Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to investigate whether a relationship exists between in vivo insulin secretion and islet mass, 8 patients suffering from severe chronic relapsing pancreatitis were studied before and after pancreatectomy by glucose-glucagon-test (per os 1.75 g glucose; i.v. glucagon 0.01 mg/kg b.w.) and by intravenous glucose-tolerance-test (iGTT) (i.v. glucose 0.33 g/kg b.w.). Postoperative in vitro assessments of pancreatic insulin and alpha-amylase content were performed, and morphometric studies were carried out. Patients were characterized by reduced c-peptide secretion when compared with healthy subjects. The c-peptide response to the glucose-glucagon-test correlated well with the morphometrically estimated exocrine and islet tissue mass (P less than 0.05) and with the content of insulin and amylase in the tissue. The findings suggest that in subjects suffering from severe chronic relapsing pancreatitis the maximal insulin response might represent a parameter for the patient's islet mass.
 ...
PMID:Relationship between insulin secretion and pancreas morphology in subjects with chronic pancreatitis. 639 55

The incidence of diabetic retinopathy was evaluated by means of fluorescein angiography in 54 patients with diabetes secondary to chronic pancreatitis or to pancreatectomy. Thirty-one percent of the patients had background retinopathy; none had proliferative retinopathy. The percentage of patients with retinopathy was the same in groups with or without a family history of diabetes. There was no correlation between the degree of metabolic control, the levels of C-peptide, glucagon, growth hormone, and the presence of retinopathy. Retinopathy was correlated with the duration of diabetes. In conclusion, diabetes caused by pancreatitis or pancreatectomy has a significant prevalence of retinopathy, which has more benign characteristics and slower evolution than the retinopathy in patients with primary diabetes.
 ...
PMID:The presence of retinopathy in patients with secondary diabetes following pancreatectomy or chronic pancreatitis. 665 14

The endocrine secretory function of rat pancreases in which pancreatitis had been induced by feeding rats a 0.5% ethionine diet was investigated. Despite loss of 50% of exocrine tissue and widespread destruction of acinar structure, pancreatic insulin and glucagon contents and 4-h fasting plasma insulin levels in vivo did not differ significantly from those of food-restricted, weight-matched controls. Plasma glucose concentrations (fasting and after oral glucose) were significantly lower than control. In isolated, perfused ethionine-treated pancreases secretin failed to stimulate insulin secretion, whereas basal insulin secretion and insulin responses to glucose, arginine, gastric inhibitory polypeptide, vasoactive intestinal peptide (VIP), and somatostatin were similar to those of controls. Basal glucagon secretion was elevated in ethionine-treated pancreases, and glucagon outputs in response to arginine, VIP, and somatostatin showed a consistent trend toward higher levels than those of controls. These findings demonstrate that ethionine-induced pancreatitis selectively impairs islet secretory function. These effects may be due to damage to islet cell membranes by exocrine enzymes and/or a direct pathogenic action of ethionine on the islets.
 ...
PMID:Altered insulin and glucagon secretion in perfused ethionine-treated rat pancreases. 675 65

Pancreatogenic diabetes (PD), secondary either to chronic calcific pancreatitis or to pancreatectomy, is characterized by higher frequency of hypoglycemic events during insulin therapy in comparison with type I insulin-dependent diabetes (IDD). Not only glucagon deficiency, but an enhanced peripheral tissue sensitivity to insulin could account for this metabolic behavior. We investigated several facets of insulin action, e.g., tissue sensitivity to insulin, insulin binding to red cells, and insulin kinetics in seven patients with PD in comparison with type I. Tissue sensitivity to insulin was evaluated by means of the glucose-insulin clamp technique as M/I x 100 ratio (mg . kg .-1 min-1/muU . ml-1), where M is the amount of glucose infused by Biostator GCIIS to clamp BG at basal level and I is the free insulin plateau concentration achieved by a primed-constant insulin infusion. At high BG 15 h after the last injection of regular insulin M/I x 100 was 7.79 (range 4.25-9.75) in PD and 4.20 (range 1.20-6.91) in D (P less than 0.05). At low and equal BG M/I x 100 was 8.55 (range 6.35-9.72) in PD and 3.42 (range 1.19-6.75) in D (P less than 0.01). The rate of endogenous glucose production was nearly totally suppressed in both groups of patients. Just before the two clamps, 125I-insulin specific binding to red cells was studied. The maximum specific binding was significantly higher in PD than in D at high BG (10.7 +/- 1.7 vs. 7.4 +/- 0.8/10(9) red cells) and at low and equal BG (12.4 +/- 1.2 vs. 6.8 +/- 0.8). Receptor concentration also was significantly higher in PD thant in D (P less than 0.02) while no significant differences were found in high affinity (Ke). Insulin kinetic data were analysed by using both "Model independent" (or noncompartmental) method and compartmental modeling. Patients with PD had significantly higher (P less than 0.05) plasma clearance of insulin.
 ...
PMID:Insulin sensitivity, binding, and kinetics in pancreatogenic and type I diabetes. 675 50

