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 investigate the relationship between metabolic control and beta cell functions in chronic pancreatitis, 30 patients were selected for study, including 10 with diabetes mellitus in insulin-dependent state (group 1, Mean age 37.6), 10 with diabetes mellitus in non-insulin-dependent state (group 2, Mean age 47.8), and 10 with normal fasting glucose levels (group 3, Mean age 42.1). Each patient received urine routine, stool fat, renal function, biochemical study such as: serum lipid and glycosylated hemoglobin, eye fundi and X-ray examinations. Beta cell function was measured by C-peptide concentration six minutes after intravenous infusion of 1 mg glucagon. The results showed that the glycosylated hemoglobin concentrations were higher in group 1 than in group 2 or 3 patients (P less than 0.05), and were higher in group 2 than in group 3 patients (P less than 0.001) as well. The cholesterol and triglyceride levels were not significantly different among three groups. Furthermore, eight and two of group 1 and 2 patients manifested pancreatic calcification on abdomen X-ray examination (P less than 0.05). All and eight of group 1 and 2 patients received insulin injection respectively. In addition, group 1 patients were more likely to develop steatorrhea, other associated diseases and uncontrolled plasma glucose levels as compared with group 2 patients. In conclusion, insulin-dependent pancreatic diabetics had more advanced disease process and were therefore more likely to get other associated diseases than noninsulin-dependent pancreatic diabetics.
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PMID:Metabolic control and B cell function in patients with diabetes mellitus secondary to chronic pancreatitis. 131 3

In a prospective clinical-experimental study, 15 patients with chronic pancreatitis operated consecutively due to 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 postoperative day, and three months after the operation. In addition to glucose levels in the peripheral venous blood, levels of insulin, C-peptide, glucagon, somatostatin, and pancreatic polypeptide were determined. As indicated by the k-value, glucose tolerance improved postoperatively in 11 patients; two patients showed no change, and one patient was worse. Only one patient developed evident diabetes mellitus immediately postoperatively. The 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 (2p less than 0.01). Duodenum-preserving pancreas head resection led to improvement of the glucose tolerance in the majority of patients; a deterioration was observed only in two cases.
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PMID:[The effect of duodenum-preserving pancreatic head resection on the endocrine pancreas function in patients with chronic head pancreatitis]. 134 82

Chronic pancreatitis is defined by a persistent destruction of the pancreatic parenchyma replaced by fibrosis. The lesions generally start in the exocrine gland, islets being attacked later in the fibrosis. The two most frequent forms are: 1. Chronic calcifying pancreatitis which is a pancreatic lithiasis responsible for more than 95% of chronic pancreatitis. In its most frequent form, calculi are built up of more than 98% calcium salts together with fibres of a degraded residue of lithostathine, a secretory protein. This disease is related (i) in most countries to alcohol, protein, fat and tobacco and (ii) in certain tropical countries to malnutrition (low-fat, low-protein diet) for some generations. A causative role for cassava and kwashiorkor is improbable. The mechanism of calcium precipitation is partly explained by the calcium-saturation of pancreatic juice and the decreased biosynthesis of lithostathine S, the secretory protein preventing crystallization. As a rule, diabetes (and steatorrhoea) appear after a clinical evolution characterized by recurrent attacks of upper abdominal pain, generally lasting some days with transiently increased concentrations of pancreatic enzymes in serum. When diabetes appears, pain frequently disappears. Complications are mostly observed in the first 10 years of clinical evolution. 2. Obstructive pancreatitis is due to an obstacle (tumours, scars) in the pancreatic duct. It is rarely a cause of diabetes. Diabetes due to chronic pancreatitis is characterized by the low incidence of ketosis and the high incidence of insulin-induced hypoglycaemia. Patients are generally thin. Serum insulin levels, either basal or stimulated, are decreased. Glucagon is less affected. Angiopathies and retinopathies are less frequent than in non-insulin-dependent diabetes. Neural complications are fairly frequent. The diagnosis is generally easy because diabetes appears at a late stage of the disease. The treatment generally requires insulin.
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PMID:Chronic pancreatitis and diabetes. 144 67

