Evidence against growth hormone-releasing factor deficiency in children with idiopathic obesity

1986 ◽  
Vol 113 (4_Suppl) ◽  
pp. S403-S410 ◽  
Author(s):  
G. VAN VLIET ◽  
D. BOSSON ◽  
E. RUMMENS ◽  
C. ROBYN ◽  
R. WOLTER
Keyword(s):  
Growth Hormone ◽  
Peak Plasma ◽  
Obese Children ◽  
Somatomedin C ◽  
Growth Hormone Releasing Factor ◽  
Gh Secretion ◽  
Lean Control ◽  
Factor Deficiency ◽  
Plasma Gh ◽  
Lean Children

Abstract The mechnisms whereby growth hormone (GH) secretion is decreased in human obsity remain obscure. We studied the response of plasma GH and prolactin (PRL) to an I.V. dose of 0.5 mcg/kg of growth hormone releasing factor (GRF) in three groups of children: lean (N=12), obese (N=15) and GRF-deficient, i.e. children with complete GH deficiency on the basis of conventional provocative testing and evidence of hypothalamic dyfunction on the basis of thyrotropin-releasing hormone testing (N=7). Mean (±SEM) peak plasma GH after GRF was blunted to the same extent in obese and in GRF deficient children (11.1 ± 2.2 and 8.3 ± 2.8 mg/ml) as compared to lean control children (34.7 ± 4.7 mg/ml). The pattern of PRL response to GRF was however different in GRF after GRF injection, and in obese and lean children, who had no acute change in PRL levels after GRF. Baseline plasma somatomedin C concentrations were low for age in GRF deficient children and tended to be high for age in obese children. On the basisi of these discrepant patterns of response of PRL to GRF and plasma somatomedin C concentration, we conculde that GRF defeciency does not account for the decreased GH secreation observed in obese children.

Growth hormone responses to growth hormone-releasing factor (1–29) in euthyroid, hypothyroid and hyperthyroid rats

1986 ◽  
Vol 109 (1) ◽  
pp. 53-56 ◽  
Author(s):  
C. Dieguez ◽  
V. Jordan ◽  
P. Harris ◽  
S. Foord ◽  
M. D. Rodriguez-Arnao ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Releasing Factor ◽  
Time Points ◽  
Gh Secretion ◽  
Hormone Responses ◽  
Plasma Gh

ABSTRACT In order to investigate whether the impaired GH secretion associated with hypothyroidism and hyperthyroidism is due to a hypothalamic or a pituitary disorder, we have studied plasma GH responses to GH-releasing factor (1–29) (GRF) in euthyroid, hypothyroid and hyperthyroid rats. Hypothyroid rats showed a significant (P< 0·001) reduction in GH responses to GRF (5 μg/kg) at 5 min (350 ± 35 vs 1950 ±260 μg/l), 10 min (366±66 vs 2320 ± 270 μg/l) and 15 min after GRF injection (395 ± 72 vs 1420 ± 183 μg/l; means ± s.e.m.) compared with euthyroid rats. Hyperthyroid rats showed a significant (P<0·05) decrease in GH responses to 5 μg GRF/kg after 30 min (200±14 vs 325 ± 35 μg/l) but not at other time-points, or after the administration of 1 μg GRF/kg. These data indicate that in hypothyroidism and perhaps hyperthyroidism there is an alteration in the responsiveness of the somatotroph to GRF administration. J. Endocr (1986) 109, 53–56

Plasma growth hormone (GH) and somatomedin C response to continuous growth hormone-releasing factor (GRF) infusion in patients with GH deficiency

1985 ◽  
Vol 110 (1) ◽  
pp. 17-23 ◽  
Author(s):  
Naomi Hizuka ◽  
Kazue Takano ◽  
Kazuo Shizume ◽  
Izumi Tanaka ◽  
Noriko Honda ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Bolus Injection ◽  
Gh Deficiency ◽  
Saline Infusion ◽  
Pulse Area ◽  
Continuous Growth ◽  
Somatomedin C ◽  
Gh Secretion ◽  
The Mean ◽  
Plasma Gh

