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

The perfused pancreas of lean and obese Zucker rats was exposed, in the presence of L-leucine, to the anomers of D-glucose, which were administered on four successive occasions in the alpha/beta/alpha/beta or beta/alpha/beta/alpha sequence. In 5 lean and 6 obese rats, alpha-D-glucose was more efficient than beta-D-glucose in both stimulating insulin secretion and suppressing glucagon release. Although D-glucose evoked a greater release of insulin and, during prolonged exposure to the hexose, a less pronounced suppression of glucagon secretion in obese than lean rats, the anomeric specificity of these secretory responses was not different in the two groups of animals. In one lean rat, however, alpha-D-glucose, while efficiently stimulating insulin release, failed on two occasions to inhibit glucagon secretion. This isolated observation raises the possibility that the anomeric specificity of functional events evoked by D-glucose in the endocrine pancreas may occasionally be perturbed.
Pancreas 1987
PMID:Anomeric specificity of the insulin and glucagon secretory responses to D-glucose in lean and obese Zucker rats. 332 84

Glucagon is structurally related to secretin but inhibits the effects of secretin and cholecystokinin (CCK) on pancreatic secretion in vivo. Because secretin is a weak stimulant of pancreatic growth and potentiates the trophic effects of CCK, we hypothesized that glucagon might inhibit CCK-induced pancreatic growth. Four groups of 10 rats were injected with saline, glucagon (30 micrograms/kg, equimolar to a known trophic dose of secretin), cerulein (0.67 microgram/kg), or glucagon plus cerulein every 8 h for 5 days. The pancreas was excised, weighed, and assayed for total content of DNA, protein, amylase, chymotrypsinogen, and lipase. In control and glucagon-alone groups, the small intestine was also removed, weighed, and assayed for DNA, protein, and disaccharidase content. Glucagon alone decreased pancreatic DNA and increased lipase content. Compared with cerulein-treated animals, animals treated with glucagon and cerulein showed significant decreases in pancreatic weight and content of protein, amylase, and chymotrypsinogen. Although glucagon had significant effects on intestinal protein, maltase, and sucrase contents in certain segments, there was no clear pattern of response. The data suggest that glucagon may be an inhibitory regulator of pancreatic growth, acting to block the effects of CCK on pancreatic hypertrophy.
Pancreas 1988
PMID:Glucagon inhibition of cerulein-induced hypertrophy of the exocrine pancreas. 336 38

Pancreas was examined in 136 patients who died at the age of 7 to 89 years of various diseases including 22 with diabetes mellitus. Amyloidosis of its islands was observed in 9 patients (aged 49 and over); 6 out of them suffered from diabetes mellitus. Number of islands with amyloidosis and amyloid quantity were determined morphometrically. Glucagon-producing A-cells and insulin-producing B-cells in the islands not involved in amyloidosis were counted in sections impregnated by Grimelius. It is found that the development of diabetes is determined not only by the islands amyloidosis but by the quantitative domination of A-cells over B-cells in the islands without amyloidosis as well being the manifestation of aging processes.
 ...
PMID:[Amyloidosis of the pancreatic islets and diabetes mellitus]. 352 15

Pancreatic function was assessed prospectively in a group of 18 treated adult coeliac patients, most of whom were asymptomatic. The para-aminobenzoic acid (PABA) test indicated exocrine pancreatic insufficiency in three patients, all of whom had persisting gastrointestinal symptoms. Arginine, 5 g intravenously, was used to stimulate pancreatic islet cells; basal and stimulated concentrations of plasma insulin, C-terminal glucagon, N-terminal glucagon, and blood glucose did not differ from asymptomatic nondiabetic control subjects. After gluten withdrawal, coeliac patients who responded clinically had no evidence of significant pancreatic impairment, but consideration of exocrine pancreatic insufficiency is worthwhile in those patients with persisting symptoms.
Pancreas 1986
PMID:Endocrine and exocrine pancreatic function in treated coeliac disease. 355 22

The capacity of autotransplanted (ATP) distal pancreas segments with systemic venous and peritoneal exocrine drainage to support physiologic control of plasma glucose levels was tested, and compared with the functions of "simulated autotransplants" (SATP) prepared with similar dissection and peritoneal exocrine drainage, but with hepatic portal venous drainage, in dogs. In ATP in the postabsorptive state, plasma levels of glucose, immunoreactive insulin (IRI) and immunoreactive glucagon (IRG1) were normal. Autotransplants resulted in impaired glucose tolerance after meals with impaired early insulin responses, and the normal brisk rise of IRG1 in the plasma was delayed and reduced through the first 30 min of feeding. In ATP, also, the response to bombesin was abnormal; the normal stimulation of release of both IRI and IRG1 was delayed in both cases. In studies of responses to oral and intravenous glucose in ATP and SATP dogs, similar mild degrees of glucose intolerance were found with both routes of administration; however, whereas in ATP dogs increases of IRI were highly exaggerated with both routes of administration of glucose, in SATP dogs plasma IRI rose from subnormal levels in the postabsorptive state through subnormal increments with both routes of administration. Further studies are necessary to determine the relative importance of denervation and reduction of the mass of the pancreas in these effects, and to assess the significance of the differences in blood insulin levels in the two preparations.
Pancreas 1987
PMID:Pancreatic endocrine responses to nutrients and bombesin after segmental pancreas autotransplantation in dogs. 355 27

