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)

A many-year prospective follow-up of patients with chronic pancreatitis has shown that the development of carbohydrate metabolism disorders in such patients is always preceded by exo-secretory pancreatic insufficiency of varying severity. Considerable enzyme-secretory pancreatic insufficiency is much more often in patients with secondary diabetes than in those with chronic pancreatitis without diabetes. Insulinemia and blood C-peptide level are regularly reduced in chronic pancreatitis with secondary diabetes but are normal in the patients with less manifest disturbances of carbohydrate metabolism, detectable by the double glucose tolerance test. Blood glucagon is increased in both groups of patients, but more so in those with secondary diabetes. A high direct correlation of the beta-cell activity and the pancreatic enzymes debit are characteristic of patients suffering from chronic pancreatitis with secondary diabetes, as well as a negative correlation, equally high, between the blood glucagon level and the pancreatic enzymes debit in the duodenal contents.
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PMID:[Exocrine and endocrine pancreatic disorders in chronic pancreatitis]. 281 62

Hormonal responses (glucagon, pancreatic polypeptide and somatostatin) to iv glucagon, iv arginine, and ingestion of a mixed meal were investigated in 6 patients with insulin-dependent diabetes secondary to chronic pancreatitis without beta-cell function, in 8 Type I (insulin-dependent) diabetics without beta-cell function, and 8 healthy subjects. No significant differences were found between the two diabetic groups regarding glucagon responses to arginine and meal ingestion. In the patients with diabetes secondary to chronic pancreatitis compared with Type I diabetics and normal controls, the pancreatic polypeptide concentrations were significantly lower and somatostatin concentrations were significantly higher after glucagon, arginine and a mixed meal. Thus, pancreatic glucagon secretion was preserved in patients with insulin-dependent diabetes secondary to chronic pancreatitis, having no residual beta-cell function. These findings suggest that pancreatic glucagon deficiency is not absolute in insulin-dependent diabetes secondary to chronic pancreatitis. A high level of somatostatin may contribute to a lower blood glucose level in patients with chronic pancreatitis.
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PMID:Pancreatic hormone secretion in chronic pancreatitis without residual beta-cell function. 289 69

Twenty-three patients with recent onset Type 1 (insulin-dependent) diabetes in whom residual insulin secreting B cells were present and 12 patients with disease of more prolonged duration (maximum 9 years), 8 of whom had residual B cells, were studied. Aberrant expression of Class II major histocompatibility complex molecules was demonstrated immunohistochemically on insulin secreting B cells in 21 out of 23 patients with recent onset disease and 6 of the patients with more prolonged disease. No such expression was seen on glucagon secreting A cells or somatostatin secreting D cells. Islets where there was marked hyperexpression of Class I major histocompatibility complex molecules on islet endocrine cells were seen in all cases in which residual B cells were present. Ninety-two per cent of insulin containing islets but only 1% of insulin deficient islets exhibited this phenomenon (p less than 0.001, Chi-squared test). There was evidence to suggest that both these abnormalities of major histocompatibility complex expression preceded insulitis within a given islet. They also appeared to be unique to Type 1 diabetes, being absent in pancreases of patients with Type 2 (non-insulin-dependent) diabetes, chronic pancreatitis, cystic fibrosis, graft-versus-host disease and Coxsackie B viral pancreatitis. The development of autoimmunity to B cells in Type 1 diabetes may be a "multistep" process in which abnormalities of major histocompatibility complex expression on islet endocrine cells are crucial events.
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PMID:Aberrant expression of class II major histocompatibility complex molecules by B cells and hyperexpression of class I major histocompatibility complex molecules by insulin containing islets in type 1 (insulin-dependent) diabetes mellitus. 330 84