Thirty patients suffering from chronic alcoholic pancreatitis (18 calcified) were entered into a study of exocrine and endocrine pancreatic function based on two maximal stimulation tests, namely the secretin-cerulein test and the glucagon test with serum assays of C peptide. The glucagon test was also performed in 19 control subjects. In addition, 10 chronic pancreatitis patients and nine controls were subjected to an oral glucose tolerance test (OGTT) with serum insulin determinations. C peptide basal values were decreased only in patients with severe pancreatic exocrine insufficiency (P less than 0.001), while delta C peptide values were also reduced in patients with moderate exocrine insufficiency (P less than 0.001). Lipase output correlated very well with delta C peptide values (P less than 0.001). While serum insulin levels during OGTT and C peptide basal values showed no significant differences between the chronic pancreatitis and control groups, delta C peptide values were significantly reduced in chronic pancreatitis patients (P less than 0.02). Both endocrine and exocrine function are impaired in chronic pancreatitis, as demonstrated by maximal tests, even in early stages of the disease.
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PMID:Exocrine and endocrine functional reserve in the course of chronic pancreatitis as studied by maximal stimulation tests. 172 34

Chronic pancreatitis is difficult to treat in patients with a nondilated duct. Patients experiencing intractable pain unresponsive to or judged untreatable by lesser procedures must decide between total pancreatectomy and resultant diabetes or a continuation of their pancreatitis. From 1977 through 1990, 26 patients underwent extensive pancreatectomy and dispersed pancreatic islet tissue autotransplantation for treatment of chronic pancreatitis pain and prophylaxis of surgical diabetes. Of these 26 patients, total (Whipple) or near-total (greater than 95%) pancreatectomy was performed in 24 patients. Of these 24 patients, pain relief could be assessed in 21 patients at 5 to 155 months (mean, 5.7 years), and 19 patients (90%) reported partial or complete remission. Of the patients who underwent total or near-total pancreatectomy, islets were injected intraportally in 22 patients and into the renal subcapsule in two patients. The latter two patients have required insulin since surgery. Of the other 22, one patient died from a complication of the pancreatectomy. Nine of the 21 evaluable recipients of intraportal islet autografts were insulin independent for at least several months after surgery. Five patients are currently insulin independent at 6 years, 4 years, 1.5 years, 9 months, and 5 months after surgery. Of the other four patients, one patient died insulin independent at 6 years, and three patients required insulin beginning 8 to 18 months after surgery. Insulin independence correlated with the number of islets recovered, which in turn correlated inversely with the degree of pancreatic fibrosis. Of our four most recent patients, three patients had mildly to moderately fibrotic glands, and higher numbers of islets were obtained. After total (Whipple) pancreatectomy, these three patients are insulin independent. A liver biopsy was performed in one patient 8 months after total pancreatectomy and islet autotransplantation; numerous clusters of islet cells staining strongly for insulin and glucagon were detected within portal triads on both wedge and needle biopsy specimens. Morbidity related to the intraportal-dispersed pancreatic islet tissue transplantation was low (no disseminated intravascular coagulation, significant portal hypertension, or hepatic dysfunction). Islet autotransplantation can be an effective and safe adjunct to extensive pancreatic resection for those patients who risk surgical diabetes for relief of their chronic pancreatitis pain.
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PMID:Autotransplantation of dispersed pancreatic islet tissue combined with total or near-total pancreatectomy for treatment of chronic pancreatitis. 185 51

Glucose counterregulation and hormonal responses after insulin-induced hypoglycemia were investigated in six patients with diabetes mellitus secondary to chronic pancreatitis, in seven with insulin-dependent (type I) diabetes mellitus, and in seven healthy subjects. Glucose counterregulation was identical in type I patients and in the patients with chronic pancreatitis, whereas both groups had impaired glucose recovery compared with the healthy subjects. The patients with chronic pancreatitis had no glucagon response to hypoglycemia, whereas epinephrine increased significantly. In an additional experiment, glucose recovery did not occur after hypoglycemia during concomitant beta-adrenoceptor blockade in these patients. In conclusion, glucose counterregulation is preserved but slightly impaired in patients with diabetes secondary to chronic pancreatitis, and the combination of total glucagon deficiency and pharmacological blockade of the metabolic actions of circulating epinephrine abolishes glucose counterregulation after hypoglycemia.
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PMID:Glucose counterregulation in diabetes secondary to chronic pancreatitis. 196 15

