Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma glucagon and insulin responses to L-arginine were compared in normal controls and patients with isolated growth hormone deficiency and acromegaly. Patients with isolated growth hormone deficiency were characterized by high plasma glucagon response and low plasma insulin response, whereas acromegalic patients showed exaggerated plasma glucagon response and almost normal insulin response. These results suggest that growth hormone is probably required for optimum function of the islets, and since hyperglucagonaemia was observed in both growth hormone deficiency and acromegaly, metabolic disturbances stemming from the respective primary diseases may affect glucagon secretion.
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PMID:Growth hormone modulation of arginine-induced glucagon release: studies of isolated growth hormone deficiency and acromegaly. 74 97

The effects of intravenous infusion of arginine (20 g/m2) after an overnight fast on plasma immunoreactive growth hormone (GH), insulin (IRI), and glucagon (IRG), and blood glucose were examined in five groups of children and adolescents: 10 normal individuals, 18 with idiopathic short stature, 6 with isolated growth hormone deficiency, 8 with panhypopituitarism, and 6 with anorexia nervosa. The mean fasting plasma GH concentration was significantly elevated in the group with anorexia nervosa (P less than 0.05), and similar to the value for the normal group in all other groups. After arginine infusion, four- to sixfold increases of plasma GH were observed in the normal children, and similar increases were seen in those with idiopathic short stature as well as in those with anorexia nervosa; whereas, in the children with isolated growth hormone deficiency or panhypopituitarism, there was no significant increase in plasma GH. Fasting blood glucose concentrations were significantly lower than normal in subjects with isolated growth hormone deficiency (P less than 0.05), panhypopituitarism (P less than 0.001), and anorexia nervosa (P less than 0.001), whereas fasting plasma IRI and IRG concentrations were similar to the values in the normal group. Plasma IRI increased eightfold at the end of the 30-min arginine infusion in the normal subjects; the increase was slightly but not significantly less in those with idiopathic short stature, and significantly less in those with isolated growth hormone deficiency (P less than 0.05), panhypopituitarism (P less than 0.001), and anorexia nervosa (P less than 0.05). Arginine infusion resulted in two- to threefold increases of plasma IRG in the normal group, and similar increases were observed in all of the other groups tested. These results suggest that whereas pancreatic beta cell responsiveness may be deficient in children and adolescents with isolated growth hormone deficiency, panhypopituitarism, or anorexia nervosa, pancreatic alpha cell responsiveness, to arginine at least, appears to be intact under these conditions.
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PMID:Plasma growth hormone, insulin, and glucagon responses to arginine infusion in children and adolescents with idiopathic short stature, isolated growth hormone deficiency, panhypopituitarism, and anorexia nervosa. 110 71

Patients suffering from deletions of chromosome 18 (p-, q-) show regularly short stature. Endocrinological investigations were performed to prove if short stature is due to pituitary insufficiency. In three female patients with deletions of chromosome 18 and retarded bone age serum growth hormone was investigated after insulin induced hypoglycemia, after glucagon-propranolol and after stimulation with growth hormone releasing hormone. Thyroid function, gonadal function and adrenal function were investigated too. All three patients showed growth hormone deficiency. In one patient there were found in addition hypothyroidism and gonadotrophine deficiency as well. In conclusion growth failure in some patients with deletions of chromosome 18 seems to due to pituitary insufficiency. In these patients treatment with recombinant growth hormone may increase growth velocity.
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PMID:[Endocrinologic disorders in deletion of chromosome 18]. 161 60

Responses of serum growth hormone (hGH) to glucagon (G), growth hormone releasing hormone (GHRH) and G/GHRH were measured in 8 normal adults and 6 patients with growth hormone deficiency (GHD). In normal adults, serum hGH reached its peak value (12.7 +/- 1.6 ng/ml) at 150 +/- 10 min, as blood glucose declined to its minimum after a transitory hyperglycemia in G test. The normal adults were responsive to GHRH test (GH peak 14.7 +/- 2.3 ng/ml at 30 +/- 0 min). In GHD, the responders to both G and GHRH tests showed a strongly positive response in G/GHRH test, with a serum hGH peak value of 34.6 +/- 4.1 ng/ml at 131 +/- 8 min being much higher than that of either single G or GHRH test (P less than 0.01), but without significant difference to the sum of the two single tests (P greater than 0.10). Among GHD patients, only 2 responded to GHRH and G/GHRH tests with hGH peak values 6.8 +/- 0.7 and 6.9 +/- 0.7 ng/ml at 45 +/- 15 and 90 +/- 0 min, respectively, both peak values being essentially similar (P greater than 0.10). We suggest that the mechanism of stimulation of pituitary hGH secretion in G test might involve inhibition of release of hypothalamic GH release inhibiting factor (GHRIF) caused by hypoglycemia after a transitory hyperglycemia following G injection. These results may further confirm our previous postulation (1986) that insulin hypoglycemia may increase hGH release by inhibiting hypothalamic cell secretion of GH release inhibiting factor.
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PMID:Reduction of the effects of growth hormone release inhibiting factor enhances plasma growth hormone response to GHRH. 256 70

