Pancreatic polypeptide: a review of its involvement in neuro-endocrine reflexes, islet-acinar interactions and ethanol-evoked physiopatologic pancreatic gland changes
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| Natura: | Artículo científico |
| Lingua: | en |
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Sociedad Argentina de Gastroenterología
2015
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| _version_ | 1876462028761071616 |
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| author | Osvaldo Manuel Tiscornia |
| author_facet | Osvaldo Manuel Tiscornia |
| contents | Pancreatic polypeptide: a review of its involvement in neuro-endocrine reflexes, islet-acinar interactions and ethanol-evoked physiopatologic pancreatic gland changes Osvaldo Manuel Tiscornia Gustavo Alberto Negri Graciela Otero Fabiana Norma López Mingorance Hipólito Waisman Patricia Graciela Tiscornia-Wasserman Medicina neuro islet flexes endocrine re acinar interactions This review was prompted by the unexpected experimental finding in canines that Tissucol-induced pancreatic duc-tal blockade elicits Pancreatic Polypeptide (PP) release and seems to be at the basis of the beneficial effects on taurocho-late-induced acute pancreatitis (AP). In the release mecha-nism of this regulatory peptide secreted by PP cells located in the periphery of Langerhans islets and scattered in the ductal epithelium, two neuroendocrine reflexes (NER) are involved. The "short" NER is evoked from the duodenum by an unknown component of bile-pancreatic secretion. The "long" NER is triggered by a vagovagal reflex. PP induces a depression of the intrapancreatic cholinergic tone. On the one hand suppressing, hormonally, nervous impulses dischar-ge from the vagal nuclear complex in the brainstem. On the other, interfering paracrinically on the cholinergic transmis-sion by acting, presynaptically, on post-ganglionic cholinergic neurons. The resulting PP-evoked fall of the intrapancrea-tic cholinergic tone depresses the hormone induced (secretin, CCK) pancreon’s secretory response. PP, with other agents, contributes to the "fail-safe" system or pancreon's brake that prevents, in pancreocytes, the evolving of a "supramaximal-ecbolic-stimulation" process. The PP involvement as a mo-dulating agent of pancreon’s reactivity is reflected by the pro-gressive increment of its plasma values in the first week of an evolving AP episode. In the AP associated to a large meal, an overpowering of the "pancreon’s brake might have a pivotal role. In experimental and clinical chronic alcoholism, a vagal neuropathy of the Pavlov inhibitory fibers that, as a conse-quence, impairs the pancreon’s brake through a depression of PP secretion is at the basis of an enhanced reactivity of the duodeno-pancreatic reflexes. The latter leads to intrapancrea-tic cholinergic hypertonus and to Vater papilla’s dysfunction. These changes, plus an enhanced pancreocyte's response to CCK, are at the core of acinar cell "supramaximal stimula-tion" with the organelle disruption that process implies. The intrapancreatic cholinergic hypertonus, the enhanced exocri-ne cell reactivity to CCK stimulation, and the augmented resistance to the pancreatic secretion flow at Oddi sphincter, explain the aggravating influence of chronic alcoholism on an episode of acute biliary pancreatitis. As the PP secretion, normally elicited by secretin, CCK, food and insulin hypogly-cemia, is depressed in the presence of an augmented number of PP cells, as it is in the cases of chronic alcoholics, cystic fibrosis patients and, also, in dogs with pancreatic fibrosis (ductal ligation), it has been inferred, besides our postulated impairment of the Pavlov inhibitory fibers in the vagus ner-ves, that the defect of PP release is localized to the common final pathway of the above stimuli, probably in or near the PP cell itself. 2015 artículo científico 2469-1119 https://www.redalyc.org/articulo.oa?id=199341085013 en http://www.redalyc.org/revista.oa?id=1993 Acta Gastroenterológica Latinoamericana application/pdf Sociedad Argentina de Gastroenterología Acta Gastroenterológica Latinoamericana (Argentina) Num.2 Vol.45 |
| format | Artículo científico |
| id | redalyc_199341085013 |
| institution | Redalyc |
