The effect of atenolol on the growth hormone response to growth hormone-releasing hormone in obese children

1992 ◽  
Vol 126 (2) ◽  
pp. 124-127 ◽  
Author(s):  
Sandro Loche ◽  
Stefano Pintus ◽  
Daniela Carta ◽  
Anna Carla Muntoni ◽  
Gabriella Congiu ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Area Under The Curve ◽  
Acute Administration ◽  
Adrenergic Blockade ◽  
Obese Children ◽  
Gh Secretion ◽  
Adrenergic Antagonist ◽  
Significant Augmentation ◽  
Obese Subjects ◽  
Β Adrenergic Receptors

We have evaluated the effect of acute administration of atenolol, a selective β-adrenergic antagonist, on the GH response to GHRH in nine obese children and in eight age-matched controls. The GH response to GHRH (1–29, 1 μg/kg iv), evaluated both as the GH peak and as integrated area under the curve, was significantly lower in the obese children than in the controls. Pretreatment with atenolol (50 or 100mg orally in subjects with body weight <or >40 kg, respectively, administered 120 min before the GHRH injection) significantly increased the GH response to GHRH in the obese subjects, such that their mean peak GH levels and mean integrated area under the curve after atenolol plus GHRH were similar to those of the control children after GHRH. Also in control children, atenolol caused a significant augmentation of the GH response to GHRH. Mean peak GH levels and mean integrated area under the curve after atenolol plus GHRH were significantly higher in the controls than in the obese children given the same treatment. These data show that inhibition of central β-adrenergic receptors counteracts the blunted GH response to GHRH present in the obese children. In view of the alleged mechanism of action of β-adrenergic blockade (inhibition of endogenous SRIH release), our data suggest that the somatostatinergic system is intact in obesity, and that the suppressed GH secretion is due to other causes.

Pyridostigmine counteracts the blunted growth hormone response to growth hormone-releasing hormone of obese children

1989 ◽  
Vol 120 (5) ◽  
pp. 624-628 ◽  
Author(s):  
S. Loche ◽  
C. Pintor ◽  
M. Cappa ◽  
E. Ghigo ◽  
R. Puggioni ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Area Under The Curve ◽  
Pyridostigmine Bromide ◽  
Acute Administration ◽  
Growth Hormone Releasing Hormone ◽  
Hormone Response ◽  
Obese Children ◽  
Significant Augmentation ◽  
Simple Obesity ◽  
Obese Subjects

Abstract. We have evaluated the effect of acute administration of pyridostigmine bromide, a cholinesterase inhibitor, on the GHRH-induced GH rise in 11 obese children and in 8 age-matched controls. The GH response to GHRH (hpGRF 1–40, 1 μg/kg iv), evaluated both as maximum GH peak and as integrated area under the curve, was significantly lower in the obese children than in the controls. Pretreatment with pyridostigmine bromide (60 mg orally 60 min before the GHRH injection) significantly increased both baseline GH levels and the GH response to GHRH in all the obese subjects, so that their mean baseline GH, peak GH levels and integrated area under the curve after pyridostigmine bromide plus GHRH were similar to those of the control children after GHRH. Also in control children pyridostigmine bromide increased (though not significantly) baseline GH levels, and caused a significant augmentation of the GH response to GHRH. Mean peak GH levels and mean integrated area under the curve after pyridostigmine bromide plus GHRH were significantly higher in the controls than in the obese children given the same treatment. Mean baseline Sm-C levels were significantly higher in the obese than in control children. These data show that enhancement of cholinergic neurotransmission, likely in the hypothalamus, counteracts the blunted GH response to GHRH present in the obese children, and that in simple obesity the potential of the pituitary to make a secretory response to a direct GH secretagogue is preserved.

GROWTH HORMONE RESPONSES TO FRUCTOSE IN DIABETES MELLITUS

1974 ◽  
Vol 75 (3) ◽  
pp. 497-502
Author(s):  
Mayer B. Davidson ◽  
Roger M. Steele
Keyword(s):  
Diabetes Mellitus ◽  
Growth Hormone ◽  
Fasting Glucose ◽  
Area Under The Curve ◽  
Oral Glucose ◽  
Gh Secretion ◽  
Significant Difference ◽  
Duration Of Disease ◽  
Hormone Responses

ABSTRACT Since fructose is normally metabolized in diabetics and has recently been shown to stimulate GH secretion, it was used to assess GH responses in diabetics. Fourteen diabetics (9 on insulin) and 8 controls matched for weight were studied. Fructose, infused over 10 min, was compared to arginine, infused over 30 min, both at 0.5 g/kg. Samples were collected at 0, 30, 60, 90 and 120 min and GH responses assessed as area under the curve minus the fasting area. There was no significant difference between the GH responses in diabetics and controls to either agent. Responses to arginine and fructose were significantly correlated (r = 0.60, P < 0.01) in all subjects, but not related to therapy, duration of disease or fasting glucose (75–287 mg/100 ml) in the diabetics. Oral glucose blunted the GH response to fructose in 2 controls. It is concluded that 1) fructose can stimulate GH secretion in male diabetics; 2) however, fructose-stimulated GH responses are not increased in diabetes mellitus.