Two different antisera which specifically reacted with either the C- or N-terminal region of pancreas glucagon were employed to determine the concentration of glucagon and glucagon-like immunoreactivity in extracts from submaxillary glands of rats. The content of glucagon and glucagon-like immunoreactivity increased with age and was found to be higher in adult males than in females. Pancreas glucagon immunoreactivity constituted only a small proportion of the total glucagon-like immunoreactivity. The role that glucagon-like peptides present in the submaxillary gland of rats might play in the glucose homeostasis remains still unknown.
 ...
PMID:Differences in the content of glucagon-like immunoreactivity in rat submaxillary glands. 374 42

Pancreas isotransplantation was performed on streptozotocin-diabetic Wistar rats. To study the influence of the graft on diabetic hyperglucagonemia, immunoreactive glucagon (IRG) and its response to alanine (peak IRG) were determined in peripheral blood at intervals for up to 8 months after the transplantation. Concentrations of IRG and immunoreactive insulin (IRI) in effluent blood from host pancreas (portal vein) and graft (caval vein) were measured 4 months after the transplantation to estimate the hormone release from both organs. Following transplantation, caval IRI increased sixfold. Portal IRI increased 180% and reached 65% of the concentration observed in control rats. Peripheral basal and peak IRG were initially restored to normal, but were later increased to levels equal to those of diabetic rats. Also portal and caval IRG concentrations were similar in recipients and diabetic rats. The results show that relatively small amounts of glucagon are released from the graft, and that the exaggerated glucagon release from the host pancreas is only transiently normalized following pancreas transplantation.
 ...
PMID:Long-term effect of pancreas transplantation on diabetic hyperglucagonemia. 674 10

Pancreatic-type glucagon (PTG) has been found in the plasma of totally pancreatectomized human beings. Arginine infusion, however, caused no increase in PTG. Pancreas-resected patients had a normal response of PTG to arginine and a subnormal increase in C peptide. Gut glucagon-like immunoreactants (gut GLI) were increased in resected patients and further increased in totally pancreatectomized patients. Gut GLI showed no change during arginine stimulation.
 ...
PMID:Immunoreactive glucagon and insulin C-peptide in man after resection of the pancreas and total pancreatectomy. 699 5

Glucagon-like peptide-I (GLP-I) is a potent incretin hormone that is now considered as a new therapeutic tool in the treatment of diabetes mellitus. In this study we characterized the effects of GLP-I on peptide hormone release from isolated human pancreatic islets. GLP-I stimulated insulin release in the presence of 10 mM glucose (2.8 mM glucose, 100%; 10 mM glucose, 166%; 10 mM glucose + 10 nM GLP-I, 222%) but had only a weak insulinotropic effect (128%) at 2.8 mM glucose. Glucagon release was inhibited by 10 mM glucose (2.8 mM glucose, 100%; 10 mM glucose, 72%) and by 10 nM GLP-I at 2.8 mM glucose (67%). Somatostatin secretion was increased by 10 mM glucose (2.8 mM glucose, 100%; 10 mM glucose, 166%). GLP-I stimulated somatostatin release in the presence of 2.8 mM glucose (172%). Pancreatic polypeptide (PP) secretion was enhanced by 10 mM glucose (2.8 mM glucose, 100%; 10 mM glucose, 236%). GLP-I induced PP release only in the presence of 2.8 mM glucose (184%).
Pancreas 1995 Aug
PMID:The effects of glucagon-like peptide-I (GLP-I) on hormone secretion from isolated human pancreatic islets. 747 79

The metabolic response to graded decreases in insulin concentration was evaluated by measuring the concentration, production, and metabolic clearance rate of glucose in response to the infusion of different galanin doses (1-12 micrograms/kg/h) in 18-h fasted dogs. Peripheral and portal concentrations of insulin and glucagon were measured simultaneously before, during, and after galanin infusions. No increases in portal or peripheral glucagon levels were seen at any dose of galanin infused but, in contrast, dose-dependent decreases of insulin levels occurred in both circulations. The metabolic clearance rate of glucose fell by approximately 25-30% at each dose of galanin infused; suggesting that the maximum effect was reached at the lowest dose. The rate of glucose production increased in a dose-dependent manner with integrated responses of 210 +/- 170, 620 +/- 80, 1,330 +/- 440, 1,920 +/- 310, 1,940 +/- 170, and 1,970 +/- 600 mg/kg at galanin doses of 1, 2, 4, 7, 10, and 12 micrograms/kg/h respectively; saturation of this response occurs at the 7 micrograms/kg/h dose of galanin. The changes in glucose production reflect most closely changes in the fractional decrease in insulin levels both in the portal and peripheral circulations. These changes appear to be mediated by insulin acting directly on the liver, because no alterations in the concentrations of the glucogenic substrates, lactate and glycerol, were seen.(ABSTRACT TRUNCATED AT 250 WORDS)
Pancreas 1994 Jul
PMID:Differential effects of a graded selective suppression of insulin secretion with galanin on glucose production and removal in dogs. 752 64


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>