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)

Hyperglucagonemia accompanies several clinical conditions characterized by increased amylase/creatinine clearance. We tested the hypothesis that glucagon may be responsible for this augmented clearance. Therefore, a constant glucagon infusion was given to eight volunteers in order to attain physiological levels comparable to those obtained during acute pancreatitis. The amylase/creatinine clearance increased from 0.84 +/- 0.8% to a mean of 1.30 +/- 1.14% (p less than 0.001). This was, however, less than the clearance of 2.94 +/- 0.23% observed during acute pancreatitis. The rise in amylase clearance during acute pancreatitis is, therefore, only partially explained by the hyperglucagonemia.
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PMID:Hyperglucagonemia--a partial explanation for the increased amylase/creatinine clearance in pancreatitis. 618 41

Glucagon effects on the kidney include increased water, creatinine, and amylase clearance. We have compared these effects in several laboratory animal species. Although every species responded to glucagon, 1 mg iv, by some alteration in renal function there were differences in the degree and direction of the changes. Glucagon caused an increase in amylase clearance in four of the six species studied and an increase in creatinine clearance in four. An increase in urine flow tended to occur in all species. An increased amylase clearance is a feature of acute pancreatitis, and raised glucagon levels have been found during attacks. It is possible that the two are causally related. In the experimental situation, timing of urine collections and species differences were found to be of critical importance in exploring this possibility.
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PMID:The effect of glucagon on urine amylase in various animal species. 619 80

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 effect of the occlusion of the pancreatic duct system with prolamine (Ethibloc) has been studied in animal experiments with dogs and mini-pigs. The solution becomes solid in the duct system and becomes disintegrated again within 11 days. This time, however, is sufficient to keep a high-grade atrophy of the exocrine parenchyma. With this method one doesn't risk the provocation of an acute pancreatitis. The endocrine function of the atrophied glands is satisfactory, no animal became diabetic. The basal jugular vein insulin shows no difference to that of the control group, but nevertheless the mean whole pancreas hormone content is reduced for insulin and somatostatin, but not for glucagon.
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PMID:Experimental studies on pancreatic duct occlusion with prolamine. 634 28

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

Patients with acute pancreatitis were studied by arginine infusion at 48--72 h. 7--10 days, and 18--21 days after onset of their illness. Plasma glucose, insulin, and glucagon values were determined. Acute pancreatitis was characterized by fasting hyperglycemia and hyperglucagonemia, associated with relative hyoinsulinemia. Arginine stimulation early in the disease (48--72 h) demonstrated hyperglycemia and hyperglucagonemia, which normalized by 18--21 days. Both phases of the normal biphasic insulin response to arginine were decreased during the initial arginine infusion. By 18--21 days, although the first phase was completely normal, the second phase of insulin secretion remained depressed. Acute pancreatitis is associated with damage to both the endocrine and exocrine pancreas. Glucose intolerance seen with this disease appears to be the result of hyperglucagonemia and relative hypoinsulinemia. Although the healing process at 3 wk is associated with return of plasma glucose and glucagon concentrations to normal, the impaired second phase insulin secretion persists.
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PMID:The glucose intolerance of acute pancreatitis: hormonal response to arginine. 699 12

In order to further investigate hormonal changes and possible metabolic consequences in acute pancreatitis, 10 cases with a mild form of the disease was studied. The influence of tissue injury per se on the hormones in question was assessed from comparison with the hormone levels in the course of myocardial infarction (MI) in 9 cases. Insulin and glucose showed no consistent changes. Glucagon was suppressed on admission, 22 +/- 10 pg . ml-1, compared with the ultimate concentration, 40 +/- 20 pg . ml-1 (p less than 0.05), and with the initial value in MI, 74 +/- 32 pg . ml-1 (p less than 0.01). Serum calcitonin (CT) was strongly elevated initially, 348 +/- 313 pg . ml-1, compared with the ultimate level, 24 +/- 7 pg . ml-1 (p less than 0.001), and with the normal initial level in MI, 43 +/- 44 pg . ml-1 (p less than 0.01). Serum CT elevations were time-related to a slight reduction in corrected serum Ca, which might reflect a biological expression of this substance. In pancreatitis, parathyroid hormone (PTH) remained normal and unchanged throughout the study, whereas patients with MI had an increased level of this hormone on admission, 0.19 +/- 0.08 microgramEq . 1(-1), compared with the ultimate concentration, 0.09 +/- 0.03 microgram/q . 1(-1) (p less than 0.02) and with the initial concentration in pancreatitis, 0.11 +/- 0.06 microgramEq . 1(-1) (p less than 0.05). Supranormal PTH levels were found in more than half of the infarction patients on days 0 and 1.
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PMID:Characteristic changes in the concentrations of some peptide hormones, in particular those regulating serum calcium, in acute pancreatitis and myocardial infarction. 701 27

Nasogastric suction, glucagon, and cimetidine are proposed treatments for human acute pancreatic because they may reduce gastric acid and exocrine pancreatic secretion. However, the functional status of gastric and pancreatic secretion during human acute pancreatitis is unknown. Thus, we compared the effects of nasogastric suction, intravenous glucagon (5 microgram/kg per hour), and cimetidine (2 mg/kg per hour) on the output of acid and pancreatic enzymes and the clinical course of human acute pancreatitis. In three subjects with acute alcoholic pancreatitis, gastric acid secretion was increased above normal and was decreased by glucagon and cimetidine used alone and in combination. In two of the three patients, duodenal output of trypsin and lipase was normal or increased and was reduced by glucagon and cimetidine given alone or in combination. Twenty patients with documented acute pancreatitis randomly received treatment with nasogastric suction, cimetidine alone, or the combination of cimetidine and glucagon. Four of the five complications observed during the trial occurred in the combination-treatment group (P less than 0.05). Administration of cimetidine alone or with glucagon did not improve the outcome when compared with nasogastric suction.
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PMID:A prospective study of the antisecretory and therapeutic effects of cimetidine and glucagon in human acute pancreatitis. 702 37

Plasma human pancreatic polypeptide (hPP) concentrations were measured in 17 patients with acute pancreatitis. On admission the mean plasma hPP concentration was 33 +/ 6,9 pmol/l (range 11-92 pmol/l), which was similar to the mean hPP concentration of 43 +/- 4 pmol/l (range 11-92 pmol/l) in age-matched healthy subjects. The plasma immunoreactive glucagon (IRG) concentration was elevated 5-fold. Nine patients were managed conventionally and received prolonged glucagon infusion, and 8 were managed conventionally and received saline infusion. Treatment was carried out in a double-blind manner. Glucagon infusion caused a further 5-fold rise in circulating IRG concentrations and an increase in the blood glucose concentration from 7,5 to 9,7 mmol/l. This was associated with a fall in hPP concentrations and a significant reduction in variability. It is suggested that plasma hPP levels are not elevated in patients with acute pancreatitis and, therefore, do not reflect acute pancreatic damage.
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PMID:Plasma pancreatic polypeptide concentrations in acute pancreatitis. 740 90

Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.
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PMID:Acute pancreatitis: a multisystem disease. 804 85


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