Pyridostigmine enhances, but does not normalise, the GH response to GH-releasing hormone in obese subjects

1990 ◽  
Vol 122 (3) ◽  
pp. 385-390 ◽  
Author(s):  
R. C. Castro ◽  
J. G. H. Vieira ◽  
A. R. Chacra ◽  
G. M. Besser ◽  
A. B. Grossman ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Acetylcholinesterase Inhibitor ◽  
Random Order ◽  
Normal Subjects ◽  
Obese Patients ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Obese Subjects ◽  
Higher Doses ◽  
Hormone Responsiveness

Abstract Obese patients are characterised by several neuroendocrine abnormalities, including characteristically a decrease in growth hormone responsiveness to GH-releasing hormone. In normal subjects, the GH response to GHRH is enhanced by the acetylcholinesterase inhibitor, pyridostigmine. We have studied the effect of this drug on GH secretion in gross obesity. Twelve obese patients were studied (mean weight 156% of ideal) and compared with a group of 8 normal volunteers. Each subject was initially studied on two occasions, in random order, with GHRH (1–29) NH2 100 μg iv alone and following pretreatment with pyridostigmine 120 mg orally one hour prior to GHRH. In obese patients, the GH response to GHRH was significantly blunted when compared to controls (GH peak: 20 ± 4 vs 44 ± 16 μg/l; mean ± sem). After pyridostigmine, the response to GHRH was enhanced in the obese subjects, but remained significantly reduced compared to non-obese subjects treated with GHRH and pyridostigmine (GH peak: 30 ± 5 vs 77 ± 20 μg/l, respectively). In 6 subjects, higher doses of GHRH or pyridostigmine did not further increase GH responsiveness in obese patients. Our results suggest that obese patients have a disturbed cholinergic control of GH release, probably resulting from increased somatostatinergic tone. This disturbed regulation may be responsible, at least in part, for the blunted GH responses to provocative stimuli.

Mediation of isoproterenol-induced thirst in rats by β2-adrenergic receptors

1978 ◽  
Vol 56 (3) ◽  
pp. 465-470 ◽  
Author(s):  
M. J. Katovich ◽  
M. J. Fregly
Keyword(s):  
Water Intake ◽  
Adrenergic Receptors ◽  
Subcutaneous Administration ◽  
Female Rats ◽  
Acute Administration ◽  
Drinking Response ◽  
Adrenergic Antagonist ◽  
Blocking Activity ◽  
Β Adrenergic Receptors ◽  
Adrenergic Blocking

Isoproterenol-induced thirst in rats has been attributed to the activation of β-adrenergic receptors. Since these receptors can be further differentiated pharmacologically into β1 and β2 types, experiments were performed using several β-adrenergic agonists and antagonists to determine the receptor type initiating the isoproterenol-induced thirst. The β1- and β2-adrenergic antagonist, d,l-propranolol (1 mg/kg, ip), blocked the increase in water intake usually accompanying acute subcutaneous administration of isoproterenol (25 μg/kg) to female rats. Since l-propranolol is known to stabilize membranes and to possess anesthetic-like properties, d-propranolol was also used. This isomer has little β-adrenergic-blocking activity but possesses anesthetic-like activity. Administration of d-propranolol (1 mg/kg, ip) failed to affect the drinking response to acute administration of isoproterenol (25 μg/kg). Practolol (125 mg/kg), a β1-adrenergic antagonist with little anesthetic properties, also had no effect on water intake of isoproterenol-treated rats. Butoxamine, a selective β2-adrenergic antagonist, attenuated the drinking response to isoproterenol. Salbutamol (150 μg/kg), a β2-adrenergic agonist, mimicked the effect of isoproterenol on water intake. These results are consistent with the suggestion that β2-adrenergic receptors mediate the isoproterenol-induced thirst in rats.