Abstract. Pituitary growth hormone (GH) responses during a 10-h iv infusion of saline or human GH-releasing factor (hGRF-44) at 500 ng/kg/h, followed by an iv bolus injection of hGRF-44 at 2 μg/kg body weight, were studied in 10 patients with GH deficiency. During saline infusion in 4 patients, small plasma GH increase were observed in 2 patients. However, during hGRF infusion in 6 patients, up to 4 or 13 pulses of GH secretion were observed. The mean integrated GH pulse area during hGRF infusion was 22.5 ± 5.2 (se) ng/ml × h, which was greater than that obtained during saline infusion. Plasma somatomedin C levels did not increase after hGRF infusion. After saline or hGRF infusion all patients responded to an iv bolus injection of the peptide. These results indicate that hGRF infusion augments GH secretion by increasing the number and amplitude of GH pulses and that the infusion does not cause pituitary somatotrophs to lose their capacity to respond to hGRF subsequently.

scholarly journals Dose-dependent relationship between severity of pediatric obesity and blunting of the growth hormone response to exercise

2010 ◽  
Vol 108 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Stacy R. Oliver ◽  
Jaime S. Rosa ◽  
Timothy D. C. Minh ◽  
Andria M. Pontello ◽  
Rebecca L. Flores ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Pediatric Obesity ◽  
Muscle Growth ◽  
Obese Children ◽  
Negative Effects ◽  
Gh Secretion ◽  
Dependent Relationship ◽  
Igf I ◽  
Plasma Gh ◽  
Response To Exercise

In children, exercise modulates systemic anabolism, muscle growth, and overall physiological development through the growth hormone (GH)-insulin-like growth factor I (IGF-I) axis. GH secretion, at rest and during exercise, changes with age and maturational status and can be blunted by hyperlipidemia and obesity, with possible negative effects on physiological growth. However, little is known about the effect of progressively more severe pediatric obesity on the GH response to exercise and its relationship to pubertal status. We therefore studied 48 early- or late-pubertal obese children [body mass index (BMI) >95th percentile, separated in tertiles with progressively greater BMI] and 42 matched controls (BMI <85th percentile), who performed ten 2-min cycling bouts at ∼80% of maximal O2 consumption, separated by 1-min rest intervals. Plasma GH and IGF-I were measured at baseline and end exercise. GH responses were systematically blunted in obese children, with more pronounced blunting paralleling increasing BMI. Although overall the GH response to exercise was greater in late-pubertal than in younger children, this blunting pattern was observed in early- and late-pubertal children. Our results reveal insight into the interaction between pediatric obesity and key modulators of physiological growth and development and underscore the necessity of optimizing physical activity strategies for specific pediatric dysmetabolic conditions.

Plasma growth hormone (GH) responses to single and repetitive subcutaneous administration of GH releasing factor (hpGRF-44) in normal and GH deficient children

1985 ◽  
Vol 108 (1) ◽  
pp. 11-19 ◽  
Author(s):  
K. Takano ◽  
N. Hizuka ◽  
K. Shizume ◽  
N. Honda ◽  
N. C. Ling
Keyword(s):  
Growth Hormone ◽  
Short Stature ◽  
Gh Deficiency ◽  
Peak Plasma ◽  
Subcutaneous Administration ◽  
Bolus Administration ◽  
Plasma Growth Hormone ◽  
Normal Children ◽  
Somatomedin C ◽  
Plasma Gh

Abstract. Synthetic human pancreatic GRF (hpGRF-44) was administered sc to 8 normal children with short stature and 11 patients with GH deficiency. After a dose of 100–200 μg hpGRF-44, mean plasma GH levels reached a peak at 15 min of 27.2 ± 6.4 (± se) ng/ml in normal children. However the responses were variable and peak plasma GH varied from 10.1 to 56.5 ng/ml. Eight of 11 patients with idiopathic GH deficiency did not respond to sc administration of 100–300 μg hpGRF-44. However, a plasma GH increase of more than 5 ng/ml occurred in 2 patients and to twice the basal level in 1 patient. Their GH values were 14.3, 5.2 and 3.4 ng/ml, respectively. After repetitive administration of hpGRF-44 (200 μg, twice a day) sc for 5 consecutive days, 2 of 8 patients restored their responsiveness, but the remaining patients did not show GH rise in response to both sc and iv bolus administration of hpGRF-44. Repetitive hpGRF-44 administrations for 5 days had no effect on somatomedin-C production.

