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Pancreatic gland located retroperitoneally accomplishes exocrine and endocrine function. The major components of neurohormonal system controlling pancreatic exocrine function include central nervous system with dorsal vagal complex DVC, the afferent (sensory) and efferent (motor) vagus nerves, the intrapancreatic ganglia, motor sympathetic nerves, enteric nerves as good as a number of hormonal substances such cholecystokinin, secretin, VIP, PYY, neurotensin, somatostatin, pancreatic polypeptide and others. Melatonin (N-acethyl-5- hydroxytryptamine) is synthesized from its precursor, L-tryptophan in four-step process. Melatonin is produced in pineal gland, retina, ciliary apparatus, Harderian gland, respiratory epithelium, kidney and mostly in the gastrointestinal tract. Melatonin receptors have been detected in the liver, spleen, intestine and also in pancreatic beta cells. The results presented so far have been suggested that melatonin takes a part in the regulation of gastric and jejunal motor activity, as well as ion and electrolytes transport in the intestinal mucosa. The protective effects of melatonin on gastric ulcer and on the bowel diseases as good as oncostatic effects of that indoloamine in gastrointestinal tumours have been described. Administration of exogenous melatonin and also melatonin precursor, L-tryptophan has revealed beneficent influence on the pancreatic ; in the course oi experimental acute pancreatitis. Leptin, a 167 amino-acid peptide takes a part in the regulation of body weight, food intake, energy expenditure. Leptin receptor has been detected in heart, placenta, lungs, liver, skeletal muscles, kidney, pancreas, spleen, prostate, ovaries, testis, small intestine and colon. Apart from adipose tissue leptin is produced in placenta, skeletal muscles, pituitary gland and primarily in the stomach. Leptin takes a part in the protection of gastric mucosa against acute damage. The presence of leptin receptor on pancreatic beta cells suggests that leptin could affect endocrine pancreatic function. That hormone influences also exocrine pancreatic secretion. Exogenous leptin, administered centrally or parenterally protects pancreatic gland from acute damage induced by subcutaneous infusion of caerulein on the course of acute experimental pancreatitis in the rats. Leptin exerts also the protective action in the ischaemic model of experimental acute pancreatitis. Ghrelin, 28-amino acid peptide is produced mainly in the gastric tissue, but its presence has been proved in hypothalamus, pituitary gland, ileum, kidney, placenta, heart, T and B lymphocytes, thyroid gland, lungs, ovaries, testis and pancreas. Ghrelin has been regarded as the most powerful orexigenic and fat deposition factor in the mammals. Numerous studies published recen ; tly described the gastroprotective role of ghrelin. Both intravenous or intracerebroventricular administration of ghrelin to the anaesthetized rats were reported to stimulate gastric acid secretion and motility . This effect has been reversed by vagotomy or atropine pretreatment, suggesting that ghrelin affects gastric function via the activation of the vagus nerve and muscarinic receptors. Recent studies have also demonstrated that ghrelin exerts the gastroprotective actions in the stomach against to stress-induced damage. Ghrelin has been also shown to modulate endocrine as well as exocrine pancreatic secretions, but the physiological role of this peptide in the modulation of pancreatic function remains unclear. It has been shown that ghrelin given intravenously is able to inhibit pancreatic exocrine secretion stimulated by cholecystokinin (CCK) in anaesthetized rats. This inhibitory effect of ghrelin on pancreatic enzyme secretion has been also observed in vitro, in pancreatic lobules. On the other hand central administration of ghrelin stimulated pancreatic exocrine secretion in conscious rats. Both gastric and pancreatic effects of ghrelin lune been shown to be mediated via vagus-dependent cholinergic pathway and probably via sensory nerves. The aim of my study was to evaluate the role of exogenous melatonin, melatonin precursor, L-tryptophan, leptin or ghrelin administer ; ed into duodenal lumen (intraduodenally i.d.) on pancreatic exocrine secretion under basal conditions or following the stimulation of this secretion with diversion of pancreato-biliary juice. I would also like to examine the involvement of CCK, sensory nerves vagal nerves and entero-pancreatic reflexes in the effects of luminally administered melatonin, L- tryptohan, leptin or ghrelin on pancreatic exocrine secretory function. The studies were performed on anesthetized rats with pancreto-biliary fistulas. The animals were surgically equipped with silicone catheters, one of them was inserted into pancreto-biliary duct and used to the collection of pancreatic secretion in 15 minutes aliquots , the other one - into duodenum for the purpose of reinfusion pancreto- biliary juice (previously collected) into the gut lumen. The examined substances (melatonin, L-tryptophan, leptin ghrelin) were dissolved in 0.5 ml of saline and administered intraduodenally as a bolus. To evaluate the role of vagal nerves in the pancreatic secretory effects melatonin, L-tryptophan, leptin or ghrelin in the rats the subdiaphragmatic vagotomy was performed tor 7 days before experiments. The involvement of sensory nerves in the effects of examined substances on the basal pancreatic enzyme secretion was studied in the lats with sensory nerves deactivated with capsaicin. Deactivation of sensory fibers was a ; ttained using capsaicin at total dose of 100 mg/kg given s.c. 10 days before the tests. To assess the effects of CCK, - receptor blockade on pancreatic secretory response to melatonin, L-tryptophan, leptin or ghrelin CCK, receptor antagonist was used. The concentration of α-amylase was measured in collected samples of pancreato- biliary juice. The results were expressed as total α-amylase output (IU/L/15 min). Plasma CCK level was estimated by radioimmunoassay method (RIA). The blood samples were taken at the end of the experiment from the abdominal vena cava and the blood was withdrawn into EDTA containing polyethylene tubes. The results of the study shows that exogenous melatonin, melatonin precursor L-tryptophan, leptin or ghrelin given into the duodenal lumen are able to pancreatic enzyme secretion under basal conditions or following the stimulation with diversion of pancreato-biliary juice. Bilateral vagotomy, deactivation of sensory nerves with capsaicin as well as CCK1 receptor blockade completely reversed the stimulatory effects of examined substances on pancreatic exocrine secretion. Intraduodenal application of melatonin, L-tryptophan, leptin or ghrelin manifested in dose-dependent increase of plasma CCK concentration. I conclude that exogenous melatonin, its precursor L-tryptophan, leptin or ghrelin administered intraduodenally could take a part in the physiologic ; al modulation of pancreatic enzyme secretion. The mechanism of the stimulatory action oi examined substances on exocrine pancreas seems to be dependent on CCK release as well as on the activation of sensory nerves and vago-vagal enteropancreatic reflexes.
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Feb 8, 2023
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| Edition name | Date |
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| ZB-120313 | Feb 8, 2023 |
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