We studied 125I-insulin binding to erythrocytes from 14 patients with diabetes secondary to chronic pancreatitis or pancreatectomy and compared the results with those found in 10 patients with type I diabetes and 25 normal controls. Patients with pancreatogenic diabetes had higher 125I-insulin binding and enhanced tissue sensitivity to exogenous insulin measured with the glucose clamp technique as compared with patients with type I diabetes. Similar binding data were obtained with monocytes from 3 patients with pancreatogenic diabetes. The increase in insulin binding seemed due mainly to an increase in receptor number. The increase in insulin binding to cells from patients with pancreatogenic diabetes in comparison with cells from normal subjects was also seen in young-erythrocyte-rich fractions and in old-erythrocyte-rich fractions obtained from the mixed population of circulating erythrocytes by centrifugation in density gradient of Percoll-Pielografin. These data, in the absence of any sign of major hematological disorders, suggest that the increase in insulin receptors seen in erythrocytes and in monocytes from patients with pancreatogenic diabetes, can mirror a general phenomenon on tissues throughout the body, including major target cells for insulin and correlate with the heightened sensitivity to insulin characteristic of these patients. In conclusion, patients with pancreatogenic diabetes have increased insulin binding as compared to controls and to patients with type I diabetes with chronic hypoinsulinemia of the same degree. Thus, in addition to insulin deficiency, other factor (s), such as glucagon deficiency, are responsible for the clinical and metabolic differences between these two conditions of insulin deficiency.
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PMID:Insulin receptors on circulating blood cells from patients with pancreatogenic diabetes: a comparison with type I diabetes and normal subjects. 330 82

Ultrasonic monitoring of the pancreas following secretin stimulation has shown to cause a marked dilatation of Wirsung duct; whether this phenomenon is due to the stimulation of pancreatic secretion and/or to the effect of secretin on the sphincter of Oddi (SO) motility is unknown. In the present study pancreatic scan after secretin was performed in 11 patients with nonpancreatic diseases after premedication with glucagon (inhibition of both pancreatic secretion and SO motility) or tyropramide (inhibition of SO motor function) and in patients with different degrees of pancreatic insufficiency. Serum immunoreactive trypsinogen (IRT) levels were measured in all the subjects during the test. Premedication with glucagon completely abolished both Wirsung enlargement and serum IRT increase, while tyropramide significantly reduced, but did not abolish, the response to secretin. These results suggest that both stimulation of pancreatic secretion and the increase of SO pressure are prerequisites for a full-blown occurrence of the secretin-induced modifications of Wirsung. Within chronic pancreatitis patients, the response to secretin was exaggerated in those with a still preserved pancreatic function and it was lacking in those with severe pancreatic insufficiency.
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PMID:Ultrasonic monitoring of Wirsung duct following secretin in controls and in chronic pancreatitis patients. 330 64

Among 88 unselected patients with chronic pancreatitis 35% (95% confidence limits 25 to 46) had insulin-dependent diabetes, 31% (21% to 41%) had non-insulin-dependent diabetes or impaired glucose tolerance (by intravenous glucose tolerance test), and 34% (24% to 45%) had normal glucose tolerance. B cell function measured by C-peptide concentration after 1 mg glucagon IV correlated with the pancreatic enzyme secretion (meal stimulated duodenal lipase content). B cell function was preserved to a greater extent (P less than .01), and glycosylated hemoglobin and fasting level of glucose were lower (P less than .01 to .05) in the 31 patients with pancreatogenic diabetes than than in 35 otherwise comparable patients with type I (insulin-dependent) diabetes, yet daily insulin dose was similar in the two groups. Glucagon stimulated C-peptide was inversely correlated to glycosylated hemoglobin in insulin-dependent patients with pancreatogenic diabetes and in type I diabetes. Since body mass indices were identical in the two groups, better glucoregulation was not due to reduced food intake or malabsorption in pancreatogenic diabetes. Rather residual B cell function and/or different secretion of other pancreatic hormones in pancreatogenic diabetes may account for different metabolic control in type I IDDM compared with insulin-dependent pancreatogenic diabetes.
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PMID:Metabolic control and B cell function in patients with insulin-dependent diabetes mellitus secondary to chronic pancreatitis. 330 47

The experiments on normal mongrel dogs and those with chronic experimental pancreatitis were performed to reveal the early changes of the endocrine pancreas function. The concentration of immunoreactive insulin and glucagon were studied in afferent vessels of the organ after intraarterial glucose-loading during pancreatic perfusion in situ. The data obtained have shown that in chronic pancreatitis the maximum secretion of insulin is decreased and delayed, as compared to normal animals. At the same time insulin-glucagon secretion ratio remains unchanged. That was indicative of the normal alpha-cell function at the early stages of the disease.
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PMID:[Characteristics of endocrine disorders in the early stages of the development of chronic experimental pancreatitis]. 331 35

