EFFECTS OF ADRENALINE ON INSULIN-INDUCED RELEASE OF GROWTH HORMONE AND CORTISOL IN MAN

1974 ◽  
Vol 75 (2) ◽  
pp. 260-273 ◽  
Author(s):  
R. Müller-Hess ◽  
C. A. Geser ◽  
E. Jéquier ◽  
J.-P. Felber ◽  
A. Vannotti
Keyword(s):  
Growth Hormone ◽  
Blood Glucose ◽  
Insulin Infusion ◽  
Human Growth ◽  
Normal Subjects ◽  
Inhibitory Effect ◽  
Control Group ◽  
Adrenaline Infusion ◽  
Plasma Ffa ◽  
Cortisol Release

ABSTRACT The influence of peripherally administered adrenaline on the secretion of human growth hormone (HGH) and cortisol was investigated in 14 normal subjects. In a control group, HGH and cortisol release was stimulated by insulin infusion for 30 min (0.1 IU/kg). This procedure was compared with a similar insulin infusion which was started 60 min after initiating an adrenaline infusion for 150 min (6 μg/min). Adrenaline did not significantly alter the basal levels of HGH and cortisol. The mean maximal HGH rise during insulin hypoglycaemia (38.9 ± 7.2 ng/ml) was significantly (P < 0.005) inhibited by simultaneously administered adrenaline (9.6 ± 3.0 ng/ml). The same action of adrenaline was also found to be effective on cortisol release. The rise in plasma cortisol after insulin infusion (16.0±1.4 μg/100ml) was suppressed by adrenaline to 6.4 ± 2.2μg/100 ml (P < 0.005). Blood glucose and plasma free fatty acids (FFA), increased by adrenaline administration, were decreased significantly after insulin infusion. These results suggest an inhibitory effect of peripheral adrenaline on insulin-induced secretion of HGH. Blood glucose and plasma FFA levels seem to have no effect on this action. Whether there is a negative feedback between HGH and adrenaline should be considered. It is possible that the inhibition of cortisol release by adrenaline is mediated by an inhibiting effect on ACTH release, in the same manner as on the release of HGH.

Effects of Adrenaline on the Dynamics of Carbohydrate Metabolism in Rats Treated Chronically with Adrenaline

1975 ◽  
Vol 53 (1) ◽  
pp. 124-128 ◽  
Author(s):  
Suzanne Rousseau-Migneron ◽  
Jacques LeBlanc ◽  
Louise Lafrance ◽  
Florent Depocas
Keyword(s):  
Blood Glucose ◽  
Clearance Rate ◽  
Glucose Production ◽  
Treated Group ◽  
Inhibitory Effect ◽  
Control Group ◽  
Metabolic Clearance ◽  
Glucose Levels ◽  
Adrenaline Infusion ◽  
Initial Clearance

Following a subcutaneous injection of adrenaline (300 μg/kg), blood-glucose levels were lower in rats treated chronically with adrenaline (300 μg/kg twice a day for 28 days) than in control rats during at least 2.5 h after the injection. To explain this difference of response, the turnover rate of glucose was measured in control and adrenaline-treated rats during adrenaline infusion (0.75 μg/kg−1 min−1), with [U-14C]glucose as tracer. It was found that the rate of appearance of glucose was greater in the control than in the adrenaline-treated group after a 120-min infusion of adrenaline. The rate of disappearance of glucose in the treated rats increased during the first 60 min of infusion and stayed at this elevated level for a subsequent 2 h, whereas in the control rats, it remained unchanged at the beginning of adrenaline infusion and significantly increased only during the second and third hours of infusion. In addition, the metabolic-clearance rate of glucose was not modified by adrenaline in the treated group, but in the control group, the initial clearance rate was significantly less than in the treated group, and decreased during the first hour of adrenaline infusion even though blood glucose reached values of 244 mg/100 ml. From these data, it is suggested that rats adapt to a chronic exogenous supply of adrenaline by a reduced increase in glucose production in response to adrenaline infusion and a better glucose utilization, which possibly indicates a decrease in the inhibitory effect of adrenaline on insulin secretion.

