Influence of Blood Glucose Levels on Growth Hormone Secretion in Sheep

1971 ◽  
Vol 136 (1) ◽  
pp. 51-55 ◽  
Author(s):  
A. Trenkle
1998 ◽  
Vol 10 (4) ◽  
pp. 941-953 ◽  
Author(s):  
Klaus Prank ◽  
Clemens Jürgens ◽  
Alexander von zur Mühlen ◽  
Georg Brabant

Diabetes mellitus is a widespread disease associated with an impaired hormonal regulation of normal blood glucose levels. Patients with insulin-dependent diabetes mellitus (IDDM) who practice conventional insulin therapy are at risk of developing hypoglycemia (low levels of blood glucose), which can lead to severe dysfunction of the central nervous system. In large retrospective studies, up to approximately 4% of deaths of patients with IDDM have been attributed to hypoglycemia (Cryer, Fisher, & Shamoon, 1994; Tunbridge, 1981; Deckert, Poulson, & Larsen, 1978). Thus, a better understanding of the complex hormonal interaction preventing hypoglycemia is crucial for treatment. Experimental data from a study on insulin-induced hypoglycemia in healthy subjects are used to demonstrate that feedforward neural networks are capable of predicting the time course of blood glucose levels from the complex interaction of glucose counterregulatory (glucose-raising) hormones and insulin. By simulating the deficiency of single hormonal factors in this regulatory network, we found that the predictive impact of glucagon, epinephrine, and growth hormone secretion, but not of cortisol and norepinephrine, were dominant in restoring normal levels of blood glucose following hypoglycemia.


1993 ◽  
Vol 128 (2) ◽  
pp. 109-115 ◽  
Author(s):  
Inger Bendtson ◽  
Anne Mette Rosenfalck ◽  
Christian Binder

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.


1996 ◽  
Vol 135 (2) ◽  
pp. 205-210 ◽  
Author(s):  
Mauro Maccario ◽  
Silvia Grottoli ◽  
Paola Razzore ◽  
Massimo Procopio ◽  
Salvatore Endrio Oleandri ◽  
...  

Maccario M, Grottoli S, Razzore P, Procopio M, Oleandri SE, Ciccarelli E, Camanni F, Ghigo E. Effects of glucose load and/or arginine on insulin and growth hormone secretion in hyperprolactinemia and obesity. Eur J Endocrinol 1996;135:205–10. ISSN 0804–4643 In hyperprolactinemic patients an exaggerated glucose-induced insulin secretion has been reported, but these results have not been confirmed by other researchers. On the other hand, there are few data concerning somatotrope secretion in this condition. In order to clarify these points, in seven normal weight hyperprolactinemic female patients (HP: age 18–46 years, body mass index = 21.8 ± 0.6 kg/m2, basal prolactin = 91.7 ± 16.5 μg/l) we studied the effects of glucose load (100 g orally) and/or arginine (0.5 g/kg infused over 30 min on insulin glucose and growth hormone (GH) levels. These results were compared with those obtained in seven patients with simple obesity (OB: age 23–48 years, body mass index = 38.3 ± 2.6 kg/m2) in whom exaggerated insulin and low GH secretion are well known. Seven normal women (NS: age 26–32 years, body mass index = 20.6 ± 1.9 kg/m2) were studied as controls. The insulin response to glucose in HP (area under curve = 11460.8 ± 1407.5 mU·min·1−1) was not significantly different from NS (7743.7 ±882.9 mU·min·1−1) and OB (14 504.8 ± 1659.9 mU·min·1−1). The arginine-induced insulin release in HP and OB was similar (4219.4 ± 631.7 and 4107.3 ± 643.2 mU·min·1−1. respectively), both being higher (p < 0.02) than in NS (2178.1 ± 290.9 mU·min·1−1). Glucose and arginine had an additive effect on insulin release in HP and NS (19 769.1 ± 3249.6 and 10996.6 ± 1201.0 mU·min·1−1, respectively) and a synergistic effect in OB (28117.3± 5224.7 mU·min·1−1). In HP the insulin response to the combined administration of glucose and arginine was not significantly different from the one in OB, and both were higher (p < 0.05) than in NS. The increase in glucose levels after glucose administered on its own or combined with arginine was higher (p < 0.02) and longer lasting in OB than in NS and HP. After arginine in OB, the glucose levels did not show the late decrease under baseline values observed in HP and NS. Glucose inhibited GH secretion both in HP and NS (p < 0.05), while arginine stimulated it in all groups, although the GH response in HP and NS was higher (p < 0.03) than in OB. The arginine-induced GH secretion was inhibited by glucose in HP and NS but not in OB. These results demonstrate that both in hyperprolactinemic patients and in obesity there is a clear increase in insulin secretion. The insulin hyperresponsiveness in hyperprolactinemia is more clearly demonstrated by combined stimulation with glucose and arginine. In spite of similar insulin hypersecretion in hyperprolactinemic and obese patients, GH secretion is reduced only in the latter; with these data the hypothesis that somatotrope insufficiency in obesity is due to hyperinsulinism is unlikely. Ezio Ghigo, Divisione di Endocrinologia, Ospedale Molinette, C.so Dogliotti 14, 10126 Torino, Italy


