pulses, and both responded briskly to exogenous GnRH. During GnRHa-induced pituitary desensitization, mean (±SEM) serum and urinary LH levels fell [11 ± 3 vs. 2 ± 0.2 IU/L (P < 0.01) and 39 ± 15 vs. 5 ± 1 IU/g creatinine (P < 0.05), respectively), and the LH response to exogenous GnRH was ablated (117 ± 20 vs. 1 ± 0.3 IU/L; P < 0.01). In contrast, despite suppression of FAS pulsatility, mean serum FAS levels rose during GnRHa treatment (204 ± 23 vs. 405 ± 50 ng/L; P < 0.01), and responsiveness to exogenous GnRH was maintained. Paradoxically, urinary FAS levels fell (3.2 ± 0.9 vs. 1.7 ± 0.4 µg/g creatinine; P < 0.05) as did its renal clearance (3.1 ± 0.5 vs. 1.3 ± 0.1 mL/min·m2; P < 0.05).

We conclude that during GnRHa-induced pituitary desensitization, the gonadotrope maintains the ability to respond to GnRH with FAS release, and the rise in serum FAS is due in part to its diminished renal clearance.

* This work was supported in part by NIH Grants HD-18169, HD-07277, RR-01066, RR-02172, and RR-08847. The data were presented in part at the 71st Annual Meeting of The Endocrine Society, Seattle, WA, June 1989.

Received April 23, 1990.




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Copyright © 1991 by The Endocrine Society