In three groups of patients with insulin-dependent diabetes following total (n = 5) or partial (n = 5) pancreatectomy or chronic pancreatitis (n = 7) and in a group of idiopathic diabetics, ketogenic capacity following insulin withdrawal and during a 24-h fast was studied. Basal glucagon values were significantly increased in all diabetic groups with no significant intergroup differences. Basal ketone body values and their increase during starvation and insulin withdrawal were high and not different in totally pancreatectomized and primary diabetics, both showing unmeasurable C-peptide levels. On the contrary, ketogenesis was reduced in partially pancreatectomized and in pancreatitis diabetics with persistent levels of C-peptide. Our data confirmed the persistence of immunoreactive glucagon after pancreatectomy and demonstrated that ketogenesis is not suppressed in pancreatectomized diabetics and depends above all on residual B-cell function. A possible ketogenic effect of extra-pancreatic glucagon-like substances cannot be excluded.
 ...
PMID:Glucagon levels and ketogenesis in human diabetes following total or partial pancreatectomy and severe chronic pancreatitis. 700 39

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.
 ...
PMID:Characteristic changes in the concentrations of some peptide hormones, in particular those regulating serum calcium, in acute pancreatitis and myocardial infarction. 701 27

In attempt to clarify changes of pancreatic endocrine function in human calcified pancreatitis at its earlier stages, an experimental model of pancreatolithiasis comparable to the human disease was produced in six dogs after incomplete ligation of the major pancreatic duct. Endocrine function was serially examined by intravenous glucose (0.5 g/kg) tolerance test and insulin (0.5 U/kg) tolerance test before and 3, 6, and 12 months after the duct ligation. Neither alpha nor beta cell dysfunction became apparent until 12 months after the ligation. The disappearance rate of glucose in an intravenous glucose tolerance test decreased from 2.92 +/- 0.41 (mean +/- SE) of the preligation value to 1.58 +/- 0.17%/min at the end of the 12 months period (p less than 0.02). Plasma insulin response to glucose was also reduced significantly. Although hypoglycemia induced during an intravenous insulin tolerance test was maximal in the 12th month, distinct response of plasma pancreatic glucagon to the hypoglycemia disappeared. Endocrine insufficiency of the pancreas observed in this experimental model was similar to that reported in human pancreatolithiasis, although the severity is less.
 ...
PMID:Pancreatic endocrine function in experimental pancreatolithiasis in dogs. 704 28

Evidence is present that plasma contains non-specific factors which interfere with the 30K glucagon assays. A correction can be made for these interference factors because the factors can be quantitated following absorption of glucagon with charcoal-dextran. Using a correction factor the range of fasting plasma immunoreactive glucagon (IRG) in 12 totally pancreatectomized patients was below detectable limit. Fasting levels of IRG were determined on the plasma from 25 liver cirrhotics complicated by abnormal GTT, 13 pancreatic diabetics with chronic calcified pancreatitis (CCP), 25 adult-onset primary diabetics and 25 healthy subjects. When all samples were measured using no correction factor, the mean levels of IRG were 358 +/- 24 (mean +/- SE), 170 +/- 26, 178 +/- 16 and 178 +/- 7 pg/ml, respectively. Using a correction factor the mean level of IRG were 177 +/- 26, 16 +/- 4, 39 +/- 9 and 20 +/- 4 pg/ml, respectively. The mean values of the interference factor were not significantly different among all five groups. During an arginine infusion the interference factor remained unchanged despite an increase in IRG. It is available but not always necessary to apply a correction factor for 30K glucagon radioimmunoassay.
 ...
PMID:Plasma pancreatic glucagon in pancreatic and primary diabetes, and liver cirrhosis: application of a correction to the radioimmunoassay for pancreatic glucagon. 714 Nov 99

