Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nature and origin of plasma immunoreactive glucagon (IRG) after pancreatectomy in humans remains controversial. Low plasma IRG levels and heterogeneity hamper accurate assessment. We studied plasma IRG levels and profiles in 12 patients 2-57 mo after a total pancreatectomy (with antrectomy and duodenectomy) for cancer (N = 9) or chronic pancreatitis (N = 3). After oral glucose, plasma IRG (with the COOH-terminal-specific 30K glucagon antibody) rose from 59 +/- 7 to a peak of 113 +/- 17 pg/ml at 60-120 min. Chromatographic profiles revealed four distinct IRG fractions. In every patient a plasma IRG fraction of 9000-15,000 Mr, detectable basally, increased markedly after oral glucose and accounted for the rise in total IRG observed in plasma. Nine of the 12 pancreatectomized subjects had no detectable 3500-Mr glucagon and the remaining 3 had very low levels. For the group as a whole, 3500-Mr IRG comprised 1-2% of the total recovered IRG. Two patients were also studied before pancreatectomy: suppressibility of glucagon (Mr 3500) was evident. After surgery this paradoxical response to oral glucose was demonstrated. Reproducibility of these responses was confirmed in two patients studied twice over 2 yr. Diabetic controls without pancreatectomy did not show this response. The absence or marked reduction of pancreatic glucagon was confirmed in five of the pancreatectomized patients after intravenous arginine or oral protein. Normal basal plasma IRG and profiles, oral glucose suppressibility, and arginine stimulation were present in five control patients with unresectable pancreatic malignancies.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Glucagon immunoreactivity and chromatographic profiles in pancreatectomized humans. Paradoxical response to oral glucose. 352 86

To determine the significance of manometric pressure of the pancreatic duct, we used a microtransducer inserted through a duodenoscope to measure pressures in the papillary sphincter zone and pancreatic main duct in 20 control subjects and 20 patients with chronic pancreatitis, and recorded the effect of exogenous glucagon or secretin. There was no significant difference between control subjects and patients with chronic pancreatitis without papillitis in the motility of the sphincter of Oddi. The pancreatic main ductal pressure was significantly higher in the patients with chronic pancreatitis (54.5 +/- 29.9 mmHg) than in the control subjects (16.2 +/- 8.7 mmHg). The viscosity of pure pancreatic juice of patients with chronic pancreatitis [5.8 centipoise (cp)] in the basal secretory state was significantly higher than that of the control subjects (1.61 cp). These data lead to the hypothesis that increased pancreatic ductal pressure in patients with chronic pancreatitis without papillitis is due not to papillary dysfunction, but to increased viscosity or other unknown factors.
 ...
PMID:Endoscopic measurement of papillary sphincter zone and pancreatic main ductal pressure in patients with chronic pancreatitis. 372 Nov 26

Radioimmunoassay was employed to study blood content of insulin, C-peptide and glucagon in 78 patients with chronic pancreatitis. It was revealed that during exacerbation, there was an increase in the content of insulin and glucagon and, to a lesser degree, in that of C-peptide. During remissions, part of the patients showed insular deficiency which increased with disease standing. When pancreatitis lasted from 1 to 5 years or from 5 to 10 years, diabetes mellitus was recorded in 9.4% of the patients and in 16% of the patients, respectively.
 ...
PMID:[Incretory changes in the pancreatic hormones in chronic pancreatitis]. 382 27

In 11 persons with normal pancreas function and 21 patients with chronic pancreatitis serum levels of insulin and C-peptide were measured under basal conditions and after maximal stimulation with glucose-tolbutamide-glucagon. Patients with the highest excretory deficiency in the secretin-pancreozymin test had the most marked impairment in endocrine function. In patients with manifest diabetes the exocrine capacity was reduced to an average of 10% of normal. The endocrine parameters correlated linearly with the exocrine ones, most markedly C-peptide reserve with pancreatic enzyme secretion.
 ...
PMID:[Reduction of insulin reserves and exocrine pancreatic secretion in chronic pancreatitis]. 388 Dec 38

The degree of correlation between exocrine pancreatic function and endocrine secretory capacity was examined in 13 chronic pancreatitis patients with secondary diabetes mellitus, 8 chronic pancreatitis patients without diabetes, and 11 healthy subjects. The two parameters were studied under maximal stimulation (volume-corrected secretin-pancreozym test and glucose-tolbutamide-glucagon provocation, respectively). A close, linear correlation was found between all endocrine variables and pancreatic acinar function (e.g. rs = 0.77 for chymotrypsin output and C-peptide release; p less than 0.0001). The correlation was less strong with pancreatic bicarbonate output (e.g. rs = 0.49 for C-peptide release; p less than 0.05). In our patients, secondary overt diabetes occurred in chronic pancreatitis when protease outputs were, on an average, reduced to about 10% of the mean maximal protease output of normal subjects.
 ...
PMID:Beta-cell reserve capacity in chronic pancreatitis. 388 12

Endocrine function of the pancreas was examined in patients with chronic pancreatitis of different etiology. Radioimmunoassay was applied to measure blood immunoreactive insulin, C-peptide and glucagon as characteristics of the hormonal activity of the pancreas. Pancreatic function was revealed to be disordered. The degree of the disorders correlated with the disease gravity and duration as well as with its progress (exacerbation or remission). As compared with patients presenting with cholepancreatitis, more remarkable alterations, which were particularly well observable during making the glucose tolerance test, were found in patients with chronic pancreatitis of alcoholic etiology.
 ...
PMID:[Endocrine function of the pancreas in chronic pancreatitis]. 391 67

