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)

19 subjects with an acute episode of pancreatitis, and 5 patients with chronic pancreatitis received intravenous glucose tolerance tests with measurement of glucose, insulin and glucagon. Patients recovering from acute pancreatitis demonstrated defects in their ability to dispose of a glucose load. 10 patients had overt glucose intolerance; of these, 4 were insulin-deficient, 3 had a loss of an acute insulin response to glucose, and 3 had marked hyperglucagonemia with normal to increased insulin levels. These abnormalities were seen in response both to intravenous glucose and intravenous arginine. Therefore, according to this study, at least three factors are clearly implicated in the production of glucose intolerance after an acute episode of pancreatitis: hypoinsulinemia, delayed insulin secretory response and hyperglucagonemia.
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PMID:Hormonal responses to intravenous glucose and arginine in patients with pancreatitis. 634 Nov 94

The injection of neoprene into the pancreatic ducts of dogs has been used to destroy exocrine function prior to pancreatic transplantation. The subsequent histological changes and the evolution of lesions over a period of 3-36 months are described. Animals were sacrificed or biopsied at various intervals (3, 15 and 36 months) and the pancreases showed the disappearance of exocrine acini and changes of chronic pancreatitis. An immunoperoxidase procedure with insulin, glucagon, somatostatin and pancreatic polypeptide antisera was used to show the persistence of pancreatic endocrine cells. After the injections, sclerosis progressively increased and secondary lesions of the islets were seen, although functional islets persisted. This technique was then applied to pancreas transplantation in man. Eight transplants from seven diabetic patients were available for examination. In four cases, there were early technical failures, but four pancreatic transplants continued to function for 28-889 days until suppuration destroyed one of the grafts and the three other patients died. The persistence of endocrine cells in sclerotic tissue was observed in histological and immunopathological examinations.
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PMID:Pathology of the pancreas after intraductal neoprene injection in dogs and diabetic patients treated by pancreatic transplantation. 635 16

In an attempt to study pancreatic A cell function at an early stage of pancreatic diabetes secondary to chronic pancreatitis, both intravenous glucose (0.5 g/kg) and insulin (0.5 U/kg) tolerance tests were performed on seven dogs with pancreatolithiasis and seven normal control dogs. Experimental pancreatolithiasis was produced 12 months after incomplete ligation of the greater pancreatic duct. Impaired glucose tolerance and reduced plasma insulin response to an intravenous glucose load were observed in the calcified group. Pancreatic release of glucagon to insulin-induced hypoglycaemia was diminished, but suppressive response of the hormone to glucose-induced hyperglycaemia was well preserved. These data suggest that the A cell response to hypoglycaemia may be impaired earlier than that to hyperglycaemia in pancreatic diabetes secondary to pancreatolithiasis.
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PMID:Plasma pancreatic glucagon response to blood glucose in experimental pancreatolithiasis in dogs. 636 79

Diabetes and carbohydrate intolerance can occur in pancreatitis. Although one-half of patients with acute pancreatitis will have some evidence of glucose intolerance during their acute illness, few will require insulin administration on either a short- or long-term basis. The diabetes seen in acute pancreatitis is likely due to a combination of factors, including alerted insulin secretion, increased glucagon release, and decreased glucose utilization by the liver and peripheral tissue. Chronic pancreatitis is often associated with diabetes mellitus, with the incidence as high as 70 percent when pancreatic calcification is present. These patients tend to be very sensitive to the effects of insulin and hypoglycemia. This is probably secondary to concurrent hepatic disease, malnutrition, and a relative decrease in glucagon reserves. The diabetes seen in chronic pancreatitis is associated with decreased insulin production. Finally, although the endocrine pancreas may influence the exocrine gland through a portal system, primary diabetes mellitus probably does not result in clinically significant alterations in pancreatic exocrine function.
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PMID:Diabetes mellitus and the exocrine pancreas. 636 37

Plasma concentrations of pancreatic glucagon, C-peptide, and pancreatic polypeptide were measured during arginine stimulation in 16 patients with chronic pancreatitis, in eight subjects with idiopathic diabetes mellitus, and in seven healthy controls. The hormone responses were compared with exocrine pancreatic function as assessed using the urinary excretion rate of p-aminobenzoic acid after oral ingestion of n-benzoyl-l-tyrosyl-p-aminobenzoic acid (BT-PABA). The increase in pancreatic glucagon levels during arginine stimulation was significantly reduced in patients with chronic pancreatitis compared to healthy controls, most markedly in those with secondary diabetes. In contrast, the glucagon response was unimpaired in patients with idiopathic diabetes. The arginine-induced increase in plasma glucagon and C-peptide concentrations correlated significantly with urinary PABA excretion in chronic pancreatitis (P less than 0.001, P less than 0.01, respectively). The responses of plasma C-peptide and pancreatic polypeptide separated pancreatitic and idiopathic diabetes less well. Thus, the glucagon response to arginine distinguished secondary diabetes due to chronic pancreatitis and idiopathic diabetes mellitus. The correlation between urinary PABA excretion and glucagon levels suggests that in chronic pancreatitis there is a parallel impairment of exocrine and endocrine function.
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PMID:Pancreatic glucagon secretion and exocrine function (BT-PABA test) in chronic pancreatitis. 638 Oct 2