The exocrine and endocrine pathophysiology of chronic calcific pancreatitis of the tropics (CCPT) remains elusive. The objective of this study was to evaluate the spectrum and correlates of the exocrine and endocrine pancreatic dysfunction in CCPT. Thirty-seven consecutive patients with a clinico-radiological diagnosis of CCPT were stratified into three subgroups: CCPT-normal glucose tolerance (NGT), CCPT-abnormal glucose tolerance (IGT) and CCPT-diabetes mellitus (DM). Ten ketosis resistant young diabetic (KRDY) patients, 10 classical insulin dependent diabetes mellitus (IDDM) patients and 18 healthy matched controls were included for comparison. Fecal chymotrypsin (FCT) levels and blood C-peptide levels (basal and post i.v. glucagon stimulation) were estimated for assessing the exocrine and endocrine pancreatic functions, respectively. Sonography was performed to evaluate the pancreatic size and ductal diameter. Pancreatic exocrine-endocrine correlation was examined by studying the C-peptide/fecal chymotrypsin ratio (CP/FCT) (CP/FCT of normal controls = 1). Mean FCT levels in all 3 subgroups of CCPT (NGT: 3.4 micrograms/g; IGT: 0.82 microgram/g; DM: 2.4 micrograms/g) were very low (87-96% reduction in exocrine pancreatic dysfunction; mean FCT in healthy controls was 22.8 micrograms/g) (P < 0.0001). In contrast, KRDY and IDDM patients displayed 50-54% reduction in pancreatic acinar function (P < 0.001). Basal and stimulated C-peptide levels progressively fell in the 3 CCPT subsets (NGT: 0.23 and 0.46 > IGT: 0.14 and 0.29 > DM 0.10 and 0.14) (P < 0.01). CCPT patients exhibited pancreatic atrophy and ductal dilation (> 3 mm).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Chronic calcific pancreatitis of the tropics (CCPT): spectrum and correlates of exocrine and endocrine pancreatic dysfunction. 760 50

Thirteen patients with pancreatic diabetes caused by calcifying pancreatitis were divided into 2 groups; 5 with diabetic autonomic neuropathy [AN(+) group] and 8 without [AN(-) group]. They were subjected to an insulin-induced hypoglycemic stress test to evaluate their blood pancreatic glucagon, adrenalin, and cortisol responses. When a blood glucose level below 45 mg/100 ml was defined to be hypoglycemia, all the patients in the AN(-) group exhibited peripheral adrenalin responses, with a significant increase (mean, 19.0 times the basal level) in the blood adrenalin level. Among the AN(+) group, on the other hand, central nervous symptoms became evident rather than the peripheral adrenalin response (the blood adrenalin level hardly exceeded the basal level). With the exception of a single patient, none exhibited responses in the blood pancreatic glucagon levels. Only one patient showed a minimal cortisol response but the remaining 12 reacted normally in the cortisol release. The findings are summarized as follows: in pancreatic diabetes, insulin-induced hypoglycemia causes little change in pancreatic glucagon secretion; when the condition is complicated with autonomic neuropathy, central nervous symptoms develop while the blood adrenalin level hardly increases. These findings indicated that patients with pancreatic diabetes complicated with diabetic autonomic neuropathy have a risk of lapsing into an acute hypoglycemic coma and difficulty in recovering from the hypoglycemic state.
 ...
PMID:Decreased counterregulatory hormone responses to insulin-induced hypoglycemia in patients with pancreatic diabetes having autonomic neuropathy. 773 13


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