Neurohumoral control of exocrine pancreatic secretion

Department of Medicine, VA Greater Los Angeles Health Care System and University of California, Los Angeles, California 90073, USA.
Current Opinion in Gastroenterology (Impact Factor: 4.29). 10/2003; 19(5):443-6. DOI: 10.1097/00001574-200309000-00001
Source: PubMed


Purpose of review:
Advancing knowledge about normal physiology of the exocrine pancreas is essential for investigations into the mechanisms of disorders of the pancreas. To this end, reports published during the past year give further insights into the complexity of the hormonal and neural interactions and processes involved in exocrine pancreatic physiology.

Recent findings:
Key findings include demonstrations of different biologic effects of cholecystokinin peptides on pancreatic secretion, underlining the importance of measurement techniques to determine specific forms of peptide hormones involved in physiologic processes; investigations of the details of the central neural pathways involved in the vago-vagal reflex in pancreatic secretion; the demonstration of the essential role for intrapancreatic nerves in mediating meal-induced responses; and identification of a modulatory role for leptin in exocrine pancreatic secretion.

These findings should not only spur further investigations into mechanisms of normal physiology but also provide impetus for application of these findings to studies of pancreatic disorders.

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    • "Further studies revealing the nature of the enteric stimuli that selec - tively activate either the excitatory or the inhibitory compo - nents of the enteropancreatic innervation should provide the needed insight into the function of this system , and lead to better insight into the integration and / or summation of vagal and intrinsic signals to the pancreas . Finally , advancing knowledge on the normal physiology of the exocrine pancreas is essential for investigations into the mechanisms of disorders of the pancreas ( Pandol , 2003 ; 2004 ) . "
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    ABSTRACT: Although the molecular machinery and mechanism of cell secretion in acinar cells of the exocrine pancreas is well documented and clear, only recently has the pharmacophysiology of pancreatic exocrine secretion come to light. Therefore, we focus in this article on the current understanding of the pharmacophysiology of pancreatic exocrine secretion. The pancreatic secretory response to ingestion of a meal is mediated via a complex interplay of neural, humoral and paracrine mediators. A major role in the control of the intestinal phase of pancreatic secretion is attributed to vago-vagal enteropancreatic reflexes. In the scheme of this control mechanism, afferents originating in the duodenal mucosa, and efferents mediating central input on the pancreatic ganglia, activate intrapancreatic postganglionic neurons. Experiments utilizing specific receptor antagonists demonstrate the involvement of both muscarinic M1 and M3 receptors expressed in pancreatic acinar cells. Cholecystokinin (CCK), originally implicated in the humoral secretion of pancreatic enzymes, through a direct action on acinar CCK receptors, is also essential to the enteropancreatic reflex mechanism. CCK stimulation of the exocrine pancreatic secretion through excitation of sensory afferents of the enteropancreatic reflexes, is a paracrine mode of CCK action, and is probably the only one in humans and the predominant one in rats. In dogs, however, CCK acts on the pancreas via both the humoral and a paracrine route. More recent experiments suggest further possible sites of CCK action. Additionally, at the brain stem, vago-vagal enteropancreatic reflexes may be modulated by input from higher brain centres, particularly the hypothalamic-cholinergic system in the tonic stimulation of preganglionic neurons of the dorsal motor nucleus of the vagus projecting into the pancreas.
    Preview · Article · Nov 2008 · Cell Biology International
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    ABSTRACT: Aunque el manejo nutricional de los pacientes con Pancreatitis Aguda Severa ha sido bien establecido por la evidencia disponible, el inicio de la vía oral en Pancreatitis Leve no ha sido igualmente estudiado. El objetivo de este estudio es evaluar el efecto del inicio temprano de la nutrición por vía oral en estos pacientes. Métodos: Realizamos un descriptivo serie de comparación de casos en los cuales comparamos la evolución y resultados del manejo de los pacientes con pancreatitis aguda antes y después de iniciar un protocolo de inicio temprano de nutrición por vía oral. Resultados: La serie incluyó 13 pacientes manejados con restitución convencional y 9 pacientes a quienes se restituyó tempranamente la nutrición oral. No existieron diferencias estadísticamente significativas en cuanto las características clínicas, etiológicas y demográficas entre los grupos. No se presentaron casos de progresión a enfermedad severa en ninguno de los grupos. La aparición de síntomas gastrointestinales como vomito y dolor después del inicio de la dieta fue similar en los dos grupos. Conclusiones: La restitución de la nutrición por vía oral basada criterios preestablecidos (la intensidad del dolor menor de 4 y un periodo mayor a 6 horas desde el último episodio emético) es segura y disminuye el periodo de ayuno inicial mas no el de estancia hospitalaria. Although the nutritional management of patients with severe acute pancreatitis has been well established by the available evidence, little attention has been paid to optimizing the dietary management of mild acute pancreatitis. The aim of this study is to evaluate the effect of early initiation of oral nutrition in these patients. 8 Methods: A descriptive comparative case series in which we compare the progress and outcome of management of patients with acute pancreatitis before and after initiating a protocol of early oral nutrition. Results: The series included 13 patients managed with conventional restitution of nutrition by mouth and 9 patients with early restitution of nutrition by mouth oral nutrition. There were no statistically significant differences in etiology, clinical characteristics, and demographic differences between the groups. There were no cases of progression to severe disease in either group. The occurrence of gastrointestinal symptoms like vomiting and pain after the start of the diet was similar in both groups. Conclusions: The restoration of oral nutrition based in preset criteria (pain intensity of less than 4 and a period longer than 6 hours after the last episode emetic) is safe and reduces the initial fasting period but not the hospital stay.
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    ABSTRACT: Ertan et al have shown that the perfusion of the proximal jejunum with a mixture of amino acids (MAA) in physiological concentration releases endogenous cholecystokinin (CCK) in man. In the present experiment, we investigate the mechanism by which jejunal MAA perfusion mediates an increase in exocrine pancreatic and biliary secretions. The effects of a bolus of topical anesthetic (oxethazaine, 0.5 mg/kg of 0.4% solution) or the simultaneous jejunal perfusion of a topical anticholinergic agent (atropine, 1 mg/liter) were studied in the same five normal patients on different days. Suppression of the response to jejunal MAA perfusion but not to intravenous infusion of CCK or jejunal saline perfusion, was noted in these normal subjects following jejunal application of oxethazaine and atropine. These results suggest a local involvement of the cholinergic mechanism for the endogenous release of CCK, while exogenous CCK acts directly on the pancreatic cells.
    No preview · Article · Oct 1975 · The American Journal of Digestive Diseases
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