Sequential Arginine and Insulin Tolerance Tests on the Same Day

Penny, Robert; Blizzard, Robert M.; Davis, Walter T.

doi:10.1210/jcem-29-11-1499

Cited by 121 publications

(30 citation statements)

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“…This seems unlikely for several reasons. First, normal subjects respond with increased GH secretion to separate stimuli presented 1 h apart (31) or even 30 min apart (32). Secondly, we have shown that the amount of GH secretion during morning naps is unrelated to the amount of GH secretion the previous night (33).…”

Section: Introductionmentioning

confidence: 72%

Suppression of sleep-related prolactin secretion and enhancement of sleep-related growth hormone secretion.

Mendelson¹,

Jacobs²,

Reichman³

et al. 1975

J. Clin. Invest.

117

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AB STRA CT Methysergide, a clinically-used blocker of serotonin receptors, was administered to 10 normal young men at a dose of 2 mg every 6 h for 48 h. After drug treatment, serum levels of growth hormone during sleep were 41.9% higher than placebo values (P < 0.001). In contrast, drug treatment was associated with a 36.4% decrease in stimulated growth hormone secretion during insulin tolerance testing (P < 0.01).These opposite effects of methysergide suggest that different mechanisms are responsible for sleep-related and insulin-induced growth hormone secretion. Accordingly, data obtained with pharmacologic stimuli may lead to erroneous inferences regarding physiologic growth hormone control mechanisms. Administration of methysergide profoundly suppressed sleep-related prolactin secretion; overall nocturnal mean prolactin fell by 70.3% from 4.30±0.19 to 1.28±0.06 ng/ml (P < 0.0001).It appears that serotonin may be a significant modulating neurotransmitter for the control of growth hormone secretion, limiting sleep-related release, and enhancing insulin-induced release. It seems likely from these data that the role of serotonin in the control of prolactin secretion is relatively more important, since serotonin receptor blockade dramatically reduced sleeprelated prolactin secretion.

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Section: Introductionmentioning

confidence: 72%

Suppression of sleep-related prolactin secretion and enhancement of sleep-related growth hormone secretion.

Mendelson¹,

Jacobs²,

Reichman³

et al. 1975

J. Clin. Invest.

117

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“…A standard AITT was performed in all but two children (24). In these two, the spontaneous 24-h GH secretion profile was performed (25).…”

Section: Methodsmentioning

confidence: 99%

Final Height in Short Children Born Small for Gestational Age Treated with Growth Hormone

2005

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The aim of this observational study was to assess the longterm growth responses to GH treatment of children born small for gestational age (SGA). GH treatment was begun before puberty and continued to final height (FH). Seventy-seven short (height SD score below Ϫ2) prepubertal children born SGA (below Ϫ2 SD for birth weight and/or birth length), with a broad range of GH secretory capacity, were treated with GH in a daily dose of 33 g/kg (0.1 U/kg), beginning before the onset of puberty. We observed a difference between adult and pretreatment projected height of 1.3 SD (9 cm) for the entire group. Among the children treated for Ͼ2 y before puberty, this mean gain (i.e. difference) in final height was 1.7 SD, whereas the mean gain was 0.9 SD among those in whom treatment was begun Ͻ2 y before puberty. Better catch-up growth was observed in the younger (r ϭ Ϫ0.56, p Ͻ 0.0001), shorter (r ϭ Ϫ0.49, p Ͻ 0.0001), and lighter (r ϭ Ϫ0.46, p Ͻ 0.0001) subjects. We conclude that GH treatment improves the final height of short children born SGA. The height gain attained before the onset of puberty is maintained to final height. The younger, shorter, and lighter the child at the start of GH treatment, the better the response. Moreover, most of these SGA individuals treated with GH reach their target height. There is a 5-to 7-fold higher risk of short stature among adults who were born SGA, compared with those born AGA (1,2). Children born SGA comprise one-third of children who are short during childhood (1). As short stature is present in 10 -15% of children born SGA (1-3), efforts have been made to understand the etiology of their growth restriction and to increase their FH.Birth length has been shown in population-based studies to be the single most important predictor of adult height (1,2). Short children born SGA keep their prepubertal height SDS to FH, whereas short children born AGA gain further 0.6 -0.7 SDS in height during puberty (4). French data show that adult men who were born SGA are, on average 7.5 cm, and women are 9.6 cm below their mid-parent target height (5). This is at the lower end of the range compared with other studies (1,6,7), which find a growth deficit of 0.7-0.9 SDS below the MPH.Either low GH secretion or reduced sensitivity to GH may account for some of the growth retardation of children born SGA (8 -10). Boguszewski et al. (11,12) reported that short children born SGA have both lower mean GH secretion rates and lower serum IGF-I (IGF-I) values than children born AGA. In children born SGA, there is a correlation between the GH dose and the growth response, mainly during prepubertal years (13-16). The majority of short children born SGA show improvement in growth rate during GH treatment, particularly if treatment is begun early (14,16). With the exception of one large study (17), however, no information is available on the FH achieved by short children born SGA and treated with GH from a young age to FH. We report here the observational data on the effect of GH therapy on final height of childr...