EFFECT OF AMINOPHYLLINE ON GROWTH HORMONE SECRETION IN MAN

1974 ◽  
Vol 76 (3) ◽  
pp. 488-494 ◽  
Author(s):  
M. Peracchi ◽  
F. Cavagnini ◽  
A. E. Pontiroli ◽  
U. Raggi ◽  
A. Malinverni ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Blood Glucose ◽  
Intravenous Infusion ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Normal Subjects ◽  
Gh Secretion ◽  
Inhibiting Effect ◽  
Plasma Ffa ◽  
Serum Gh

ABSTRACT The effects of intravenously administered aminophylline on growth hormone (GH) secretion have been studied in sixteen normal subjects and four acromegalic patients. Intravenous infusion of theophylline ethylenediamine 480 mg over a 30 min period did not alter the blood glucose and serum GH levels in six normal subjects but raised the plasma FFA by 88 %. By contrast, in four acromegalic patients theophylline administration resulted in a fall of the serum GH levels by 17.6–51.7 %, mean 36.5%. In ten normal subjects the infusion of the drug clearly blunted the GH response to insulin hypoglycaemia without modifying the decrease in blood glucose and plasma FFA induced by insulin: mean peak GH values decreased from 32.7 ± 3.39 to 21.4 ± 4.10 ng/ml (P < 0.025). These data seem to indicate that theophylline has an overall inhibiting effect on the hypothalamic-hypophyseal axis for GH secretion.

Circadian Variation of the Blood Glucose, Plasma Insulin and Human Growth Hormone Levels in Response to an Oral Glucose Load in Normal Subjects

Diabetes ◽  
1974 ◽  
Vol 23 (2) ◽  
pp. 132-137 ◽  
Author(s):  
N. J. Aparicio ◽  
F. E. Puchulu ◽  
J. J. Gagliardino ◽  
M. Ruiz ◽  
J. M. Llorens ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Blood Glucose ◽  
Plasma Insulin ◽  
Circadian Variation ◽  
Human Growth ◽  
Normal Subjects ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load ◽  
Glucose Plasma

Failure of Human Growth Hormone and Human Placental Lactogen to Affect Glucose Consumption by Human Erythrocytes and Leucocytes In Vitro

1972 ◽  
Vol 50 (10) ◽  
pp. 1014-1017
Author(s):  
Catherine L. Tanser ◽  
Nannie K. M. de Leeuw
Keyword(s):  
Growth Hormone ◽  
Glucose Oxidase ◽  
Human Growth Hormone ◽  
Glucose Utilization ◽  
Human Growth ◽  
Glucose Consumption ◽  
Inhibitory Effect ◽  
Placental Lactogen ◽  
Human Placental Lactogen

The effect of human growth hormone (HGH) and human placental lactogen (HPL) on glucose consumption by erythrocytes and leucocytes in vitro was investigated. Glucose consumption was measured by determining glucose utilization during 3 h incubation at 37 °C, using the glucose oxidase method.HGH and HPL showed no effect on glucose consumption by erythrocytes, and HPL showed no effect on glucose consumption by leucocytes in vitro. Our results do not confirm previous reports of an inhibitory effect of HGH on glucose consumption by erythrocytes in vitro.

Altered lipid kinetics in adjuvant recombinant human growth hormone-treated multiple-trauma patients

1994 ◽  
Vol 267 (4) ◽  
pp. E560-E565 ◽  
Author(s):  
M. Jeevanandam ◽  
S. R. Petersen
Keyword(s):  
Growth Hormone ◽  
Multiple Trauma ◽  
Human Growth Hormone ◽  
Recombinant Human Growth Hormone ◽  
Human Growth ◽  
Whole Body ◽  
Constant Infusion ◽  
Control Group ◽  
Trauma Patients ◽  
Oxidation Rates