The present investigation defined the pattern of pancreatic, pituitary and adrenal responses after insulin-induced hypoglycemia in chronic calcific pancreatitis (CCP) related to alcohol abuse, and assessed the role of some of these hormones in the counterregulation of blood glucose. We studied 6 Black men with recently diagnosed CCP, all showing radiological evidence of pancreatic calcification and normal glucose tolerance, as well as 7 matched nonobese male controls. After a standard iv insulin tolerance test inducing marked hypoglycemia, patients with CCP showed significantly impaired mean plasma pancreatic glucagon and pancreatic polypeptide responses compared to the controls. Mean basal plasma somatostatin levels tended to be higher in chronic pancreatitis and remained so throughout the test without altering consistently; in the controls somatostatin peaked significantly at 30 min. Concerning extrapancreatic hormonal changes, plasma growth hormone, prolactin and total catecholamines responded normally in CCP, but plasma cortisol rose to significantly higher levels than controls at 60 and 120 min after the injection of insulin. This, coupled with the brisk output of catecholamines, may have prevented the heightened sensitivity to insulin anticipated because of their hypoglucagonemia. We conclude that patients with CCP show impaired pancreatic hormone release after insulin hypoglycemia with the exception of somatostatin; there is also an excessive rise in plasma cortisol, possibly related to the long standing abuse of alcohol in the past.
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PMID:Hormonal profile after insulin-induced hypoglycemia in chronic calcific pancreatitis. Pancreatic, pituitary and adrenal responses. 639 52

The incidence of diabetic retinopathy was evaluated by means of fluorescein angiography in 54 patients with diabetes secondary to chronic pancreatitis or to pancreatectomy. Thirty-one percent of the patients had background retinopathy; none had proliferative retinopathy. The percentage of patients with retinopathy was the same in groups with or without a family history of diabetes. There was no correlation between the degree of metabolic control, the levels of C-peptide, glucagon, growth hormone, and the presence of retinopathy. Retinopathy was correlated with the duration of diabetes. In conclusion, diabetes caused by pancreatitis or pancreatectomy has a significant prevalence of retinopathy, which has more benign characteristics and slower evolution than the retinopathy in patients with primary diabetes.
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PMID:The presence of retinopathy in patients with secondary diabetes following pancreatectomy or chronic pancreatitis. 665 14

Pancreatic and gut hormones have been measured in 39 patients with chronic pancreatitis, 16 of whom had severe pancreatic insufficiency. Patients with pancreatic insufficiency had significantly diminished fasting levels and postprandial rises of pancreatic polypeptide which were less than 20% of normal. Patients with chronic pancreatitis, with or without exocrine insufficiency, had two- to threefold higher plasma levels of motilin and enteroglucagon than controls. Plasma levels of insulin, pancreatic glucagon, gastric inhibitory polypeptide and gastrin were similar to normal in these patients. The pattern of response of these hormones to a test breakfast differs markedly from those seen in other gut disease states and may reflect pathophysiological mechanisms.
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PMID:Pancreatic and gastrointestinal hormones in chronic pancreatitis. 675 14

In order to clarify the pancreatic endocrine functions in mild chronic pancreatitis, the response of insulin to oral glucose load and the response of glucagon and human pancreatic polypeptide (HPP) to insulin-induced hypoglycemia were investigated in five normal controls and eight patients with chronic pancreatitis but without diabetes mellitus. Although insulin and glucagon responses in patients with chronic pancreatitis tended to be lower than those in normal subjects, the differences between the two groups were not statistically significant. In contrast, HPP response to hypoglycemia in the patients was markedly impaired and significantly lower than that in normals (p less than 0.02). This finding indicates that the impairment of HP response is the earliest and most definite manifestation among pancreatic endocrine abnormalities in chronic pancreatitis.
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PMID:Impaired response of human pancreatic polypeptide to insulin-induced hypoglycemia in chronic pancreatitis without diabetes mellitus. 676 60

A patient with chronic pancreatitis underwent 95% pancreatectomy and islet autotransplantation. The pancreatic tissue was prepared by mincing and collagenase digestion, and then embolized into the liver via the portal vein. The patient has been followed with metabolic studies for 1 year. Fasting normoglycemia returned 3 weeks following operation. Intravenous glucose tolerance tests revealed K values that were similar before operation (1.06), and 3 weeks (0.96) and 4 months (1.09) after operation. Four months after islet transplantation, peripheral, portal, and hepatic vein insulin levels were determined simultaneously following an infusion of glucose (0.25 gm/kg) into the portal vein. During a 10-minute interval, right hepatic vein insulin increased fourfold, left hepatic vein insulin increased twofold, and peripheral vein insulin doubled. During this time portal vein insulin remained constant. In addition, significant levels of pancreatic glucagon were present in both hepatic veins, but were undetectable in the portal vein. At 6 months the patient became hyperglycemic and subsequently has required insulin therapy. Restudy at 10 months following islet transplantation revealed a marked drop in K value (0.34), and no evidence of graft function in the liver. These studies represent convincing evidence of transplanted intrahepatic islet cell function for a 6-month period following operation. The grafts for unknown reasons ceased to function at 6 months.
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PMID:Metabolic studies following intrahepatic autotransplantation of pancreatic islet grafts. 676 46


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