Corticotrophin-releasing hormone does not inhibit growth hormone-releasing hormone-induced release of growth hormone in control subjects but is effective in patients with eating disorders

1994 ◽  
Vol 140 (2) ◽  
pp. 327-332 ◽  
Author(s):  
M Rolla ◽  
A Andreoni ◽  
D Bellitti ◽  
M Ferdeghini ◽  
E Ghigo ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Eating Disorders ◽  
Young Women ◽  
Animal Studies ◽  
Area Under The Curve ◽  
Inhibitory Influence ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Not Otherwise Specified ◽  
Normal Women

Abstract Previous studies have shown that corticotrophin-releasing hormone (CRH) inhibits GH secretion in response to GH-releasing hormone (GHRH) in normal women and men, and animal studies suggest that this effect is mediated by an increased release of somatostatin from the hypothalamus. It has been reported that there are abnormalities in the neuroendocrine regulation of the hypothalamo-pituitary-somatotrophic axis and the hypothalamo-pituitary-adrenocortical axis in patients with eating disorders. The present study therefore investigated the ability of CRH to inhibit the GH response to GHRH in eight young women with anorexia nervosa (AN) and in seven young women with eating disorders which were not otherwise specified (NOS). We also compared the effect of CRH in the patients with the response it caused in ten control women. In contrast to a previous report, combined i.v. administration of 50 μg human CRH (hCRH) and 50 μg GHRH(1–29) caused a GH response in control women which was higher, although not significantly so, than that induced by GHRH alone (area under the curve (AUC) 988·5 ±506·0 compared with 1568·4 ±795·6 (s.e.m.) ng/ml per 120 min for GHRH alone and GHRH plus hCRH respectively). Conversely, the administration of hCRH given together with GHRH markedly inhibited the GH response induced by the latter in both AN patients (AUC 2253·0 ±385·7 compared with 1224·4 ±265·7 ng/ml per 120 min for GHRH and GHRH plus hCRH respectively; P<0·005 and NOS patients (AUC 2827·4±281·1 compared with 308·5 ± 183·4 ng/ml per 120 min for GHRH and GHRH plus hCRH respectively; P<0·0001). These results (1) refute the suggestion that there is an inhibitory influence of CRH over GH secretion under normal conditions, (2) indicate that this inhibitory influence exists in patients with eating disorders, and (3) imply that, in the latter, hypothalamic somatostatinergic function is, at least in part, preserved. Journal of Endocrinology (1994) 140, 327–332

Acute effects of cortisone acetate on growth hormone response to growth hormone-releasing hormone in normal adult subjects

1990 ◽  
Vol 122 (2) ◽  
pp. 206-210 ◽  
Author(s):  
Andrea Giustina ◽  
Mauro Doga ◽  
Corrado Bodini ◽  
Angela Girelli ◽  
Fabio Legati ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Random Order ◽  
Serum Cortisol ◽  
Cortisone Acetate ◽  
Acute Administration ◽  
Acute Effects ◽  
Gh Secretion ◽  
Normal Man ◽  
The Relationship ◽  
Dose Dependent

Abstract Glucocorticoids have been shown to inhibit GH secretion in normal man when administered in large amounts for several days. The aim of our study was 1. to investigate the acute effects of a single dose of glucocorticoids on GH secretion in normal man; 2. to look at the relationship between the increase in serum cortisol concentration and GH response to the stimuli. Six healthy volunteers received on three occasions in random order an iv injection of GHRH (1–29) NH2, 100 μg, alone or 60 min after oral administration of either 25 or 50 mg of cortisone acetate. Mean stimulated GH levels, GH peak and integrated GH concentration were significantly lower after GHRH plus cortisone 25 mg than after GHRH alone. Mean GH levels at 15 and 30 min after GHRH injection and the peak GH level showed a further decrease after GHRH plus cortisone 50 mg. We conclude that acute administration of pharmacological doses of glucocorticoids is able to inhibit GH response to GHRH, probably through enhancement of endogenous somatostatin release. Moreover, this pharmacological effect of glucocorticoids seems to be dose-dependent and thus directly related to serum cortisol concentrations.