The response of growth hormone, cortisol, and catecholamines to hypoglycaemia produced by a continuous intravenous infusion of insulin was investigated in 10 normal subjects and 15 patients with pituitary disease. The insulin infusion rate was started at 2 U/hour for adolescents, 4 U/hour for adults, and 6 U/hour for patients with acromegaly. If required the rate was increased during the test depending on changes in blood glucose, measured by a Reflomat with low reading glucose oxidase strips. Stopping the infusion when the blood glucose concentration had fallen to 2.0 mmol/l (36 mg/100 ml) resulted in a maximum further fall of 0.7 mmol/l (13 mg/100 ml) and a subsequent spontaneous rise in blood glucose concentration. The rise was identical in normal subjects and in patients with hypopituitarism, further evidence that pituitary hormones--in contrast to glucagon and catecholamines--are relatively unimportant in the recovery from hypoglycaemia. The only patient who required intravenous glucose to restore normoglycaemia was a patient with longstanding insulin dependent diabetes. A comparison with the conventional bolus injection test showed that continuous intravenous insulin infusion was more reliable in producing adequate but not excessive hypoglycaemia and the hormone responses were equivalent. The continuous intravenous insulin infusion may offer particular advantages in the investigation of growth hormone deficiency.
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PMID:Testing the anterior pituitary: hypoglycaemia produced by continuous intravenous insulin infusion. 641 Dec 30

A 5-year-old male with the Aarskog syndrome is described. He had abnormal facies, short stature, short fingers with interdigital webbing, a saddle type scrotum and mild mental retardation. In addition, he had isolated growth hormone deficiency as evidenced by the insulin, arginine, and propranolol-glucagon tests. An arginine test after short-term stimulation with estrogen further supported this diagnosis. His mother had minor abnormalities of the hands and feet, and slight mental retardation.
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PMID:Aarskog syndrome with isolated growth hormone deficiency. 722 81

A total of 5,473 pharmacological provocative growth hormone release tests were carried out in 3,143 children. Mean age was 9 years 9 months (range 3-16 years) and mean bone age was 7 years 6 months (range 2-14 years). Tests were of 9 different types: 1) arginine (n = 625); 2) clonidine (n = 339); 3) insulin (n = 198); 4) ornithine (n = 162); 5) insulin + arginine (n = 203); 6) clonidine + betaxolol (n = 2,003); 7) L-dopa (n = 685); 8) glucagon = propranolol (n = 443); 9) glucagon + betaxolol (n = 815). All growth hormone determinations were performed using the same radioimmunoassay. Distribution of values obtained with each test was gausso-logarithmic. Mean peak levels with their 95% confidence limit were as follows: 1) 10.2 and 0.45; 2) 11.5 and 0.7; 3) 11.8 and 0.8; 4) 14.2 and 1.2; 5) 14.3 and 0.9; 6) 15.7 and 1.1; 7) 19.8 and 2.1; 8) 20.8 and 2.3; 9) 21.0 and 2.5. These data indicate low specificity, with up to two-fold differences in mean peak levels from one test to another; proportions of peaks under 10 ng/ml ranged from 29% to 69%. Thus, the rate of patients diagnosed with growth hormone deficiency may vary substantially according to the test used. To reduce these discrepancies, we suggest adjustment of test results using a weighting coefficient of 1) 1.9; 2) 1.48; 3) 1.4; 4) 1.16; 5) 1.06; 6) 1.01; 7) 0.73; 8) 0.69; 9) 0.66.
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PMID:[Statistic study of 5,473 somatotropin secretion stimulation pharmacologic tests (n=9). Proposed weighting coefficient]. 823 89

To determine whether the increases in growth hormone that occur during sleep alter carbohydrate tolerance the following morning, two groups of volunteers were studied on two occasions. In one group saline alone was injected and infused (i.e. no octreotide) on one occasion and on the other octreotide was injected at 23.00 hours to inhibit endogenous growth hormone secretion followed by saline infusion to create a state of relative nocturnal growth hormone deficiency. In the other group the octreotide injection was followed on one occasion by a constant growth hormone infusion designed to maintain growth hormone concentrations at "basal" levels throughout the night whereas on the other it was followed by a constant infusion plus two supplemental growth hormone infusions given at midnight and 02.30 hours to mimic the normal nocturnal rise in growth hormone. The next morning, subjects were fed a radiolabelled mixed meal. The differences in the nocturnal growth hormone concentrations had no effect on the glucose, insulin, C-peptide and glucagon concentrations following breakfast ingestion nor did they alter postprandial rates of glucose production, disappearance or substrate oxidation. Thus, the normal nocturnal rise in growth hormone does not appear to be an important regulator of carbohydrate tolerance the following morning.
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PMID:Failure of nocturnal changes in growth hormone to alter carbohydrate tolerance the following morning. 975 25

