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)

Growth hormone release-inhibiting hormone (somatostatin), a hypothalamic peptide that inhibits the release of growth hormone and also the secretion of insulin glucagon, and gastrin, was found in the rat stomach and pancreas in a concentration similar to that in the hypothalamus, as measured by radioimmunoassay. Somatostatin was also found in the duodenum and jejunum, but in a smaller concentration. Gel filtration of the extracts of the pancreas and stomach on Sephadex G-25 yielded two immunoreactive peaks, one corresponding in each case to the somatostatin tetradecapeptide. The hormone was not detected in other viscera or the ovaries. The results imply that somatostatin may be synthesized in the pancreas and the stomach in addition to the brain, and may be involved in local regulatory mechanisms for pancreatic and gastric secretion as well as secretion of growth hormone.
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PMID:Somatostatin: abundance of immunoreactive hormone in rat stomach and pancreas. 5 79

The parathyrin receptor in renal cortex has been investigated by studying the binding of 125I-labelled parathyrin, or of unlabelled parathyrin detected with 125I-labelled antibodies, to a partially purified plasma membrane fraction. The kinetics of hormone uptake demonstrated a biphasic response in both systems at 22 degrees C but this phenomenon was not detectable at 37 degrees C. Specific displacement of lactoperoxidase labelled 125I-labelled parathyrin occurred with 8 ng unlabelled bovine parathyrin. The apparent affinity constant was 2.3-10(8) M(-1) and the apparent binding capacity of the membranes 1.25 pmol/mg protein. Using the labelled antibody technique the receptor showed maximal binding at pH 7.0-7.5. As little as 80 pg bovine parathyrin produced a significant increase in binding of labelled anti-bovine parathyrin antibody and saturation of binding sites was demonstrated at 2.5 pmol/mg protein. Oxidized hormone showed undetectable binding. Treatment of membranes with phospholipases A or D, or Trypsin greatly reduced subsequent hormone binding. Prior incubation of membranes with 1-34 synthetic parathyrin decreased the binding of intact hormone whereas gastrin, insulin and glucagon had no effect. Growth hormone and calcitonin slightly increased parathyrin binding.
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PMID:Characterization of the parathyrin receptor in renal plasma membranes by labelled hormone and labelled antibody binding techniques. 17 66

The glucose, insulin, and adenosine 3',5'-monophosphate (cyclic AMP) responses to intravenous glucagon were found to be impaired in growth hormone deficient children. The delta plasma glucose response in 22 normal children was 54.5 mg/dl compared to 38.4 mg/dl in the 11 growth hormone deficient children; t = 2.74, P less than 0.02. For serum insulin, the comparative values were 65.3 muU/ml (n = 20) vs. 29.8 muU/ml (n = 11); t = 3.03, P less than 0.01. For urinary cyclic AMP, the comparative values were 0.46 mumol/m2 (n = 22) vs. 0.18 mumol/m2 (n = 10); t = 2.48, P less than 0.02. Growth hormone therapy resulted in a significant improvement in the glucose, insulin, and cyclic AMP responses to intravenous glucagon in the growth hormone deficient group of children.
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PMID:Impaired glucose, insulin, and adenosine 3',5'-monophosphate responses to glucagon in growth hormone deficient children. 18 73

Growth hormone secretion has been evaluated in patients with Addison's disease given T.R.H., A.C.T.H. or Glucagon i.v., or L-DOPA p.o. In those with the idiopathic, auto-immune variety the mean response to glucagon and L-DOPA was reduced when compared with that documented for patients in whom tuberculosis caused the lesion. Growth hormone plasma concentrations barely changed after T.R.H. and A.C.T.H., irrespective of the aetiology of the disease.
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PMID:Growth hormone secretion in Addison's disease. 21 Jul 6

Five insulin-dependent diabetics with poor metabolic control were examined at the beginning and after a three-day application of artificial endocrine pancreas (AEP). Pancreatic alpha cell function evaluated by arginine infusion (0.5 g/Kg b.w. over 30 minutes) showed no significant differences between the beginning and during artificial beta cell aplication, but the increment in plasma glucagon level over basal values observed in both tests appeared significantly higher at 30 and 60 min in comparison with a control group. Growth hormone response to arginine infusion was clearly reduced in the second test. C-peptide concentration appeared very low in basal conditions and during arginine infusion; no improvement was observed after three days of AEP application. Urinary excretion of norepinephrine markedly increased at the beginning of the study, reversed almost to normal during AEP treatment, while minor changes were observed in urinary excretion of epinephrine. The Concentration of glycosylated hemoglobin, markedly higher than normally before the connection with AEP, showed a slight but significant decrease during glucose-controlled insulin infusion. Finally, 2,3-diphosphoglycerate was normal and no modifications were observed in the course of the study.
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PMID:Variation induced by a three-days application of the artificial beta-cell on glucagon, growth hormone and catecholamine secretion, glycosylated hemoglobin, and erythrocyte 2,3-diphosphoglycerate concentration. 39 95