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“…Serum samples were collected at -20, 0, 15, 30, 45, and 60 min, and in most patients at 90 and 120 min. TSH, serum thyroxine, free thyroxine (T4) (16), and GH concentrations (17), and serum HPr concentrations (18,19) were measured as previously reported. No cross-reaction between TSH, HPr, or GH could be demonstrated in the assay systems.…”

Section: Methodsmentioning

confidence: 99%

Human prolactin and thyrotropin concentrations in the serums of normal and hypopituitary children before and after the administration of synthetic thyrotropin-releasing hormone

Foley¹,

Jacobs²,

Hoffman³

et al. 1972

J. Clin. Invest.

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A B S T R A C T Synthetic thyrotropin-releasing hormone (TRH) was administered to normal children and hypopituitary patients in a dose of 7 jg/kg i.v. over 30-60 sec. Serum thyrotropin (TSH) and prolactin (HPr) concentrations were measured by radioimmunoassay before and at 15-min intervals for 2 hr after TRH. In 20 normal children HPr rose from a mean baseline value of 7.0±1.2 (SEM) ng/ml to a mean peak value of 39.5±5 ng/ml.In 11 patients with growth hormone (GH) deficiency without TSH deficiency, HPr values rose from a mean baseline of 3.6±0.8 ng/ml to a mean peak value of 13.9+-2.8, a significantly less peak response as compared with normal children (P < 0.005). The TSH responses to TRH, however, were statistically indistinguishable from those of normal children.In 10 patients with GH and TSH deficiency both the mean baseline HPr levels (25.0+5 ng/ml) and the mean peak HPr levels after TRH (68.5+10 ng/ml) were significantly higher (P < 0.005 and < 0.025) than those of normal children. Similar comparisons were also true for the peak TSH responses (P < 0.05). Two panhypopituitary patients released no TSH and only small amounts of HPr after TRH. After thyroid replacement therapy in eight of the patients with GH and TSH deficiency, the mean HPr baseline levels (7.6+1.0 ng/ml) and peak levels (23.3+4.6 ng/ml) after the same dose of TRH were significantly less than their pretreatment levels (P<0.001 and <0.01) and were within the range for normal children.Synthetic TRH stimulates the simultaneous release of TSH and HPr in normal children and most hypopituitary patients. When the concentrations of thyroxine (T4) and triiodothyronine (T3) are low, the levels of HPr before and after TRH are elevated. After thyroid replacement therapy, HPr levels decrease to normal.T4 and/or T3 may condition the production or effects of prolactin-inhibiting factor (PIF) activity. The TSH and HPr responses after TRH in hypopituitary patients will determine whether the primary defect resides in the pituitary or hypothalamus, but cannot delineate the hypothalamic defect as a deficiency of hypothalamic hormone production or neurohumoral transmission.

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Sequential Arginine and Insulin Tolerance Tests on the Same Day

Cited by 121 publications

References 0 publications

Suppression of sleep-related prolactin secretion and enhancement of sleep-related growth hormone secretion.

Suppression of sleep-related prolactin secretion and enhancement of sleep-related growth hormone secretion.

Final Height in Short Children Born Small for Gestational Age Treated with Growth Hormone

Human prolactin and thyrotropin concentrations in the serums of normal and hypopituitary children before and after the administration of synthetic thyrotropin-releasing hormone

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