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)

The vicinity of several hormone-producing glands as part of the anatomy of the intestinal tract and the resulting interaction has been confirmed by the discovery of hormonal factors of a specifically gastro-intestinal origin. Today we are mainly interested in the interaction between intermediary metabolism and incretory intestinal function; this is characterized by the joint action of conventional glandular hormones such as insulin and pancreatic glucagon as well as by the incretion of diffuse intestinal organs, hormones such as secretin, pancreozymin, motilin, VIP and GIP. The latter are at present subject of active research with the object of discovering their physiological significance be it as tissue hormones or as humoral agents with a "long distance" impact; their role within pathophysiology is also of interest. GIP ("gastric inhibitory peptide"), apart form acting upon the intestinal tract, also causes a marked rise in insulin production; this GIP possibly is the factor responsible for the difference in glucose tolerance following i. v. or oral administration of glucose, something that scientists have been trying to discover for a long time. We have also endeavored to investigate somatostatin. This substance was originally discovered as a hypothalamic factor with inhibitory action on growth hormone secretion; in the meantime, however, cells containing and possibly also producing somatostatin have also been detected in the intestine and particularly in the islets of Langerhans (D-cells). Since somatostatin inhibits insulin secretion and especially glucagon release as well as the exretory functions of the stomach and of the pancreas, the significance of this hormone possibly is that of a tissue hormone with inhibitory action on adjacent cells. As factor inhibiting both endocrine and exocrine secretory processes it would combine these two complexes. The possible therapeutic significance of somatostatin administration to diabetics would lie in the saving of insulin. A third sector of present-day research deals with the interaction between the calcium metabolism and the hormones involved as well as the intestine. We know that patients suffering from primary hyperparathyroidism are prone to contract stomach ulcers and pancreatitis; patients with a gastrinoma and a hyperfunction of the epithelial bodies suffer from a Zollinger-Ellison-sindrome and this again suggests association with endocrine polyadenomatosis (Wermer syndrome). The inhibitory action of the parathormone antagonist calcitonin on the exocrine functions of the intestinal tract, such as the acid secretion of the stomach and the enzyme secretion of the pancreas, have already given rise to some considerations and experiments relative to treatment. It is to be hoped that because of all the joint observations cited above there will be better intergration of research both from the aspect of gastro-enterology and endocrinology. This might hopefully elucidate some of the unresolved problems ranging from basic research to practical application.
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PMID:[Interaction between gastrointestinal hormones and endocrine regulation]. 0 83

Recent data seem to support a tubular defect as the mechanism of the elevated renal clearance of amylase relative to creatinine in acute pancreatitis. Glucagon has been proposed by some to be an important factor in this phenomenon. To examine the role of glucagon as this "tubular dysfunction factor", we investigated the effect of intravenously infused glucagon on the fractional excretion of amylase and the tubular handling of a low molecular weight protein, beta2 microglobulin, in normal, healthy volunteers. At glucagon levels far in excess of those seen in pancreatitis, the clearance ratio of beta2 microglobulin relative to creatinine increased, whereas the clearance ratio of amylase relative to creatinine did not increase above the normal range. The dissociation between beta2 microglobulin clearance and amylase clearance allows one to question the theory that tubular dysfunction is the mechanism of the elevated renal clearance of amylase relative to creatinine in acute pancreatitis. Glucagon does not appear to be the sole factor responsible for the elevation of renal clearance of amylase relative to creatinine in acute pancreatitis.
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PMID:Effect of glucagon infusion on the renal clearance of amylase relative to creatinine. 8 90