We evaluated carbohydrate tolerance in nine thin cystic fibrosis (CF) patients and in six controls, measuring responsiveness to the following insulinotropic secretagogues: oral glucose, IV glucose, and IV tolbutamide. Glucose responses segregated patients into two groups: Group I with normal carbohydrate tolerance associated with normal to slightly increased insulin responses, and Group II with impaired carbohydrate tolerance associated with insulinopenia. This latter group included one patient with frank diabetes. The CF patients demonstrated a significant positive correlation between insulin secretion, in response to each secretagogue, and pancreatic exocrine function as measured by serum pancreatic amylase isoenzyme concentration. Pancreatic alpha-cell function, as reflected by basal plasma glucagon concentrations, also correlated well with exocrine function in the CF patients, excluding the diabetic individual. The enteroinsular axis of the CF group was intact as reflected by normal plasma gastric inhibitory polypeptide concentrations in Group I and by elevated levels, basally and in response to oral glucose, in the insulinopenic Group II patients. Furthermore, those patients with impaired tolerance demonstrated a greater magnitude of insulinopenia compared to controls following IV glucose and possibly IV tolbutamide, than following oral glucose. Thus, these data suggest that loss of carbohydrate tolerance in patients with CF, like that seen with classical chronic pancreatitis, 1) parallels the loss of exocrine function, 2) is associated with appropriate enteroinsular signaling, and 3) can be detected earlier or more easily following testing with direct IV secretagogues than following oral glucose stimulation.
 ...
PMID:Carbohydrate tolerance in cystic fibrosis is closely linked to pancreatic exocrine function. 608 38

Ten patients who had been totally duodeno-pancreatectomized and totally (N = 1) or partially gastrectomized (N = 9) for chronic pancreatitis (N = 9) or pancreatic carcinoma (N = 1) were investigated. None had a measurable basal level of either plasma C-peptide or a C-peptide response to i.v. glucagon. Immunoreactive glucagon (IRG) was present in all patients, and the mean level (69 +/- 8 pg/ml) was not significantly different from the mean observed in normal subjects (81 +/- 16 pg/ml). Plasma IRG was unequivocally stimulated by arginine in 2 of the 10 subjects. The effect of somatostatin on plasma glucose and IRG during an oral glucose tolerance test was studied in 5 of the 10 patients. The effects of somatostatin on spontaneous hyperglycemia, plasma growth hormone, and IRG after withdrawal of insulin treatment was studied in 4 patients. Somatostatin blunted both the hyperglycemic and paradoxical IRG responses to the glucose challenge, and reduced the spontaneous rise of blood glucose that occurred after insulin withdrawal. This latter effect was not related to clear-cut changes in plasma growth hormone or in IRG. These data confirm the existence of circulating IRG in pancreatectomized patients and demonstrate the presence of circulating IRG in a completely gastrectomized and pancreatectomized patient. The somatostatin-induced improvement in glucose tolerance in the oral glucose tolerance test seems to be related to a reduction of the paradoxical IRG response. In contrast, the inhibition by somatostatin of the rise in blood glucose which occurs after insulin withdrawal does not seem to be mediated through IRG or growth hormone.
 ...
PMID:Glucagon immunoreactivity and antidiabetic action of somatostatin in the totally duodeno-pancreatectomized and gastrectomized human. 611 86

Plasma immunoreactive glucagon, C-peptide and substrates (glucose, lactate, and alanine) were measured in 21 pancreatectomized patients and 28 patients with chronic calcifying pancreatitis during arginine infusion. Results were compared with those obtained in control and in insulin-dependent diabetic subjects, and in pancreatectomized subjects receiving a combined infusion of glucagon and arginine or somatostatin and arginine. Plasma immunoreactive glucagon in the pancreatectomized patients was 230 +/- 26 pg/ml (control subjects 100 +/- 13 pg/ml, p less than 0.001), but was unchanged following arginine or somatostatin. Following ethanol extraction of plasma it became undetectable. Similar results were obtained in patients with chronic pancreatitis. In contrast to the insulin-dependent diabetic subjects, no changes in blood glucose, lactate, and alanine concentrations were found during arginine infusion in the pancreatectomized or pancreatitis patients. Addition of glucagon restored the metabolic response to arginine in the pancreatectomized patients. Our results confirm previous smaller studies that in pancreatectomized patients, A cell function is absent or insignificant.
 ...
PMID:Absence of islet alpha cell function in pancreatectomized patients. 612 Aug 75

Exocrine pancreatic function was evaluated by a Lundh meal test and a secretin-cholecystokinin test in 16 patients with chronic pancreatitis. B cell function was assessed by measuring the concentration of C-peptide after stimulation with oral glucose and intravenous glucagon. The Cc-peptide response to intravenous glucagon and oral glucose was closely correlated (r = 0.88, p less than 0.01). Plasma C-peptide after glucagon was significantly correlated to the post-prandial concentration of lipase (r = 0.72, p less than 0.001), amylase (r = 0.64, p less than 0.05) and to amylase output (r = 0.64, p less than 0.05). Eight out of nine patients treated with insulin had residual B cell function, but it diminished significantly with increasing duration of diabetes. We conclude that B cell function is correlated to pancreatic enzyme secretion and that patients with insulin-treated diabetes secondary to chronic pancreatitis have a residual insulin secretion similar to that of patients with Type 1 (insulin-dependent) diabetes.
 ...
PMID:B cell function in patients with chronic pancreatitis and its relation to exocrine pancreatic function. 618 47


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>