Neurohumoral control of exocrine pancreatic secretion

Abstract

Reports over the past year provide significant advances in our knowledge of the neurohumoral control of exocrine pancreatic secretion, especially related to human physiology. Major findings include those demonstrating that human pancreatic acinar cells do not respond to cholecystokinin stimulation and that a major circulating form of cholecystokinin is CCK-58. These findings establish that in humans, cholecystokinin causes pancreatic secretion via a neural circuit after interacting with neural sensory receptors in the mucosa of the intestine and that CCK-58 is the likely form of cholecystokinin that stimulates the neural pathways. Other findings demonstrate significant differences in the pancreatic secretory response in humans as a function of the type of nutrient delivered to the gut, especially the fact the elemental diets and medium-chain triglycerides cause much less stimulation of pancreatic secretion than do complex diets. Finally, convincing evidence demonstrating that pancreatic proteases cause inhibition of pancreatic secretion in humans has been presented. In addition to new insights into the neurohumoral control of pancreatic secretion, these findings provide information relevant to both the pathogenesis of pancreatic disorders and their treatment.