17 oral glucose tolerance tests with simultaneous estimation of plasma insulin, were carried out in 15 patients with chronic pancreatitis of which 7 were of calcific type. Among these patients, 10 had obvious diabetes and 3 chemical diabetes. The disorders of glucose regulation were more common in the calcific form of the disease. Serum insulin was then lower and not stimulant. The curves of plasma insulin obtained in non-calcific pancreatitis were variable. In hyperinsulinism, the oral glucose tolerance test showed flat or normal curves. In hypoinsulinism, the glucose tolerance tests were either normal or strongly pathological. This insulinism, as shown by this study of chronic pancreatitis, seems to be linked to an imbalance in the cell distribution of the islets of Langerhans. The role of glucagon appears preponderant.
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PMID:[Study of insulin secretion in chronic pancreatitis]. 18 95

Acute pancreatitis may present as the mild edematous type or the more rare and dangerous hemorrhagic form. The effects of the latter are believed to be due to the activation of pancreatic enzymes, notably trypsin. Therefore attempts are being directed towards suppression of pancreatic enzyme activation in the management of the condition. Aprotinin and glucagon are the agents for this purpose that have received most attention. Patients with acute hemorrhagic pancreatitis are subject to respiratory failure, which is not detectable early by clinical evidence, so that early monitoring of pulmonary function by the determination of arterial blood-gas pressures is desirable. This is borne out by the findings in six fatal cases.
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PMID:Symposium on pancreatitis: 1. Conservative management of acute pancreatitis. 30 73

Glucagon has been claimed to be an effective treatment for pancreatitis, but the studies reporting this were either uncontrolled or did not use concurrent controls, and none were double blind. To evaluate the efficacy of glucagon for alcohol-related pancreatitis, we performed a controlled, randomized, double blind study. Twenty-six patients with pancreatitis associated with alcohol ingestion received either glucagon or placebo in addition to intravenous fluids, nasogastric suction, and meperidine as needed. There were no statistically significant differences between the group which received glucagon and the group which did not in any of 12 parameters which included symptoms, signs, laboratory tests, and requests for analgesia. We conclude that glucagon in addition to conventional therapy is no better for the treatment of alcoholic pancreatitis than conventional therapy alone.
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PMID:Failure of glucagon in the treatment of alcoholic pancreatitis. 34 25

Glucagon can depress normal animal and human pancreatic exocrine secretions and modify experimentally-induced pancreatitis in animals. It has yet to be demonstrated that glucagon has any efficacy in the treatment of the diseased pancreas in man. Glucagon might act on the exocrine pancreas by 1. reducing pancreatic blood flow, 2. decreasing gastric secretion, 3. lowering serum calcium levels by the release of calcitonin, 4. acting to inhibit the secretin mechanism, 5. causing a hyperglycemia and 6. degranulating pancreatic acinar cells. While a reduction in pancreatic blood flow, an inhibition of the secretin mechanism and a hyperglycemia seemed to have been ruled out as possible mechanisms of action, there is too little available data to effectively speculate on the mechanism(s) of action of glucagon on the exocrine pancreas.
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PMID:The effect of glucagon on the exocrine pancreas. A review. 36 5

Acute pancreatitis was induced in 245 rats by retrograde instillation of Na-taurocholate into the pancreatic duct. Mortality rate in animals treated 6-hourly with glucagon (1 mg/kg) after induction of pancreatitis was 50% as compared to 30% deaths in the controls treated with 0,9% NaCl (chi2-test: p less than 0,05). Mortality rate in animals treated 6-hourly with the same dose of glucagon before induction of pancreatitis was 36,5% as compared to 28% deaths in the corresponding controls (chi2-test: p greater than 0,05). Glucagon in lower doses (0,1-0,5 mg/kg every 6 hours) did not alter mortality rates as compared to animals treated with 0,9% NaCl. 2. A nonletal form of pancreatitis was induced in 26 rats by ligation of the pancreatic duct. Injection of glucagon (1 mg/kg) seemed to suppress amylase activities in blood for a short period of appr. 1 hour. However, 7 and 9 hours after induction of pancreatitis, amylase activities were significantly higher in animals treated one or two times with glucagon as compared to untreated controls. It is concluded that glucagon in the high dose of 1-4 mg/kg/24 hours does not only not influence the course of acute experimental pancreatitis in rats but can even deteriorate it.
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PMID:A controlled trial of glucagon in acute experimental pancreatitis in rats. 60 26

