The Secretion of Growth Hormone in Response to Insulin Infusion under Conditions of Normo- and Hypo-glycaemia

1975 ◽  
Vol 49 (3) ◽  
pp. 21P-21P
Author(s):  
T. E. T. West ◽  
P. H. Sönksen ◽  
D. P. Frost
Keyword(s):  
Growth Hormone ◽  
Insulin Infusion ◽  
Hypo Glycaemia

Counterregulation of insulin-induced hypoglycaemia in primary hypothyroidism

1986 ◽  
Vol 111 (4) ◽  
pp. 516-521
Author(s):  
Nina Clausen ◽  
Per-Eric Lins ◽  
Ulf Adamson ◽  
Bertil Hamberger ◽  
Suad Efendić
Keyword(s):  
Growth Hormone ◽  
Insulin Infusion ◽  
Primary Hypothyroidism ◽  
Constant Rate Infusion ◽  
Counterregulatory Hormones ◽  
Insulin Metabolism ◽  
Hormonal Responses ◽  
Glucose Levels ◽  
Constant Rate ◽  
Rate Infusion

Abstract. Hypothyroidism has been alleged to modulate insulin action and influence the secretion of growth hormone and catecholamines. We recently investigated the influence of hypothyroidism on glucose counterregulatory capacity and the hormonal responses to insulin-induced hypoglycaemia in 6 patients with primary hypothyroidism (age 32–52 years, TSH-values 66–200 mU/l). Hypoglycaemia was induced in the hypothyroid state and again when the subjects were euthyroid. After an overnight fast a constant rate infusion of insulin (2.4 U/h) was given for 4 h. Glucose was measured every 15 min and insulin, C-peptide, glucagon, epinephrine, norepinephrine, growth hormone and cortisol every 30 min for 5 h. During insulin infusion somewhat higher concentrations of the hormone were obtained in the hypothyroid state and simultaneously glucose levels were 0.5 mmol/l lower. As expected, basal norepinephrine levels were higher in hypothyroidism. However, no increase in circulating norepinephrine during hypoglycaemia was registered in the two experiments. The responses of counterregulatory hormones showed an enhanced response of cortisol, similar responses of growth hormone and epinephrine while the glucagon response was paradoxically impaired. Our findings suggest that hypothyroidism alters insulin metabolism, and that the glucagon response to hypoglycaemia is impaired in this condition.

The influence of insulin on circulating ghrelin

2003 ◽  
Vol 284 (2) ◽  
pp. E313-E316 ◽  
Author(s):  
Daniel E. Flanagan ◽  
Mark L. Evans ◽  
Teresa P. Monsod ◽  
Frances Rife ◽  
Rubina A. Heptulla ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Energy Homeostasis ◽  
Insulin Infusion ◽  
Significant Rise ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Physiological Regulator ◽  
Underlying Mechanisms ◽  
Mean Glucose

Ghrelin is a novel peptide that acts on the growth hormone (GH) secretagogue receptor in the pituitary and hypothalamus. It may function as a third physiological regulator of GH secretion, along with GH-releasing hormone and somatostatin. In addition to the action of ghrelin on the GH axis, it appears to have a role in the determination of energy homeostasis. Although feeding suppresses ghrelin production and fasting stimulates ghrelin release, the underlying mechanisms controlling this process remain unclear. The purpose of this study was to test the hypotheses, by use of a stepped hyperinsulinemic eu- hypo- hyperglycemic glucose clamp, that either hyperinsulinemia or hypoglycemia may influence ghrelin production. Having been stable in the period before the clamp, ghrelin levels rapidly fell in response to insulin infusion during euglycemia (baseline ghrelin 207 ± 12 vs. 169 ± 10 fmol/ml at t = 30 min, P < 0.001). Ghrelin remained suppressed during subsequent periods of hypoglycemia (mean glucose 53 ± 2 mg/dl) and hyperglycemia (mean glucose 163 ± 6 mg/dl). Despite suppression of ghrelin, GH showed a significant rise during hypoglycemia (baseline 4.1 ± 1.3 vs. 28.2 ± 3.9 μg/l at t = 120 min, P < 0.001). Our data suggest that insulin may suppress circulating ghrelin independently of glucose, although glucose may have an additional effect. We conclude that the GH response seen during hypoglycemia is not regulated by circulating ghrelin.

