Alterations in the Pulsatile Properties of Circulating Growth Hormone Concentrations during Puberty in Boys*

Abstract

To investigate the mechanisms subserving physiological alterations in circulating GH concentrations during puberty, we assessed the GH pulse characteristics of 60 24-h serum GH profiles obtained from healthy male volunteers of normal stature (aged 7-27 yr) whose physical development spanned the entire pubertal range. Subjects were divided into five study groups based on degree of sexual maturation. The mean 24-h concentration of GH was greater in late pubertal boys than in all other groups (P less than 0.001). This elevation primarily reflected a greater size, rather than number, of GH pulses, whether assessed as mean GH pulse area (P = 0.004 vs. all other groups), mean GH pulse amplitude (P = 0.001), or sum of the GH pulse areas (P less than 0.001). GH pulse frequency was indistinguishable among all groups (P greater than 0.05). However, circadian GH rhythms varied significantly in amplitude and mean values (but not in phase) throughout puberty. Plasma insulin-like growth factor-I levels were greatest in the late pubertal boys (1.98 +/- 0.15 U/mL) and remained elevated in the postpubertal group (1.44 +/- 0.18). The mean value for the adult men (0.74 +/- 0.06) was indistinguishable from that of prepubertal boys (0.90 +/- 0.13). In addition, all assessed characteristics of GH pulses and circadian rhythms in adults were equal to or less than corresponding values in prepubertal boys. We conclude that circulating GH concentrations transiently increase during mid- to late puberty in normal boys, primarily through augmentation of the size of GH pulses, but return to or below prepubertal levels during early adulthood.

Clinical Usefulness of Urinary Growth Hormone Measurements in Normal and Short Children According to Different Expressions of Urinary Growth Hormone Data

“…' In our series, UGH excretion (ng/24 h) clearly differed in some groups (GH-deficient versus prepubertal controls or idiopathic short children; prepubertal versus pubertal; adult controls versus acromegalic patients), as already reported (3,12,(14)(15)(16)(17)(18)(20)(21)(22)(23). However, the increased GH secretion in puberty (24,25) reflected in UGH excretion (12, 15, 17, 22) disappeared when UGH was expressed as ng/g Cr. Previous reports have documented that Cr excretion varies as a function of body muscle mass (26); thus, to express UGH per g of Cr may result in falsely low UGH values in puberty, as has been suggested by others (18,20).…”

GH as a co-gonadotropin: the relevance of correlative changes in GH secretion and reproductive state

“…The pubertal growth spurt and increase in GH pulse amplitude in boys is similarly correlated with a rise in serum testosterone and IGF-I (Martha et al 1989). GH, IGF-I and testosterone levels are higher in boys with precocious puberty than in age-matched controls, and treatment with GnRH analogs to inhibit excess testosterone secretion corrects the high GH and IGF-I levels (Harris et al 1985).…”

“…GH, IGF-I and testosterone levels are higher in boys with precocious puberty than in age-matched controls, and treatment with GnRH analogs to inhibit excess testosterone secretion corrects the high GH and IGF-I levels (Harris et al 1985). Moreover, the induction of puberty by exogenous androgen or GnRH induces high-amplitude GH secretion (Blizzard et al 1989, Foster et al 1989. Very small doses of testosterone, similar to those observed in early puberty, are sufficient to increase GH pulse amplitude (Guistina et al 1997), GHRH-induced GH release (Mauras et al 1989a) and circulating IGF-I levels (Parker et al 1984).…”

“…For instance, GH secretion over a 24-h period is similar in post-pubertal and prepubertal males, despite elevated androgens in post-pubertal males (Martha et al 1989). Indeed, chronic sex steroid exposure may desensitize the GH axis to testosterone (or estrogen) stimulation .…”

Desmopressin and low-dose ACTH test in rheumatoid arthritis

“…In fact, it is possible to hypothesize that the reduced baseline and ACTHstimulated DHEA levels found in RA could be partially due to a decreased adrenal P450 17,20 lyase activity. It is well known that androgens are positive regulators of the growth hormone (GH)±IGF-I axis (27). Previous literature data have shown that, in comparison with controls, RA patients have, almost signi®cantly, reduced plasma IGF-I levels and clearly reduced plasma IGF-II and insulin-like growth factor-binding protein-3 levels which, however, are increased in synovial¯uid (28).…”