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Differential Regulation of Serum Immunoreactive Luteinizing Hormone and Bioactive Follicle-Stimulating Hormone by Testosterone in Early Pubertal Boys^*

Departments of Pediatrics and Biostatistics, University of Michigan Hospitals Ann Arbor, Michigan 48109-0718

Address all correspondence and requests for reprints to: Jeanne M. Hassing, M.D., Ph.D., Division of Pediatric Endocrinology, University of Michigan Hospitals, MPB D-3252/Box 0178, Ann Arbor, Michigan 48109-0718.

The microheterogeneity and bioassayable activity of serum FSH (B-FSH) can be regulated by exogenous GnRH in boys with idiopathic hypogonadotropic hypogonadism and by estrogen in a woman with gonadal dysgenesis, presumably via hormonally mediated changes in the degree of FSH glycosylation. To test the hypothesis that testosterone (T) regulates the circulating forms of B-FSH, we raised the serum T levels of early pubertal boys to adult levels. In this model, high dose T inhibits the pubertal nocturnal augmentation of LH secretion, apparently through decreased GnRH secretion. This model allowed us to test a second hypothesis, that B-FSH is a sensitive indicator of hypothalamic GnRH release. The boys were studied on two consecutive weekends, during which they received either saline (S) or T infusions. Beginning at noon on the study day, after an overnight acclimatization, the boys received either S or T at 33% or 100% of the adult male production rate. Blood was sampled from 2000-0800 at 10-min intervals for immunoactive LH and FSH (I-FSH) and for B-FSH, as determined by the in vitro Sertoli cell aromatase induction assay, and at 30-min intervals for T. Gonadotropin levels were analyzed as mean hourly or 3-h concentrations and as pulse profiles by two established objective peak detection programs, Cluster and Detect.

During S treatment, mean LH increased after the onset of sleep (P = 0.0006) and, after plateauing for several hours, declined to baseline in the early morning hours. Mean levels of B-FSH were also minimally (but significantly) increased after the onset of sleep (P = 0.046) and paralleled the decline noted for LH. Mean levels of I-FSH did not demonstrate a diurnal rhythm. The effect of T was gonadotropin specific. High dose T abolished the nocturnal elevation in mean LH concentrations, but had no effect on the nocturnal elevation of B-FSH (P < 0.05) or on I-FSH levels.

The LH pulse frequency was greatest from 2300-0450 h, during S treatment (P = 0.016). The pulse frequency of B-FSH was also minimally increased after the onset of sleep (P = 0.045). The T infusion abolished the nocturnal increase in LH pulse frequency, without an effect on B-FSH pulse frequency. B-FSH pulse frequency exceeded LH pulse frequency during S treatment (8.0 ± 0.7 pulses/12 h vs. 5.5 ± 0.4), and B-FSH pulses persisted throughout the night. The pulse amplitudes of LH and B-FSH were not affected by T.

We conclude that acute infusion of T does not regulate serum B-FSH levels in early pubertal boys. In addition, we have found differential regulation of LH and B-FSH secretion. Although both gonadotropin assays demonstrate a nocturnal rhythm in secretion, T abolishes the nocturnal enhancement of mean LH and LH pulse frequency without an effect on mean B-FSH or B-FSH pulse frequency. We propose that B-FSH is released in response to either low amplitude GnRH pulses, which are insufficient to elicit a LH pulse, or another FSH-releasing factor.

^* Presented in part at the 70th Annual Meeting of The Endocrine Society, June 1988, and the Society for Pediatric Research, May 1989, Washington, DC. This work was supported by NIH Grants HD-18515, HD-07048, and HD-16000.

Received June 19, 1989.

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