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)

To evaluate beta-cell function in patients with pancreatic cancer, the glucagon stimulation test was performed in seven patients with pancreatic adenocarcinoma, seven patients with type I diabetes mellitus, seven patients with type II diabetes mellitus, and in seven healthy controls. C-peptide serum levels were determined before and after a 1-mg i.v. glucagon injection. Basal C-peptide values were normal or slightly increased in pancreatic cancer and type II diabetic patients and low in type I diabetic patients. Following glucagon stimulation, no significant increase was observed in C-peptide values of type I diabetics and pancreatic cancer patients, whereas significant increases occurred in controls and type II diabetics. It is concluded that the altered beta-cell function found in pancreatic cancer patients may lead to hyperglycemia, which is frequently associated with this tumor type.
Pancreas 1994 May
PMID:Beta-cell function in pancreatic adenocarcinoma. 802 55

Effects of prostaglandin (PG) E1 on ischemia-reperfusion (I-R) injury to the pancreas was evaluated using isolated in vivo perfused dog pancreas. Pancreatic endocrine and exocrine functions were stimulated with 10(-12) M cholecystokinin octapeptide (CCK-8). This amount of CCK-8 promoted production of insulin, glucagon, PGI2, and thromboxane (Tx) A2 in the pancreas. Sixty minutes of ischemia and subsequent reperfusion induced damage to pancreatic ductular, acinar, and beta cells. Intra-arterial administration of PGE1 at a dose of 0.5 microgram/kg/min throughout the experiment prevented the I-R injury, reducing plasma lipid peroxides, and elevating PGI2 without changing TxA2 in the pancreas. PGE1 thus appears to protect pancreatic function from I-R injury both by depressing the effect of free-radicals and by decreasing TxA2/PGI2 which predicts cell injury.
Pancreas 1994 May
PMID:Prostaglandin E1 protects dog pancreas from ischemia-reperfusion injury. 802 58

In a prospective clinical-experimental study, 15 consecutive patients with chronic pancreatitis, operated on because of severe pain, were examined for the effects of a duodenum-preserving resection of the pancreas head on endocrine pancreas function. This was done by means of oral and intravenous glucose tolerance testing before the operation, on the 10th or 11th day postoperatively, and 3 months after the operation. In addition to glucose levels in the peripheral venous blood, levels of insulin, C-peptide, glucagon, and pancreatic polypeptide were determined. As indicated by the k value, glucose tolerance improved postoperatively in 10 patients (66.6%); three patients (19.9%) showed no change, and one patient (6.6%) was worse. Only one patient (6.6%) developed evident diabetes mellitus immediately postoperatively. Pre- and postoperative levels of insulin and C-peptide showed no significant differences. The fasting levels of glucagon were significantly lower postoperatively than before the operation (p < 0.01). The stimulation of pancreatic polypeptide after oral glucose was significantly lower postoperatively (p < 0.01). Duodenum-preserving pancreas head resection does not lead to an impairment of glucose tolerance in the majority of patients; a deterioration was observed only in few cases (13.3%).
Pancreas 1994 Jan
PMID:Glucose homeostasis and endocrine pancreatic function in patients with chronic pancreatitis before and after surgical therapy. 810 71

This study determined whether in vivo endotoxin treatment alters the ability of epinephrine to inhibit immunoreactive insulin (IRI) secretion or to stimulate immunoreactive glucagon (IRG) secretion from the in vitro perfused rat pancreas preparation. Insulin and glucagon secretion were measured from pancreases obtained from control and endotoxin-treated rats. The pancreases were perfused with 240 mg/dl glucose in the presence and the absence of 13.6 nM epinephrine. The absolute ability of epinephrine to inhibit glucose-induced IRI secretion was similar for both "control" and "endotoxic" pancreases. However, since endotoxic pancreases hypersecrete insulin, the relative ability of epinephrine to inhibit insulin secretion was reduced in endotoxic compared with control pancreases. Epinephrine did not appreciably alter IRG secretion in control pancreases. However, epinephrine prevented a progressive decrease in IRG secretion in endotoxic pancreases. The results suggest that the relative inability of epinephrine to inhibit the excess insulin secretion due to endotoxin treatment contributes to endotoxin-induced hyperinsulinemia. Furthermore, the additional observation that epinephrine supported glucagon secretion in the endotoxic pancreas in the face of high glucose levels suggests epinephrine may play a deleterious role with respect to glucose homeostasis during endotoxicosis. The results provide a partial mechanism to explain endotoxin-induced hyperinsulinemia and also demonstrate a possible role for epinephrine with regard to the production of elevated glucagon levels during endotoxicosis.
Pancreas 1993 Jul
PMID:The effect of epinephrine on insulin and glucagon secretion from the endotoxic rat pancreas. 836 65