A possible immunogenetic basis for diabetes in chronic pancreatitis was explored by studying 19 patients with both disorders, most of whom required treatment with insulin. In contrast to patients with insulin-dependent (Type 1) diabetes, patients with diabetes and chronic pancreatitis had residual beta cell function but blunted C-peptide responses to intravenous glucagon, absence of circulating islet cell antibodies, and HLA-DR types similar to control subjects and patients with chronic pancreatitis without diabetes. Diabetes complicating chronic pancreatitis is therefore not associated with the biochemical or immunogenetic markers characteristic of Type 1 diabetes.
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PMID:Evidence against an immunogenetic basis for diabetes in chronic pancreatitis. 332 10

To evaluate the role of glucagon in insulin-mediated glucose metabolism, we studied four men and four women, ranging in age from 30-73 yr (mean +/- SEM, 54 +/- 5) who had undergone complete pancreatic resection for cancer or chronic pancreatitis 16-58 mo previously. The patients had undetectable C-peptide levels and established lack of biologically active 3500 mol wt glucagon. Euglycemic insulin clamp studies were performed with a 40 mU X m-2 X min-1 insulin infusion in the basal, post-absorptive, insulin-withdrawn state, before and during the last 3 h of a 72-h glucagon replacement-dose infusion (1.25 ng X kg-1 X min-1). In four patients, hepatic glucose production was determined by a primed-constant infusion of 3-[3H]glucose. Monocyte insulin-binding studies, pre- and postglucagon, were performed in all patients. The 72-h glucagon infusion, resulting in mean plasma glucagon levels of 124 +/- 7 pg/ml, caused a significant rise in the mean plasma glucose level (249 +/- 8 versus 170 +/- 13 mg/dl preglucagon) and a sixfold increase in mean 24-h glucose excretion. Both with and without glucagon, euglycemic hyperinsulinemia achieved identical and complete suppression of hepatic glucose production. The mean glucose utilization rate (4.70 +/- 0.36 mg X kg-1 X min-1 preglucagon) was significantly decreased by glucagon replacement (3.83 +/- 0.31 mg X kg-1 X min-1, P less than 0.02). Mean glucose clearance was also diminished with glucagon (4.49 +/- 0.32 versus 5.73 +/- 0.45 ml X kg-1 X min-1 preglucagon, P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Basal glucagon replacement in chronic glucagon deficiency increases insulin resistance. 351 31

Reported are eight patients with idiopathic chronic pancreatitis and two patients with alcoholic pancreatitis who had near total distal pancreatectomy for disabling pain and underwent simultaneous segmental pancreatic autotransplantation of the body and tail of the gland to the femoral area in an attempt to prevent or delay the onset of diabetes. The median follow-up period was 31 months, and follow-up study in nine patients ranged from 24 to 54 months. Patency of the grafts was determined by angiography and selected percutaneous venous assays for insulin. Islet cell function was determined by oral glucose tolerance tests, intravenous (I.V.) glucose tolerance tests, and I.V. glucagon stimulation studies. Segmental autotransplantation was technically successful in eight patients, only one of whom required insulin (at 2 years after grafting). The other seven patients with technically successful grafts have remained insulin independent, including two patients who later underwent pyloric preserving pancreatoduodenectomy for completion pancreatectomy. Variable pain relief was observed in patients who underwent near total pancreatectomy, but pain was unrelieved in those patients who underwent limited distal resection. Patients with idiopathic pancreatitis appear to have better pain relief and preservation of endocrine function than alcoholic patients. Segmental pancreatic autotransplantation prevents or delays the onset of diabetes mellitus and should be considered as an alternative for those patients who require extensive pancreatic resection for chronic pancreatitis.
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PMID:Segmental pancreatic autotransplantation with pancreatic ductal occlusion after near total or total pancreatic resection for chronic pancreatitis. Results at 5- to 54-month follow-up evaluation. 352 8


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