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)

By using both immunofluorescence and peroxidase-anti-peroxidase procedures to detect cells producing the four islet hormones, supplemented by biochemical, biological, and radioimmunological assays of tissue extracts, it has been shown that insulin seems to be the most original hormone, apparently occurring already in invertebrates in cells of open type in the alimentary tract mucosa. Insulin cells also predominate in the first islet organ, namely that of the cyclostomes. The order of appearance in the endocrine pancreas during the subsequent evolution is: somatostatin; glucagon; and the pancreatic polypeptide. Even in lower vertebrates pancreatic polypeptide cells occur in those parts of the pancreas situated in close proximity to the gut.
J Histochem Cytochem 1979 Sep
PMID:Immunocytochemical studies of the evolution of islet hormones. 38 30

Pancreatic endocrine function was studied in 13 patients who had undergone massive bowel resection. The patients were divided into two groups: one month after operation (short-term group), and three or more months after operation (long-term group). Oral administration of glucose caused a persistent low insulin secretion in almost all the patients and the glucose tolerance curve showed a diabetic pattern in four. In contrast, the insulin response to intravenously infused arginine was impaired in the short-term group, but was at an approximately normal level in the long-term group. Pancreatic glucagon response to intravenous arginine, however, remained unchanged in both groups. Interruption of the enteroinsular axis as the result of massive bowel resection probably plays a major part in this discrepancy of the behaviour of insulin in the long-term group.
Gut 1979 Sep
PMID:Effect of massive bowel resection on enteroinsular axis. 38 43

Unspecific binding of immunoglobulins to gastrin G cells, glucagon A cells and somatostatin D cells of the gastric mucosa or pancreas, as well as to the calcitonin-somatostatin cells of rabbit thyroid has been found to occur through a non antigen-antibody mechanism mediated at least in part by the C1q fraction of complement. The phenomenon represents a major drawback in hormone immunohistochemistry, which can be prevented by incubating the specific anti-hormone sera with anti-C1q antibodies or with complement-fixing immunocomplexes.
Histochemistry 1979 Sep
PMID:Complement-mediated unspecific binding of immunoglobulins to some endocrine cells. 38 92

The direct effect of insulin on the secretion of insulin (as measured by C-peptide), glucagon, gastric inhibitory polypeptide, and gastrin was studied in normal subjects by infusing insulin while the plasma level of glucose was maintained in the normal fasting range (euglycemic clamp). Insulin-induced hypoglycemia resulted in increases in circulating glucagon and gastric inhibitory polypeptide, a decrease in C-peptide, and no change in gastrin levels. In contrast, during the euglycemic clamp, insulin was found to behave a direct suppressive effect on the secretion of glucagon, C-peptide, and gastrin, but no effect on levels of gastric inhibitory polypeptide.
J Clin Endocrinol Metab 1978 Sep
PMID:Direct effect of insulin on secretion of insulin, glucagon, gastric inhibitory polypeptide, and gastrin during maintenance of normoglycemia. 40 Jul 22

This study explored the relationship between metyrapone blockade of endogenous cortisol secretion and the plasma concentration of basal ketone bodies in insulin-dependent diabetic man. Endogenous cortisol secretion was reduced with metyrapone administration (as assessed by a reduction in plasma cortisol and an increase in deoxycortisol concentration) and then simulated with two different schedules of exogenous cortisol administration. Our results demonstrate that administration of metyrapone suppresses plasma cortisol concentration which may then be elevated by the oral ingestion of cortisol. The suppression of endogenous cortisol secretion with metyrapone results in a 50% reduction in basal plasma ketone body concentration. When endogenous cortisol secretion was simulated with the oral administration of 30 mg cortisol, plasma ketone body concentration returned to that concentration observed in the control study. When 60 mg cortisol were administered in divided dosages to the diabetic subjects, hyperketonemia resulted. These results suggest that the normal diurnal variation in plasma cortisol concentration may modulate the basal plasma ketone body concentration in diabetic man. The mechanism of this modulation may be a direct effect of cortisol or may be secondary to cortisol's lipolytic activity and/or its effects on elevating plasma glucagon concentration.
J Clin Endocrinol Metab 1978 Sep
PMID:Modulation of basal ketone body concentration by cortisol in diabetic man. 40 Jul 24