The long-term effects of streptozotocin (30-70 mg/kg) were studied on plasma glucose and insulin levels, islet morphology, and glucose-stimulated insulin secretion in rats. In addition, the protective effect of short-term (7 days) insulin treatment on streptozotocin-induced diabetes was examined. Streptozotocin administration at dose levels exceeding 40 mg/kg resulted in a long-term, stable hyperglycemia with no insulin response to glucose at 3 months and with a marked derangement of islet morphology (few insulin cells, accumulation of glucagon cells). In contrast, at 30 and 40 mg/kg, streptozotocin induced a transient diabetes. Thus, the blood glucose levels, being elevated at days 1-7, returned to normal levels within 10 days after streptozotocin administration and the glucose-induced insulin secretion, being absent at day 1, was normal at 3 months. Furthermore, the islet morphology was also normal in these groups at 3 months. Short-term (7 days) insulin treatment normalized the long-term diabetes in rats given 50 mg/kg streptozotocin, but not in rats given 60 or 70 mg/kg streptozotocin. Thus, after insulin treatment, all rats receiving 50 mg/kg streptozotocin returned to normoglycemia within the following 2 weeks, and the glucose-induced insulin secretion was normal after 3 months, as was islet morphology.(ABSTRACT TRUNCATED AT 250 WORDS)
Pancreas 1993 Jan
PMID:Long-term diabetogenic effect of streptozotocin in rats. 841 9

Insulin and glucagon metabolism in the pancreas with obstructive jaundice caused by complete ligation of the common bile duct and in the cholestatic liver caused by hepatic duct ligation was evaluated experimentally using dogs. The isolated perfused pancreas in obstructive jaundiced dogs, which showed a low insulin response in the peripheral blood after intravenous glucose administration, revealed depression of insulin production and no change of glucagon production in response to cholecystokinin octapeptide. The extraction of insulin in the cholestatic lobe of the liver was decreased compared with that in the noncholestatic lobe. The extraction of glucagon, on the other hand, in the cholestatic lobe and in the noncholestatic lobe showed no significant difference. So the imbalance of glucose metabolism in obstructive jaundice does not depend on the enhanced extraction of insulin in the liver, but on the depression of insulin production in the pancreas.
Pancreas 1993 Mar
PMID:Metabolism of insulin and glucagon in liver and pancreas in dogs with obstructive jaundice. 846 Jan 1

The nonobese diabetic (NOD) mouse is an animal model that shares a number of clinical, genetic, and immunologic characteristics with human insulin-dependent diabetes mellitus. Since little is known about the morphometric cell profiles in the endocrine pancreas of these NOD animals, it was of interest to assess their changes in morphometry within the pancreatic islet cell types during two stages of this syndrome. Prediabetic (6-week-old) and diabetic (16-week-old) NOD female mice, as well as normal C57BL/6 female mice (15 weeks old), were used. Light microscopic immunocytochemical and morphometric methods were employed to study the endocrine cell populations. The immunoperoxidase technique for the identification of insulin, glucagon, somatostatin, and pancreatic polypeptide, as well as the point-counting method, was used on serial sections of pancreas tissue. Compared to those of normal and prediabetic mice, pancreata from diabetic animals showed a decrease in both the number of islets and the volume density of the endocrine component. Analysis of islet tissue revealed a significant diminution of B-cell volume density, as well as an increased A-, D-, and PP-cell volume density. A parallel variation in the number of B and non-B cells was also found. In addition, when the total pancreatic tissue surface was taken as reference, the fractional area occupied by all the different types of islet cells was seen to be diminished in a variable fashion. We conclude that the diabetic syndrome of NOD mice not only severely affects the B-cell mass, but also causes marked changes in the non-B endocrine-cell populations.
Pancreas 1995 Nov
PMID:Quantitative immunohistochemical changes in the endocrine pancreas of nonobese diabetic (NOD) mice. 853 57