Insulin was withdrawn from 7 patients with Type I (insulin-dependent) diabetes and 4 patients with insulin-dependent diabetes secondary to chronic pancreatitis, both groups without residual beta-cell function. Median plasma glucagon concentrations rose slightly, but significantly after withdrawal of insulin in Type I diabetic patients (from 14 (range: 11-16) to 19 (14-25) pmol/l by 6 h), but not in the patients with secondary diabetes. This was accompanied by a significantly higher increase in blood glucose concentration from 5.1 (4.9-5.7) to 15.2 (12.9-18.1) mmol/l by 6 h in Type I diabetic patients compared with patients with secondary diabetes (from 4.9 (4.3-6.7) to 13.1 (10.9-13.5) mmol/l) (p less than 0.01). Beta-hydroxybutyrate increased to a similar extent in the two groups, whereas no significant increases were found in glycerol and lactate in any of the groups. Increased secretion of glucagon is not essential for the development of hyperglycemia and ketonemia in patients with diabetes secondary to chronic pancreatitis, but may augment the degree of hyperglycemia in Type I diabetic patients compared with patients having secondary diabetes.
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PMID:The effect of insulin withdrawal on intermediary metabolism in patients with diabetes secondary to chronic pancreatitis. 202 8

The mechanisms of carbohydrate metabolism abnormality were studied in 128 patients suffering from chronic pancreatitis by means of simultaneous measurement in the blood of glucose, insulin, C-peptide and glucagon concentrations both on an empty stomach and after the glucose tolerance test (50 g glucose). Five types of the hormonal mechanisms of hyperglycemia were revealed, caused by derangement of beta-cells for the most part, more rarely by alpha-cells of the pancreas and impairment of interregulation of those cells in chronic pancreatitis. The rate of the hormonal mechanisms of carbohydrate metabolism abnormality was shown to depend on the gravity and duration of chronic pancreatitis whereas blood sugar and insulin response to intravenous injection of glucose in patients with chronic pancreatitis to have characteristic features in common to type I and II diabetes.
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PMID:[Hormonal mechanisms of carbohydrate metabolism disorders in chronic pancreatitis]. 204 24

Morphology of pancreas (either esocrine, either endocrine) was studied in 29 cases of surgically treated chronic pancreatitis (27 cases of chronic calcifying pancreatitis and 2 cases of chronic obstructive pancreatitis). Parenchymal sclerosis in chronic calcifying pancreatitis (CCP) which represents the goal of our study was graded as mild (10 cases), moderate (10) and severe (7). Immunoperoxidase staining (PAP method) for insulin, glucagon, somatostatin, pancreatic polipeptide (PP), vasoactive intestinal polipeptide (VIP) and gastrin, was used to investigate endocrine pancreas. Acinar sclerosis and endocrine damage were closely related. Progression of sclerosis into islet appears to follow vascular pedicles producing a fragmentation into small cell groups as final result. In all cases of moderate or severe sclerosis, A/B cell ratio was increased due to the reduction of insulin positive cells. "Adenoma-like complexes", i.e., apparent concentration of islets, resulting from the loss of the acinar component, were observed in 7 cases with moderate or severe sclerosis. Nesidioblastosis was a prominent feature in all cases but one, with a positivity for insulin in 11 cases, for glucagon in 13, for somatostatin in 6 and for PP in 17. No positivity for gastrin was observed, while VIP was detected in a few ganglia. An increased amount of PP cells in islet and budding from the ducts was noticed and their presence outside the pancreatic head was demonstrable in 4 out of the 7 distal pancreatectomy specimens. Our data confirm the secondary involvement of the endocrine pancreas in the sclerotic acinar process.
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PMID:[Anatomopathologic pictures of chronic pancreatitis]. 209 39

Insulinemia, concentration of C-peptide and glucagon in the blood was studied in chronic hepatitis patients showing moderate tolerance disorders to glucose and diabetes mellitus developed against the background of chronic pancreatitis. Both groups showed hyperglucagonemia. Basal hypoinsulinemia and reduction of the C-peptide level revealed only in patients suffering of chronic pancreatitis with secondary diabetes mellitus. Reduced reaction of beta-cells of the pancreas to physiologic stimulation by pancreosozymin were observed also in less significant disorders of tolerance to glucose. The authors discuss the significance of changes in the sequential development of different degrees of disorders of the carbohydrate metabolism in patients with chronic recurrent pancreatitis.
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PMID:[The indices of pancreatic incretory activity in patients with chronic pancreatitis and disordered carbohydrate metabolism]. 209 92


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