GROWTH-HORMONE AND CORTISOL RESPONSES TO INSULIN INFUSION IN PATIENTS WITH DIABETES MELLITUS

The Lancet ◽  
1972 ◽  
Vol 300 (7769) ◽  
pp. 155-160 ◽  
Author(s):  
P.H. Sönksen ◽  
M.C. Srivastava ◽  
ChristineV. Tompkins ◽  
J.D.N. Nabarro
Keyword(s):  
Diabetes Mellitus ◽  
Growth Hormone ◽  
Insulin Infusion ◽  
Patients With Diabetes ◽  
Cortisol Responses

Nocturnal versus diurnal hormonal counterregulation to hypoglycemia in Type 1 (insulin-dependent) diabetic patients

1993 ◽  
Vol 128 (2) ◽  
pp. 109-115 ◽  
Author(s):  
Inger Bendtson ◽  
Anne Mette Rosenfalck ◽  
Christian Binder
Keyword(s):  
Growth Hormone ◽  
Blood Glucose ◽  
Insulin Infusion ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Diabetic Patients ◽  
Hormonal Responses ◽  
Nocturnal Hypoglycemia ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic

Asymptomatic hypoglycemia in IDDM patients seems to be more frequent during the night than during the day, with reported frequencies as high as 56%. Hormonal counterregulation to diurnal and nocturnal hypoglycemia was studied in 10 insulin-dependent diabetic patients without diabetic complications in order to test whether hormonal responses were lower at night than during daytime. A lower catecholamine response might imply less marked symptoms and therefore one reason why patients are not awakened by hypoglycemia. Blood glucose was stabilized to around 6 mmol/1 by iv insulin infusion and hypoglycemia was induced by increasing the insulin infusion rate—in the night studies at 01.30, in the day studies at 08.00. Blood glucose nadirs were 1.5±0.4 (1.2–1.9) mmol/1 at night and 1.9±0.3 (1.3–2.2) mmol/l during the day; in three patients the nadirs were identical during both the night and day. One patient had no adrenaline response to daytime hypoglycemia. In general, nocturnal hypoglycemia elicited greater catecholamine responses correlated to the duration of hypoglycemia. Glucagon responses showed a great heterogeneity independently of diabetes duration and hypoglycemic level. Growth hormone secretion was reduced during the night study; however, no refractory periods were found after sleep-related growth hormone secretion. In conclusion: counter-regulatory hormonal responses tend to be greater at night than during the day and do not explain why patients are not awakened by nocturnal hypoglycemia.

Growth Hormone and Glucose Interrelationships in Diabetes: Studies with Insulin Infusion During Continuous Blood Glucose Analysis

1969 ◽  
Vol 29 (3) ◽  
pp. 319-327 ◽  
Author(s):  
VAHAB FATOURECHI ◽  
GEORGE D. MOLNAR ◽  
FREDERICK J. SERVICE ◽  
EUGENE ACKERMAN ◽  
JOHN W. ROSEVEAR ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Blood Glucose ◽  
Insulin Infusion ◽  
Continuous Blood Glucose Analysis ◽  
Glucose Analysis

scholarly journals 600 EFFECT OF CRANIAL RADIATION DOSE ON GROWTH HORMONE RESPONSE TO ARGININE AND INSULIN INFUSION

1978 ◽  
Vol 12 ◽  
pp. 463-463 ◽  
Author(s):  
W Perry Dickinson ◽  
D H Berry ◽  
L Dickinson ◽  
M Irvin ◽  
H Schedewie ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Radiation Dose ◽  
Insulin Infusion ◽  
Growth Hormone Response ◽  
Hormone Response ◽  
Cranial Radiation

Uridine triphosphate and RNA synthesis during diabetes-induced renal growth

1980 ◽  
Vol 238 (4) ◽  
pp. E349-E357
Author(s):  
P. Cortes ◽  
N. W. Levin ◽  
F. Dumler ◽  
A. H. Rubenstein ◽  
C. P. Verghese ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Rna Synthesis ◽  
Insulin Infusion ◽  
Renal Cortex ◽  
Plasma Concentrations ◽  
Synthesis Rate ◽  
Renal Growth ◽  
Rna Content ◽  
And Control

UTP, CTP, and RNA synthesis were studied in the renal cortex of diabetic and control rats in vivo. The incorporation of UTP into RNA (nmol/h DNA) was used as estimate of RNA synthesis rate. Two to three days after streptozotocin injection, UTP and CTP ppol size and orotate incorporation into UTP and RNA were greater in diabetic animals than in controls. In addition, RNA content and RNA synthesis rate were increased. These changes were corrected by insulin infusion. In diabetic animals, additional increases in UTP pool, RNA content, and RNA synthesis rate followed contralateral nephrectomy. This increase in RNA content was greater than in uninephrectomized controls. The changes in the diabetic renal cortex were not accompanied by increased plasma concentrations of growth hormone. The increase in RNA content in the diabetic renal cortex is probably due to increased RNA synthesis. Increased synthesis of pyrimidines and expansion of the UTP pool may make this substrate more readily available for the synthesis of UDP sugars and may facilitate the synthesis of basement membrane in diabetes.

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.

Normalization of the Growth Hormone and Catecholamine Response to Exercise in Juvenile-Onset Diabetic Subjects Treated with a Portable Insulin Infusion Pump

Diabetes ◽  
1979 ◽  
Vol 28 (8) ◽  
pp. 785-788 ◽  
Author(s):  
W. V. Tamborlane ◽  
R. S. Sherwin ◽  
V. Koivisto ◽  
R. Hendler ◽  
M. Genel ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Insulin Infusion ◽  
Infusion Pump ◽  
Juvenile Onset ◽  
Catecholamine Response ◽  
Response To Exercise
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