2012 ◽  
Vol 6 (S3) ◽  
Author(s):  
Daniel P Sherbet ◽  
Tongjin Zhao ◽  
Robert L Li ◽  
Michael S Brown ◽  
Joseph L Goldstein

2007 ◽  
Vol 293 (5) ◽  
pp. E1303-E1310 ◽  
Author(s):  
Suzanne M. Breckenridge ◽  
Bharathi Raju ◽  
Ana Maria Arbelaez ◽  
Bruce W. Patterson ◽  
Benjamin A. Cooperberg ◽  
...  

Conclusions drawn from the pancreatic (or islet) clamp technique (suppression of endogenous insulin, glucagon, and growth hormone secretion with somatostatin and replacement of basal hormone levels by intravenous infusion) are critically dependent on the biological appropriateness of the selected doses of the replaced hormones. To assess the appropriateness of representative doses we infused saline alone, insulin (initially 0.20 mU·kg−1·min−1) alone, glucagon (1.0 ng·kg−1·min−1) alone, and growth hormone (3.0 ng·kg−1·min−1) alone intravenously for 4 h in 13 healthy individuals. That dose of insulin raised plasma insulin concentrations approximately threefold, suppressed glucose production, and drove plasma glucose concentrations down to subphysiological levels (65 ± 3 mg/dl, P < 0.0001 vs. saline), resulting in nearly complete suppression of insulin secretion ( P < 0.0001) and stimulation of glucagon ( P = 0.0059) and epinephrine ( P = 0.0009) secretion. An insulin dose of 0.15 mU·kg−1·min−1 caused similar effects, but a dose of 0.10 mU·kg−1·min−1 did not. The glucagon and growth hormone infusions did not alter plasma glucose levels or those of glucoregulatory factors. Thus, insulin “replacement” doses of 0.20 and even 0.15 mU·kg−1·min−1 are excessive, and conclusions drawn from the pancreatic clamp technique using such doses may need to be reassessed.


1993 ◽  
Vol 40 (5-6) ◽  
pp. 204-208
Author(s):  
J. Lebl ◽  
Edith Schober ◽  
H. Frisch ◽  
Susanne Sagmeister ◽  
Gabriele H&auml;usler

2015 ◽  
Vol 112 (4) ◽  
pp. 1226-1231 ◽  
Author(s):  
Yuanyuan Zhang ◽  
Fei Fang ◽  
Joseph L. Goldstein ◽  
Michael S. Brown ◽  
Tong-Jin Zhao

Plasma growth hormone (GH) and hepatic autophagy each have been reported to protect against hypoglycemia in the fasted state, but previous data have not linked the two. Here we demonstrate a connection using a mouse model of fasting in a fat-depleted state. Mice were subjected to 1 wk of 60% calorie restriction, causing them to lose nearly all body fat. They were then fasted for 23 h. During fasting, WT mice developed massive increases in plasma GH and a concomitant increase in hepatic autophagy, allowing them to maintain viable levels of blood glucose. In contrast, lethal hypoglycemia occurred in mice deficient in the GH secretagogue ghrelin as a result of knockout of the gene encoding ghrelin O-acyltransferase (GOAT), which catalyzes a required acylation of the peptide. Fasting fat-depleted Goat−/− mice showed a blunted increase in GH and a marked decrease in hepatic autophagy. Restoration of GH by infusion during the week of calorie restriction maintained autophagy in the Goat−/− mice and prevented lethal hypoglycemia. Acute injections of GH after 7 d of calorie restriction also restored hepatic autophagy, but failed to increase blood glucose, perhaps owing to ATP deficiency in the liver. These data indicate that GH stimulation of autophagy is necessary over the long term, but not sufficient over the short term to maintain blood glucose levels in fasted, fat-depleted mice.


1974 ◽  
Vol 76 (3) ◽  
pp. 488-494 ◽  
Author(s):  
M. Peracchi ◽  
F. Cavagnini ◽  
A. E. Pontiroli ◽  
U. Raggi ◽  
A. Malinverni ◽  
...  

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.


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