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Eighteen healthy children were given 50 micrograms synthetic AVT intranasally and samples of serum for GH, magnesium and alpha-amino-nitrogen were drawn 30, 60 and 120 minutes later. There was a significantly different mean of GH peak level (13.1 +/- 3.02 microU/ml) which occurred generally at 30 minutes. The number of GH responders (i.e. peak level greater than 15 microU/ml) was of 7/18. The means of chemical determinations elicited little though opposite changes: slight increases in magnesium and slight decrease in alpha-amino-nitrogen. In a separate day, a sleep test of 30 minutes-duration performed in the morning resulted in a significantly greater GH peak level (28.2 +/- 9.7 microU/ml) but the number of GH responders was nearly the same (6/18). The serum magnesium levels following sleep decreased slightly and unsignificantly. The involvement of serotonergic neurons in mediating GH-releasing effects of AVT is briefly discussed.

Intravenous glycine injection (250 mg/kg of body weight) resulted in growth hormone release in normal children but not in those with growth hormone deficiency diagnosed by insulin-induced hypoglycaemia. In the latter significantly higher peak concentrations of serum alpha-amino nitrogen were also found. False negative responses to glycine (no GH release) were observed in two patients of short stature but normal pituitary function. In them the peak levels of serum alpha-amino nitrogen were lower than in those with hypopituitarism. We propose the clinical use of glycine as an inexpensive and innocuous procedure for the detection of GH deficiency in children. A post-glycine GH peak greater than 10-0 mu/l seems to be a good index of an intact GH reserve.

Intravenous insulin (0.1 U/kg body weight) and oral 1-proline (100 mg/kg body weight) tolerance tests were performed in 22 healthy and 30 short-statured children and adolescents and blood glucose, serum immunoreactive growth hormone (GH), immunoreactive insulin (IRI) and 1-proline were determined. The peak level of serum GH was significantly higher following insulin than after 1-proline. The proline loading correctly identified the normality of GH axis in 12 out of 22 controls and in 3 out of 7 normopituitary short-statured patients. The serum 1-proline levels consideration did not improve much the ability of 1-proline load to detect either the normal GH responsiveness or the pituitary insufficiency. The mechanism of GH stimulatory properties of 1-proline in some healthy subjects is not known.

Sleep and exercise are considered physiologic stimuli of growth hormone (GH) release from the pituitary. They were used to some extent for the assessment of GH reserve in growth disorders of supposedly pituitary origin. In order to better establish the diagnostic value of the sleep test, we studied 34 children of both sexes aged 6-14 having various degrees of shortness of stature associated with bone age retardation (range of the latter: 3-10 years). Eight healthy controls of the same age were also subjected to the sleep test. The latter was begun at 10:00-11:00 a.m. generally in a dark room under polygraphic control. The subjects were fed a standard breakfast at 8:00-8:30 a.m. After thirty minutes of steep or after reaching the IVth stage of slow-wave sleep, the children were awakened and samples of venous blood for GH determinations were drawn. Two other GH reserve tests were also performed in other days, usually insulin-induced hypoglycemia and glycine intravenous loading. Except sleep, no other GH provocative tests were performed in controls. In normal GH reserve children (21/34) according to other tests, the sleep test was positive (i.e. peak values greater than 15 microU/ml) in 7 cases and the mean GH response was not significantly smaller than the peak recorded after insulin-induced hypoglycemia. In abnormal GH reserve, presumably hypopituitary children (13/34) according to other tests, the sleep confirmed the other tests in 8 cases. In five cases of clinically and endocrinologically "hypopituitary" dwarfism, the sleep test revealed a normal response.(ABSTRACT TRUNCATED AT 250 WORDS)

In hypopituitary short-statured patients glycine intravenous injection (250 mg/kg of body weight) provokes a mild and inconstant stimulation of IRI release followed by a significant fall down. Though insiginificant (P 0.064), the prevalence of IRI responsive individuals to glycine in the patients group of idiopathic etiology could be of pathophysiological importance.

A solution of 10% glycine (250 mg/kg of body weight) was injected in within 5-10 minutes in 22 healthy, sexually immature children who were previously tested for insulin-induced hypoglycemia. Blood specimens were collected before, 10, 30, 60 and 120 minutes after injection for glucose, HGH and total alpha-amino nitrogen determination. The mean peak post-glycine level of serum HGH was 11.47 +/- 1.558 ng/ml (+/- SEM) and did not differ significantly from the corresponding post-insulin mean value (15.63 +/- 0.247 ng/ml). The highest post-stimulatory mean value (8.88 +/- 1.694 ng/ml) was observed 30 minutes after the end of the injection of glycine. Glycine is a reliable GH stimulating agent, which may be tentatively used for detection of hyposomatotropism in children.

Proline (100 mg/kg b.w.) was given per os and after 30 minutes 10% glycine was i.v. injected to 25 healthy children of both sexes. A positive response (an increase of over 5 ng/ml of serum level of GH) was found in 21 of the 25 children. The insulin test showed a positive response in 24 of the 25 children. It was concluded that the decrease in glycine dosage from 250 mg/kg b.w. (earlier reports by the same authors) to 100 mg/kg b.w. (present data) is generally compensated by l-proline priming. The IRI serum levels were almost unchanged. By l-proline priming, the glycine test can also be applied to subjects with body weight over 40 kg, in doses of 100 mg/kg b.w. for exploring the secretory reserve of the somatotropic axis.

Orally given 1-proline in high dosage (500 mg/kg b.w.) resulted in growth hormone (GH) release in 9 healthy, sexually immature children investigated (5 boys and 4 girls). A slight, unsignificant decrease of the mean prolactin level was also noted. Serum immunoreactive insulin (IRI), follicle-stimulating hormone (FSH) and luteinizing hormone (LH) concentrations in serum were not influenced. The possible use of proline loading in high dosage for the detection of GH deficiency especially in small children and in infants is suggested.

In order to assess the dopaminergic tonus, urinary determinations of HVA and DOPAC and also of noradrenaline (NA), adrenaline (A), and methoxyhydroxyphenylglycol (MHPG) were performed in 86 obese children, 11 growth hormone (GH)-deficient short children and also in 40 control children. Part of the obese patients were subjected to a low carbohydrate, low calorie diet and also to short-term (9-14 days) courses of diethylpropion (DEP) 50 mg/day, meclofenoxate (MEC) 100 mg/day and thyroid extract (THE) 1-2 mg/kg/day. The GH-deficient patients received only THE in substitutive (5-10 mg/kg/day) doses. Significative correlations between DOPAC and age, weight and height were found in controls. In the obese group a significantly increased mean level of HVA was found (1.45 +/- 0.09 mg/24 h vs 1.15 +/- 0.10 in controls). The excretion of DOPAC was slightly greater but far from significance. There was also a significant decrease of HVA but not DOPAC in the DEP-treated obese. The rest of the drugs and the diet alone were not effective in any way. Normal levels in all metabolites except NA and A were found in GH-deficient short children. The therapy with thyroid extract did not alter the excretion levels. These findings indicate that in infantile obesity the dopaminergic tonus is somewhat increased but its pathophysiological significance is doubtful. In GH-deficient short children of standard appearance the dopaminergic tonus seems to be undistinguishable from normal.