Effect of Growth Hormone-Releasing Factor on Plasma Growth Hormone, Prolactin and Somatomedin C in Hypopituitary and Short Normal Children

1985 ◽  
Vol 22 (1-2) ◽  
pp. 32-45 ◽  
Author(s):  
Guy Van Vliet ◽  
Dani&egrave;le Bosson ◽  
Claude Robyn ◽  
Margareta Craen ◽  
Paul Malvaux ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Plasma Growth Hormone ◽  
Normal Children ◽  
Somatomedin C ◽  
Growth Hormone Releasing Factor

Is there a place for urinary growth hormone measurement?

1993 ◽  
Vol 128 (3) ◽  
pp. 197-201 ◽  
Author(s):  
Maria N Moreira-Andrés ◽  
Francisco J Cañizo ◽  
Federico Hawkins
Keyword(s):  
Growth Hormone ◽  
Screening Method ◽  
Small Sample ◽  
Point Of View ◽  
Intrasubject Variability ◽  
Gh Secretion ◽  
Lack Of Information ◽  
Low Levels ◽  
Plasma Gh ◽  
Serum Gh

The evaluation of growth hormone (GH) secretion is an important problem in pediatric endocrine practice. The diagnosis of GH insufficiency is based on the finding of a "blunted" GH response to GH provocative tests or on the demonstration of a decreased endogenous secretion. From a practical point of view, these methods are uncomfortable, expensive and time consuming. Recently, very sensitive specific assays to measure human GH in urine have been developed. We present a discussion of available data on these tests in order to estimate their role in the evaluation of a short or slowly growing child. The present available assays allow measuring very low levels of GH in a small sample of untreated urine. The main limitations of urinary GH measurement are the intrasubject variability, wide normal range, overlapping results in several GH secretory states and lack of information on GH pulsatility. However, most of these limitations also apply to other tests of GH secretion. The advantage of urinary GH tests is that they provide, in an easy procedure, information on serum GH concentration. There is good correlation between urinary and serum GH concentration and several findings suggest that urinary GH excretion reflects changes in plasma GH levels during the period of urine collection. Therefore, the usefulness of urinary GH measurement is that of a simpler and cheaper screening method for assessing integrated serum GH concentration in clinical practice.

Growth hormone-releasing factor enhances sleep in rats and rabbits

1988 ◽  
Vol 255 (2) ◽  
pp. R310-R316 ◽  
Author(s):  
F. Obal ◽  
P. Alfoldi ◽  
A. B. Cady ◽  
L. Johannsen ◽  
G. Sary ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Motor Activity ◽  
Eye Movement ◽  
Brain Temperature ◽  
Sleep Onset ◽  
Temporal Correlation ◽  
Diurnal Rhythms ◽  
Sleep Regulation ◽  
Growth Hormone Releasing Factor ◽  
Gh Secretion

Previously, it was suggested that a hypothalamic mechanism links somatotropin [growth hormone (GH)] secretion to sleep regulation, and this may explain the temporal correlation between GH release and nonrapid eye movement sleep (NREMS) on sleep onset. The purpose of these experiments was to study whether growth hormone-releasing factor (GRF), a hypothalamic peptide responsible for stimulation of GH secretion, also has the capacity to promote sleep in rats and rabbits. Artificial cerebrospinal fluid or GRF (human GRF-[1-40], 0.01, 0.1, and 1 nmol/kg) was intracerebroventricularly injected to rats at dark onset, and the electroencephalogram (EEG), brain temperature (Tbr), and motor activity were recorded for 24 h. Rabbits received the same doses of GRF during the light period, and sleep-wake activity was monitored for 6 h. GRF promoted NREMS and rapid eye movement sleep (REMS) and increased EEG slow-wave activity in both rats and rabbits. NREMS increased in postinjection hour 1 after low doses of GRF, whereas the effect was more prolonged after higher doses. REMS increased in response to the low and middle doses of GRF in postinjection hour 1 in rats and in hour 2 after each dose in rabbits. The diurnal rhythms of sleep-wake activity, motor activity, and Tbr were not affected in rats. Because GRF promotes sleep and also stimulates GH secretion, it is a likely candidate for linking GH secretion and sleep regulation.

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