Beta-cell function in growth hormone (GH)-deficient (GHD) adults is poorly documented. Beta-cell function was therefore studied in 10 GHD adults (age, 40+/-3 years; weight, 79.3+/-4.8 kg; body mass index [BMI], 27.5+/-1.3 kg x m(-2)) before and after 6- and 24-month recombinant human GH (rhGH) therapy (0.24 IU x kg(-1) x wk(-1)) compared with 10 age-, sex-, weight-, and BMI-matched control subjects. With rhGH therapy, fat-free mass (FFM) increased (48.2+/-4.9, 52.5+/-4.8, and 59+/-6.8 kg, respectively) and fat mass (FM) decreased (33.8%+/-2.8%, 28.0%+/-3.0%, and 29.4%+/-2.5%, respectively), as did serum cholesterol. Oral glucose tolerance initially deteriorated at 6 months, but improved toward the control value by 24 months. Fasting insulin (FI) increased significantly, as did the acute insulin response to oral glucose (deltaAIR(OGTT)/deltaG) at 30 minutes (FI: pretreatment 9.8+/-0.8, 6 months, 14.0+/-1.8, 24 months 12.5+/-1.6 v control 11.4+/-1.9 mU x L(-1); deltaAIR(OGTT)/deltaG: pretreatment 201+/-24, 6 months 356+/-41, 24 months 382+/-86 v control 280+/-47 mU x mmol(-1)). However, the acute insulin response to intravenous (IV) glucose (AIR(G)) and IV glucagon at euglycemia and hyperglycemia did not change with rhGH therapy and were similar to the control group values. Importantly, the expected reciprocal relationships (as observed for the control group) between the various insulin secretory parameters and insulin sensitivity (SI) either were not present or were statistically weak in GHD subjects, despite the 35% decrease in SI by 24 months of rhGH therapy. In particular, over time, there was an attenuation of insulin secretion with respect to the ongoing insulin resistance with rhGH therapy, particularly for AIR(G) at 24 months. After 5 days of rhGH withdrawal, insulin secretion decreased and SI improved in GHD subjects. It is concluded that the current long-term rhGH treatment regimens appear to impact on insulin secretion such that the normal relationships between insulin secretion and SI are altered despite the favorable impact on body composition and serum lipid profiles.
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PMID:Insulin secretion in growth hormone-deficient adults: effects of 24 months' therapy and five days' acute withdrawal of recombinant human growth hormone. 1058 46

The aim of this study was to evaluate the 24-h pattern of blood pressure in adults with growth hormone deficiency using ambulatory blood pressure monitoring. We therefore evaluated the mean systolic and diastolic blood pressures, systolic and diastolic blood pressure loads and diurnal blood pressure rhythm. We used an auscultatory-type monitor, the measurements being made at 10-15 min intervals during the day and 20-30 min intervals at night. We included patients with a growth hormone peak of less than 3 ng/ml in at least two stimulation tests: the insulin tolerance and glucagon tests. The exclusion criteria were mental illnesses, pregnancy, diabetes mellitus, blood pressure higher than 160/90 mmHg, the use of growth hormone in the previous 12 months, severe acute illnesses, chronic liver or kidney disease and a history of malignancy. The results were interpreted according to the II Brazilian Consensus for the utilization of ambulatory monitoring. The study population comprised 27 adult patients with growth hormone deficiency, 11 male and 16 female, with an age range of 21-62 years. Five had developed the condition during childhood, whereas the remainder had adult-onset growth hormone deficiency. The mean systolic (115 +/- 16.7 mmHg) and diastolic blood pressure loads (75.51 +/- 1.90 mmHg) were normal. There was a tendency towards a lower blood pressure in patients with childhood-onset growth hormone deficiency when compared with their adult-onset counterparts. Men had a lower systolic blood pressure than women, the same pattern being found for mean diastolic blood pressure. Multiple regression analysis showed that age was the only independent variable with the statistical power to explain the variance of blood pressure in this group of patients. The incidence of non-dippers was 37.03%. Growth hormone deficiency thus seems to be associated with a change in the 24-h blood pressure pattern, with a high incidence of non-dippers.
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PMID:Ambulatory monitoring of blood pressure in growth hormone-deficient adults. 1204 25


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