The amylase/creatinine clearance ratio (Cam/Ccr ratio) was determined in 239 subjects. In 87 hospitalised patients without pancreatic disease (controls) the Cam/Ccr ratio was 3.02 +/- 0.69 (mean +/- ISD). The ratio was above the normal range in all patients with acute pancreatitis but was normal in those with chronic pancreatitis and carcinoma of the pancreas. In 18 patients with choledocholithiasis a raised ratio distinguished those with pancreatitis as assessed independently by the surgeon at laparotomy from those with a macroscopically normal pancreas. Raised Cam/Ccr ratios were also found in diabetics with ketoacidosis and in three patients with fulminant alcoholic liver disease. Though a positive correlation was found between the Cam/Ccr ratio and serum creatinine concentration, abnormally high ratios did not occur in 30 patients with chronic renal failure. A significant increase in Cam/Ccr ratios was produced in six healthy volunteers by intravenous injection of glucagon. However, it is unlikely that hyperglucagonaemia alone accounts for the increased Cam/Ccr ratio seen in acute pancreatitis, as no correlation was found between the clearance ratio and the plasma glucagon concentration in a series of patients. In two other patients in whom excess circulating pancreatic polypeptide was detected the Cam/Ccr ratio was normal. It is concluded that, in view of the sensitivity and relative specificity of finding an increased Cam/Ccr ratio in acute pancreatitis, its determination should be valuable clinically, especially in those cases of hyperamylasaemia where the cause is in doubt. The mechanism whereby the ratio is increased is unknown, and it is unlikely that either glucagon or pancreatic polypeptide is a major factor in its production.
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PMID:Mechanism and specificity of increased amylase/creatinine clearance ratio in pancreatitis. 60 90

Pancreatitis was induced in 11 miniature pigs by infusing a bile salt-trypsin solution into the pancreatic duct. Seven animals served as sham-operated controls. Serum ionized calcium, total calcium, albumin, total protein, inorganic phosphorus, urea nitrogen, magnesium, insulin, glucagon, and hematocrit were determined every six to 12 h over a period of one week in both test and control animals. We observed significant decreases in ionized and total calcium, modest decreases in albumin, and significant increases in the inorganic phosphorus, urea nitrogen, and hematocrit in the pancreatitic pigs. The latter two findings were consistent with early acute hypovolemia. Glucagon and insulin appeared to play no role in the hypocalcemia. Glucagon concentrations increased to the same degree in both test and control animals, probably as a result of the stress of being handled and operated on. The highest concentrations of inorganic phosphorus and the lowest concentrations of both ionized and total calcium were seen 18 h after the induction of pancreatitis in the test animals. These findings suggest that parathyrin (parathormone) was not being secreted in adequate amounts, or that the target organs were unresponsive to parathyrin.
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PMID:Biochemical changes in a porcine model of acute pancreatitis. 65 76

Differences in metabolic homeostasis in 12 patients with initial vs. eight patients with repeated attacks of acute pancreatitis have been compared during the acute phase of the disease. As a group, subjects with a previous history of pancreatitis had significantly lower glucagon concentrations (P less than 0.002) for the over all 24-hour study period. Conversely, the serum concentrations of blood sugar, insulin, growth hormone, gastrin, cortisol, nonesterified fatty acids, triglycerides and cholesterol failed to distinguish between the two patient groups. Likewise, immunoreactive plasma parathyroid hormone and calcitonin levels were comparable in both patient populations. Of the measurements considered, it would appear therefore that plasma immunoreactive glucagon is the best indicator of previous pancreatic inflammation. Evaluation of parenchymal integrity during an episode of acute pancreatitis would be of prognostic and therapeutic value in this disease.
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PMID:First 24 hours of acute pancreatitis. A biochemical and endocrine evaluation of initial versus repeated attacks. 69 15


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