Effects of octreotide on insulin-like growth factor I and metabolic indices in growth hormone-treated growth hormone-deficient patients

1993 ◽  
Vol 129 (5) ◽  
pp. 399-408 ◽  
Author(s):  
Torben Laursen ◽  
Jens OL Jorgensen ◽  
Hans Ørskov ◽  
Jens Møller ◽  
Alan G Harris ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Animal Studies ◽  
Area Under The Curve ◽  
Insulin Like Growth Factor ◽  
Gh Secretion ◽  
Factor I ◽  
Igf I ◽  
Growth Factor I ◽  
Igfbp 3

Animal studies have demonstrated that in addition to inhibiting growth hormone (GH) secretion octreotide inhibits in a direct manner hepatic or peripheral insulin-like growth factor I (IGF-I) generation. To test this hypothesis in humans we studied ten GH-deficient patients with frequent blood sampling during 38 h on two occasions. Regular GH therapy was discontinued 72 h prior to each study period. At the start of each study a subcutaneous (sc) injection of GH (3 IU/m2) was given (at 18.00 h). In a single-blinded crossover design, patients received a continuous sc infusion of either octerotide (200 μg/24 h) or placebo (saline). The pharmacokinetics of GH were similar on the two occasions. The area under the curve±sem of serum GH was 142.5±53.6 μg·l−1·h−1 (octreotide) and 144.8±41.8 μg·l−1·h−1 (placebo), (p=0.73); Cmax (μg/l) was 12.5±1.47 (octreotide) and 12.8±1.42 (placebo) (p=0.83), and Tmax (h) was 6.1±0.97 (octreotide) and 5.2±0.65 (placebo) (p=0.49). Growth hormone administration was associated with an increase in serum IGF-I (μg/l), which was identical during the two studies, from 85.3±19.4 to 174.25±30.3 for octreotide and from 97.0±26.4 to 158.8±28.2 for placebo. Mean IGF-I levels (μg/l) were 138.2±25.1 (octreotide) and 134.5±28.6 (placebo) (p=0.78). Similarly, the increase in IGF binding protein 3 (IGFBP-3) levels was identical. Mean IGFBP-3 levels (μg/l) were 2303±323 (octreotide) and 2200±361 (placebo) (p=0.25). Mean insulin levels were significantly lower during octreotide treatment (39.9±17.9 mU/l) than during placebo (59.7±17.8 mU/l) (p<0.05). Mean blood glucose levels were elevated significantly during octreotide infusion (5.98±0.23 mmol/l for octreotide and 5.07±0.16 mmol/l for placebo; p=0.001). Glucagon levels decreased non-significantly (p=0.07) and IGFBP-1 levels tended to increase during infusion of octreotide although not significantly (p=0.41). Levels of the lipid intermediates were identical on the two occasions. Alanine and lactate levels were significantly increased during octreotide infusion. Mean levels of blood alanine (μmol/l) were 470.8±24.2 (octreotide) and 360.1±17.8 (placebo) (p<0.02). Mean levels of blood lactate were 1038±81.0 (octreotide) and 894.4±73.8 (placebo) (p<0.04). We conclude that short-term continuous sc infusion of octreotide has no direct effect on the generation of IGF-I or the pharmacokinetics of exogenous GH in GH-deficient man.

A possible relationship between serum transferrin, growth hormone secretion and height velocity in children

1980 ◽  
Vol 93 (2) ◽  
pp. 134-138 ◽  
Author(s):  
M. Donnadieu ◽  
R. M. Schimpff ◽  
P. Garnier ◽  
J. L. Chaussain ◽  
J. C. Job
Keyword(s):  
Growth Hormone ◽  
Growth Regulation ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Height Velocity ◽  
Obese Children ◽  
Gh Secretion ◽  
Growth Promoting

Abstract. Since transferrin (Tf) in vitro has a growth-promoting activity and is associated with NSILA properties, the aim of this work was to study in vivo the relationships between Tf, somatomedin activity (SM), growth hormone (GH) secretion, and height velocity in children. An iv infusion of ornithine hydrochloride was given to 23 controls; the induced rise of GH was accompanied by a simultaneous fall of SM (r = −0.711, P < 0.001) and was preceded by a fall of Tf (r = −0.610, P < 0.01). In 17 obese children SM was within the normal range, when Tf levels were higher and arginineinduced GH peaks lower than in the controls, and a negative correlation was found between Tf basal levels and GH peaks (r = −0.608, P < 0.01). In 9 children with confirmed hypopituitarism the Tf levels were significantly lower than in the controls. In 14 children with confirmed or suspected hypopituitarism a single im injection of hGH (6 mg) failed to induce Tf variations over 24 h. In 39 of these children the height velocity was significantly correlated with Tf basal levels (r = 0.701, P < 0.001). These data suggest that transferrin is involved in growth regulation, and that GH secretion is related to transferrin levels by a feed-back mechanism.

Sign in / Sign up

Export Citation Format

Share Document