Experimentally, biliary obstruction can produce morphological and functional changes in the pancreatic gland, whereas pancreatic obstruction may have short-term (hyperamylasemia, pancreatic edema, and lysosomal hydrolase redistribution) or long-term (acinar cell atrophy and interstitial fibrosis) effects. We created a pancreaticobiliary duct obstruction in rats to evaluate (a) exocrine and endocrine anatomobiochemical pancreatic modifications; (b) structural and functional liver alterations; and (c) the relationship, if any, between the alterations found in the two organs. Forty-five male Sprague-Dawley rats were subdivided on the basis of period of obstruction (from 1 to 28 days). In each rat serum we evaluated amylase, cholestatic and cytolytic indices, and glucose. In frozen pancreatic samples we measured insulin, glucagon, and DNA; in the liver the DNA content was determined. Histologically, ductal dilation and proliferation were evaluated for the liver, zymogen granules, and Langerhans' islets, and atrophy for the pancreas. Fibrosis was evaluated for both the liver and the pancreas. Short-term common pancreaticobiliary duct ligation caused an increase in serum amylase levels and mild pancreatic edema. Longer-term obstruction had either similar or different effects on the two organs. In the pancreas it caused fibrosis and exocrine and endocrine atrophy, but not acute pancreatitis. In the liver the main phenomena observed were fibrosis, ductal dilation, and proliferation.
Pancreas 1995 Nov
PMID:Effects of pancreaticobiliary duct obstruction on the exocrine and endocrine rat pancreas. 853 59

Pancreatic duct bicarbonate secretion is mediated primarily by secretin-induced elevation of intracellular cyclic AMP, although little is known of the effects of other physiological regulators on pancreatic duct cyclic AMP metabolism. We investigated the effects of secretin and several other potential agonists on cyclic AMP levels in isolated guinea pig main and interlobular pancreatic duct segments and in cultured duct epithelial monolayers. Secretin (0.1 microM) caused a five- to eightfold elevation of cyclic AMP in both isolated ducts and cultured monolayers (EC50 = 0.15 nM). Main duct segments, while responsive, were less so than segments of interlobular duct. In isolated duct segments, carbachol, bombesin, cholecystokinin, substance P, calcitonin gene-related peptide, glucagon, insulin, isoproterenol, neurotensin, and prostaglandin E2 did not significantly alter resting or secretin-stimulated cyclic AMP levels. In contrast, 0.1 microM vasoactive intestinal peptide significantly increased cyclic AMP to a level comparable to that evoked by an equal concentration of secretin. Somatostatin significantly attenuated the effects of a submaximal (physiological) dose of secretin on duct cyclic AMP levels without altering resting cyclic AMP levels, suggesting that somatostatin's effects on pancreatic duct fluid secretion are mediated by inhibition of adenylyl cyclase activity.
Pancreas 1995 Oct
PMID:Regulation of cyclic AMP levels in guinea pig pancreatic ducts and cultured duct epithelial monolayers. 857 80

The effects of autonomic nervous activation, initiated by 2-deoxy-D-glucose (2-DG)-induced neuroglycopenia, or endocrine and exocrine pancreatic secretion were investigated in the conscious pig. Pigs were surgically fitted with permanent pancreatic duct and duodenal reentrant cannulas, allowing long-term sampling of pancreatic juice, and a jugular vein catheter for blood sampling and infusion of 2-DG. 2-DG was administered as a 5-min intravenous infusion at three dose levels to conscious pigs. 2-DG (400 mg/kg) was found to elevate plasma glucagon and insulin levels (p < 0.01). In contrast, exocrine pancreatic secretion, measured as volume, total protein output, and output of trypsin activity was not affected by 2-DG at the dose levels of 75, 200, and 400 mg/kg. Secretin (440 pmol/kg/h), however, stimulated pancreatic exocrine output of fluid (p < 0.01), protein (p < 0.01), and trypsin (p < 0.05). It is concluded that autonomic nervous activation by 2-DG-induced neuroglycopenia, in the conscious pig under basal conditions, elevates the plasma levels of glucagon and insulin but does not affect exocrine pancreatic secretion. 2-DG-induced neuroglycopenia is, thus, a suitable model for studying autonomic neural influences on the porcine endocrine pancreas.
Pancreas 1995 Oct
PMID:Stimulation of endocrine, but not exocrine, pancreatic secretion during 2-deoxy-D-glucose-induced neuroglycopenia in the conscious pig. 857 81


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