Adjuvant recombinant human growth hormone therapy during the postinjury period may improve the efficiency of utilization of body energy stores. In a group of 20 severely injured highly catabolic hypermetabolic adult multiple-trauma victims, we have investigated the basic lipid kinetics of trauma (study I) and its modification after 7 days of intravenous feeding (total parenteral nutrition) with (group H, n = 10) or without (group C, n = 10) daily rhGH (0.15 mg somatotropin.kg-1.day-1) intramuscular injections (study II). Whole body lipolysis rate (2-stage primed constant infusion of 10% glycerol), substrate net oxidation rates (indirect calorimetry), and plasma levels of hormones were determined. Compared with the control group (group C) the treatment group (group H) showed significantly (P = 0.006) enhanced rates of lipolysis and free fatty acid reesterification (10 +/- 2 to 18 +/- 2 kcal.kg-1.day-1, P = 0.05). As a function of resting energy expenditure (REE), a trend of increased net glucose oxidation [32 +/- 10 vs. 56 +/- 7% REE, not significant (NS)] and decreased fat (40 +/- 8 vs. 25 +/- 5% REE, NS) and protein oxidation rates (28 +/- 2 vs. 19 +/- 2% REE, P = 0.007) were also indicated. The simultaneous operation of increased lipolytic and reesterification processes may allow the adipocyte to respond rapidly to changes in peripheral metabolic fuel requirements in injury.

Effects of exogenous growth hormone pretreatment on the pituitary growth hormone response to growth hormone-releasing hormone alone or in combination with pyridostigmine in Type I diabetic patients

1991 ◽  
Vol 125 (5) ◽  
pp. 510-517 ◽  
Author(s):  
Andrea Giustina ◽  
Simonetta Bossoni ◽  
Corrado Bodini ◽  
Antonino Cimino ◽  
Giuseppe Pizzocolo ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Blood Glucose ◽  
Normal Subjects ◽  
Diabetic Patients ◽  
Type I ◽  
Gh Secretion ◽  
Glucose Levels ◽  
Group A ◽  
Group B ◽  
And Control

Abstract. We evaluated the effects of iv pretreatment with exogenous GH on the GH response to GHRH either alone or in combination with pyridostigmine in 14 Type I diabetic patients and 6 normal subjects. All the subjects received an iv bolus injection of biosynthetic human GH, 2 IU; 2 h later they received either a. pyridostigmine, 120 mg orally, or b. placebo, 2 tablets orally, followed 1 h later by iv injection of GHRH(1-29) NH2, 100 μg. In normal subjects the median GH peak after GH+GHRH was 1.8, range 1.2-6.9 μg/l. Pyridostigmine enhanced the GH response to GHRH in all subjects. The median GH peak after pyridostigmine+ GH+GHRH was 32.7, range 19.8-42.1 μg/l (p<0.001 vs GHRH alone). Seven diabetic subjects had median GH peaks after GH+GHRH >6.9 μg/l (the maximum GH peak after GH+GHRH in normal subjects) (group A: median GH peak 35.7, range 21.7-55 μg/l). The other diabetic subjects had GH peak lower than 6.9 μg/l (group B: median GH peak 4.4, range 2.1-6.5 μg/l). Pyridostigmine significantly increased the GH response to GHRH in group B patients (median GH peak 29.3, range 15.7-93.4 μg/l, p<0.001 vs GH+GHRH alone), but not in group A patients (median GH peak 39.9, range 21.9-64.9 μg/l). Group A diabetic patients were younger and had higher HbA1c and blood glucose levels than group B patients. In those diabetic patients with an exaggerated GH response to GH+GHRH, pyridostigmine failed to cause the increase in GH secretion observed in diabetic and control subjects with no responses to GH+GHRH. It can be suggested that elevated 24-h GH levels in some Type I diabetic patients may be due to decreased somatostatinergic tone which in turn causes altered autoregulation of GH secretion. We hypothesize that this finding is a consequence of a reset of the hypothalamic control of GH secretion caused by a chronically elevated blood glucose level in this subpopulation.

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