Oral glucose tolerance tests were done in eight insulin-requiring pancreatic diabetic patients to study the effect of withdrawal of insulin treatment on gut hormone release. Basal levels of gastric inhibitory polypeptide (GIP), glucagon-like immunoreactivity, and immunoreactive glucagon levels rose on insulin withdrawal, more so in patients on short-acting insulin, and were lowered by insulin treatment. Insulin treatment did not affect the GIP, glucagon-like immunoreactivity, or IRG responses to oral glucose. Improved glucose tolerance was greater in patients receiving soluble insulin than in those receiving lente insulin, and there was a significant positive linear correlation between basal plasma GIP and blood glucose levels in these patients. Therefore, it is suggested that insulin treatment lowers basal hormones levels, possibly via a metabolic effect, whereas the hormone responses to oral glucose may be controlled by several factors unrelated to insulin administration or changes in glucose homeostasis.
J Clin Endocrinol Metab 1978 Sep
PMID:Gastric inhibitory polypeptide in acquired pancreatic diabetes: effects of insulin treatment. 40 Jul 25

The cardiovascular effects of glibenclamide, gliclazide and carbutamide were studied on myocardial contractile force, cardiac output, mean arterial pressure and heart rate in 43 intact, 14 pancreatectomized and 18 adrenalectomized dogs. It is shown that a positive inotropic and hypertensive effect of hypoglycaemic sulphonylureas develops without the mediation of glucagon, insulin or adrenaline. Contrary to the other investigated sulphonylureas, glibenclamide reduced myocardial contractile force and arterial blood pressure.
Diabetologia 1977 Sep
PMID:The direct effect of hypoglycaemic sulphonylureas on myocardial contractile force and arterial blood pressure. 40 40

1) In electively immuno-induced carcinomas of the exocrine pancrease in Mice, where A (glucagon) and B (insulin) endocrine cells persist, cells with a pancreatic polypeptide immunoreactivity are also detected, even in late evolution stages. These cells, like D cells, containing somatostatin, are localized only in the pancreatic remains surrounding the anaplasic carcinomatous tissue: islets, adenomatous parenchyma, and ductular epithelium. Ultrastructure of these cells shows their active elaboration of numerous chracteristic secretion granules. (2) Immunocytoenzymatic detection of gastrin is negative in the exocrine and endocrine pancreatic tissues. However one of the anti-gastrin sera used gives a positive reaction, in some carinomatous cells only. Does this immunoreactivity characterize a polypeptide specific to the pancreatic carcinomatous cell?
C R Acad Hebd Seances Acad Sci D 1977 Sep 12
PMID:[Presence of "pancreatic polypeptide" cells, and gastrin immunoreactivity in immuno-induced exocrine pancreas carcinoma]. 41 May 28

The study was undertaken to assess the effects of glucagon on biliary tract opacification during intravenous cholangiography. Two series of infusion cholangiograms were obtained at two investigating centres designated A and B. In series A, 41 patients had ioglycamide infusions at a rate of 0.2833 g min-1 over 1 h. In series B, 31 patients had ioglycamide infusions at a rate of 0.3886 g min-1 over 30 min. Radiographs were taken in both series, immediately at the end of the infusion, 10 min later and 30 min after the infusion. Two mg of intravenous glucagon was injected into alternate cases in both series A and B immediately after the first radiograph was taken at the completion of the ioglycamide infusion. Two observers in each series than assessed the radiographic opacification of the biliary system without prior knowledge of which patients had received the glucagon. Delineation of the biliary system was considered better in both series in those patients who received glucagon when compared with the controls. Gallbladder opacification was definitely increased in series A in those receiving glucagon, and a similar tendency was shown in series B. The amount of contrast in the upper intestine was increased in series A in the glucagon group, but not in series B. It is concluded that glucagon improves visualisation of the biliary tract, especially the gallbladder at infusion cholangiography.
Clin Radiol 1979 Sep
PMID:The effect of glucagon on infusion cholangiography. 46 52

Bombesin acts within the brain to produce a prompt and sustained hyperglycemia, hyperglucagonemia, and relative or absolute hypoinsulinemia. Bombesin does not decrease plasma glucose turnover. Acute adrenalectomy but not hypophysectomy prevents hyperglycemia and hyperglucagonemia after intracisternal administration of bombesin. Administration of bombesin into the lateral ventricle of awake, unrestrained animals results in elevation of plasma glucose, preceded by a significant increase in plasma epinephrine and no increase in plasma norepinephrine or dopamine. Systemic administration of somatostatin prevents bombesin-induced hyperglycemia and hyperglucagonemia. These data support the conclusion that bombesin acts within the brain to increase sympathetic outflow resulting in increased adrenalmedullary epinephrine secretion, followed by depression of plasma insulin and elevation of plasma glucagon and glucose.
Endocrinology 1979 Sep
PMID:Central nervous system action of bombesin: mechanism to induce hyperglycemia. 46 25


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