Glucagon, growth hormone, and cortisol secretion was studied in seven male insulin-dependent diabetics under conventional subcutaneous insulin therapy and after three days of blood glucose normalization attained by the artificial endocrine pancreas (Biostator-GCIIS). The diurnal hormonal profiles under the two types of therapy were compared. Six healthy male students served as control group. A three-day period of blood glucose normalization in insulin-dependent diabetic can restore glucagon secretion to normal. Growth hormone secretion is decreased but not completely normalised. Cortisol secretion is slightly decreased. It is concluded that prolonged normoglycemia achieved by means of an artificial endocrine pancreas may completely control endocrine abnormalities in insulin-dependent diabetics.
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PMID:The effect of three days of blood glucose normalization by means of an "artificial endocrine pancreas" on the concentrations of growth hormone, glucagon, and cortisol in juvenile diabetics. 39 97

The effect of intravenous somatostatin on blood levels of metabolites and hormones has been examined in normal subjects who performed a 30-minute period of bicycle exercises at 70% maximal exercise capacity. The results have been compared with control studies in the same subjects. Measurements were made of blood levels of lactate, glucose, free fatty acids, glycerol, acetoacetate, 3-hydroxybutyrate, insulin, glucagon, growth hormone (hGH) and prolactin. Growth hormone and glucagon release were suppressed during exercise with somatostatin and there was a subsequent elevation during recovery. There was slight post-exercise depression of insulin, but no alteration of plasma prolactin secretion. Blood glucose was reduced during exercise with somatostatin and increased during recovery. The elevation of ketone bodies after exercise was greater in the investigation with somatostatin, but there were no significant changes in other metabolites. Somatostatin, although causing inhibition of hGH release, appeared to have no significant effect upon fatty acid mobilization during exercise.
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PMID:The effect of somatostatin on metabolic and hormonal changes during and after exercise. 47 77

In a group of aged nondiabetic and diabetic subjects and in a group of young subjects the glycemic, insulin, growth hormone and glucagon response to intravenous arginine was studied. A prompt increase in blood glucose, serum insulin and glucagon levels was observed, but glucose and glucagon peaks were significantly higher in older non diabetic and diabetic subjects. Growth hormone secretion did not show any difference between aged nondiabetic and young subjects, on the contrary it is lower in diabetics. These findings might suggest the hypothesis of the glucose intolerance during old age due to increased release of glucagon.
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PMID:[Raised glucagon levels of the blood induced by arginine: relation to blood sugar, blood insulin and STH in aged non-diabetics and diabetics]. 66 51

Growth hormone injected daily in 6 dogs for 6 days caused a 20-fold elevation in fasting serum immunoreactive insulin (IRI) without appreciable change in serum glucose in 1 day. In the somatotrophic diabetes that occurred after 2 days, the hyperinsulinaemia was maintained and the serum IRI/glucose (I/G) ratio declined from the early high level but remained elevated. During this treatment, in response to glucose infusion, the rise in serum IRI above the initially high fasting level was 16 times the normal. In response to glucagon, the rise in IRI was twice the normal and the rise in glucose was more prolonged, resulting in a decline in the I/G ratio. In response to arginine infusion, the rise in serum IRI was 8 times the normal and the rise in the I/G ratio was twice normal. Following a meal, the rise in serum IRI was 8 times the normal. Thus, with growth hormone treatment the insulin secretory responses to these stimulating factors were magnified over the already elevated fasting level of secretion. The insulin content of the pancreas was reduced to less than 10% of normal by growth hormone treatment for 6 days, due apparently to elevation of the rate of secretion over the rae of formation of insulin.
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PMID:Somatotrophic diabetes: insulin release responses to arginine and glucagon in dogs. 70 Feb 82

We report a female small for date neonate, who developed transient diabetes mellitus (TDN) five days after birth and required insulin therapy for five weeks. At the onset of the disease, plasma insulin concentration was extremely low. At four weeks of age, after insulin withdrawal, the patient was still hyperglycemic, and basal insulin values assayed over a period of 24 h were mostly inadequate. Glucagon secretion was not suppressed. Growth hormone levels were lower than those of three small for date infants of the same age. At three months of age, the patient was still intolerant to an oral glucose load, insulin secretion remained inadequate while glucagon paradoxically increased 30 min after glucose challenge. The oral glucose tolerance values were in the normal range at six months of age. We conclude that TDN is caused by a transitory defect of insulin secretion, which would also explain the glucagon response as a consequence of insulin deficiency. We found no evidence associating the insulin antagonists observed in our study with the pathogenesis of this illness.
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PMID:[Transient diabetes mellitus in a dystrophic newborn infant]. 71 99


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