Exocrine Enzyme Secretion Research Articles

Eurytrema coelomaticum infection: correlation between parasite burden and impairment of pancreatic exocrine enzyme secretion

ABSTRACT: Eurytrema coelomaticum is a trematode reported in the pancreatic ducts of ruminants. It is conjectured that may cause disorders in the pancreas, as well as digestive and metabolic processes dependent on them. This study, determined if there is an impairment of exocrine pancreatic function, and correlated it with parasite burden. Pancreas, blood, and fecal samples were collected from 119 bovines at a abattoir. Stool samples were subjected to the gelatin and x-ray film digestion tests (to detect the presence of trypsin in feces). Using blood samples, the following biochemical tests were performed: amylase, lipase, glucose, fructosamine, cholesterol, triglycerides, total protein, albumin, and globulins. Analyses were correlated with pancreatic parasite burden. Cattle with a high parasitic load presented higher incidence of negative tests in both gelatin digestion and x-ray film digestion tests (P < 0.001) when compared to non-parasitized animals and those with a low parasitic load. Changes in those tests only occurred if the parasitemia was moderate or severe. The activity of the amylase and lipase enzymes was significantly higher in animals with low parasitemia (P < 0.05), compared to non-parasitized animals and with a high parasitic burden. In this study, in cases of high parasitemia, negative results were observed in both gelatin and x-ray film in the feces digestion tests. However, the low infection of E. coelomaticum, higher levels of serum amylase and lipase that also indicated loss of pancreatic exocrine functions were reported.

892 PKD3 Is the Predominant PKD Isoform Expressed in the Exocrine Pancreas and Regulates Hormone-Induced Exocrine Enzyme Secretion

892 PKD3 Is the Predominant PKD Isoform Expressed in the Exocrine Pancreas and Regulates Hormone-Induced Exocrine Enzyme Secretion

Effect of glycolysis on pancreatic microcirculation and cellular functions in anesthetized rats.

It has been reported that aerobic glycolysis in the pancreas contributes less than 10% to oxidative phosphorylation based on in vitro experiments using pancreatic tissue segments. However, its contribution to aerobic glycolysis in vivo remains uncertain. We investigated the effect of inhibiting glycolysis on O2 metabolism in microvessels, exocrine enzyme secretion, and the blood glucose level in the pancreas of anesthetized rats in vivo. Inhibition of glycolysis, by superfusing the pancreas of anesthetized rats with 2-deoxyglucose (10 mM) or sodium fluoride (2 mM), significantly decreased O2 release from erythrocytes flowing in the microvessels by 30-40%. Inhibiting glycolysis did not affect the exocrine secretion of pancreatic juice but decreased the secretion of total protein by approximately or = to 40%. Inhibiting glycolysis decreased blood glucose levels by approximately or = to 40% and increased glucagon release twofold. Aerobic glycolysis may play more important roles in the regulation of O2, metabolism, pancreatic exocrine enzyme secretion and the blood glucose level in rat pancreas.

Increased plasma pancreatic polypeptide in chronic alcohol abuse.

Post-prandial plasma gastrointestinal hormone profiles were measured in nine chronic alcoholics, one and fourteen days after complete alcohol withdrawal. Basal plasma pancreatic polypeptide concentration (PP--mean +/- SE mean) was significantly greater in alcoholics (control, 28 +/- 5 pmol/l; alcoholics, post-withdrawal day 1, 62 +/- 14 pmol/l, P less than 0.05; and post-withdrawal day 14, 89 +/- 17 pmol/1, P less than 0.005). The total integrated (TIR) PP response following a test breakfast was similarly elevated (control, 442 +/- 63 units; alcoholics, day 1, 1310 +/- 231 units, P less than 0.005; day 14,1066 +/- 66, P less than 0.005). Basal and TIR values for gastrin, gastric inhibitory peptide, insulin and glucagon were similar in alcoholics and controls. As PP has been shown to inhibit pancreatic exocrine enzyme secretion, these findings may help explain the abnormal pancreatic function seen frequently in alcoholics.

Pancreatic exocrine function in severe human chronic renal failure.

Patients with chronic renal failure have an abnormal immunoreactive gastrointestinal hormone profile, which is characterised by raised fasting serum concentrations of hormones that have antagonistic effects on exocrine pancreatic function. In addition, in this present study we have found that in renal insufficiency cholecystokinin disappears slowly from the plasma after a constant intravenous infusion of the hormone (p = 0.05 compared with healthy subjects). To evaluate whether the stimulatory or inhibitory hormones have a predominant effect, pancreatic exocrine function under conditions of mannitol perfusion of the duodenum and continuous intravenous cholecystokinin stimulation was studied in eight patients who had severe chronic renal failure and eight age-matched and sex-matched control subjects. Compared with healthy subjects, patients with renal insufficiency had hypersecretion of trypsin in response both to mannitol perfusion of the duodenum and to cholecystokinin stimulation (p less than 0.05). No significant differences in lipase secretion were noted between the patients with renal insufficiency and control subjects. These findings are consistent with the hypothesis that, of the abnormally raised fasting serum concentrations of gastrointestinal hormones found in renal insufficiency, hormones that stimulate rather than inhibit pancreatic exocrine function predominate. Secondly, the dissociation between trypsin and lipase outputs in chronic renal failure may suggest a differential trophic influence of stimulatory hormones -- that is, hypercholecystokininaemia -- on pancreatic exocrine enzyme secretion.