| language | en |
| publishDate | 2015 |
| publisher | Sociedad Argentina de Gastroenterología |
| spellingShingle | Pancreatic polypeptide: a review of its involvement in neuro-endocrine reflexes, islet-acinar interactions and ethanol-evoked physiopatologic pancreatic gland changes Osvaldo Manuel Tiscornia Medicina neuro islet flexes endocrine re acinar interactions Pancreatic polypeptide: a review of its involvement in neuro-endocrine reflexes, islet-acinar interactions and ethanol-evoked physiopatologic pancreatic gland changes Osvaldo Manuel Tiscornia Gustavo Alberto Negri Graciela Otero Fabiana Norma López Mingorance Hipólito Waisman Patricia Graciela Tiscornia-Wasserman Medicina neuro islet flexes endocrine re acinar interactions This review was prompted by the unexpected experimental finding in canines that Tissucol-induced pancreatic duc-tal blockade elicits Pancreatic Polypeptide (PP) release and seems to be at the basis of the beneficial effects on taurocho-late-induced acute pancreatitis (AP). In the release mecha-nism of this regulatory peptide secreted by PP cells located in the periphery of Langerhans islets and scattered in the ductal epithelium, two neuroendocrine reflexes (NER) are involved. The "short" NER is evoked from the duodenum by an unknown component of bile-pancreatic secretion. The "long" NER is triggered by a vagovagal reflex. PP induces a depression of the intrapancreatic cholinergic tone. On the one hand suppressing, hormonally, nervous impulses dischar-ge from the vagal nuclear complex in the brainstem. On the other, interfering paracrinically on the cholinergic transmis-sion by acting, presynaptically, on post-ganglionic cholinergic neurons. The resulting PP-evoked fall of the intrapancrea-tic cholinergic tone depresses the hormone induced (secretin, CCK) pancreon’s secretory response. PP, with other agents, contributes to the "fail-safe" system or pancreon's brake that prevents, in pancreocytes, the evolving of a "supramaximal-ecbolic-stimulation" process. The PP involvement as a mo-dulating agent of pancreon’s reactivity is reflected by the pro-gressive increment of its plasma values in the first week of an evolving AP episode. In the AP associated to a large meal, an overpowering of the "pancreon’s brake might have a pivotal role. In experimental and clinical chronic alcoholism, a vagal neuropathy of the Pavlov inhibitory fibers that, as a conse-quence, impairs the pancreon’s brake through a depression of PP secretion is at the basis of an enhanced reactivity of the duodeno-pancreatic reflexes. The latter leads to intrapancrea-tic cholinergic hypertonus and to Vater papilla’s dysfunction. These changes, plus an enhanced pancreocyte's response to CCK, are at the core of acinar cell "supramaximal stimula-tion" with the organelle disruption that process implies. The intrapancreatic cholinergic hypertonus, the enhanced exocri-ne cell reactivity to CCK stimulation, and the augmented resistance to the pancreatic secretion flow at Oddi sphincter, explain the aggravating influence of chronic alcoholism on an episode of acute biliary pancreatitis. As the PP secretion, normally elicited by secretin, CCK, food and insulin hypogly-cemia, is depressed in the presence of an augmented number of PP cells, as it is in the cases of chronic alcoholics, cystic fibrosis patients and, also, in dogs with pancreatic fibrosis (ductal ligation), it has been inferred, besides our postulated impairment of the Pavlov inhibitory fibers in the vagus ner-ves, that the defect of PP release is localized to the common final pathway of the above stimuli, probably in or near the PP cell itself. 2015 artículo científico 2469-1119 https://www.redalyc.org/articulo.oa?id=199341085013 en http://www.redalyc.org/revista.oa?id=1993 Acta Gastroenterológica Latinoamericana application/pdf Sociedad Argentina de Gastroenterología Acta Gastroenterológica Latinoamericana (Argentina) Num.2 Vol.45 |
| title | Pancreatic polypeptide: a review of its involvement in neuro-endocrine reflexes, islet-acinar interactions and ethanol-evoked physiopatologic pancreatic gland changes |
| topic | Medicina neuro islet flexes endocrine re acinar interactions |
| url | https://www.redalyc.org/articulo.oa?id=199341085013 |