Cholecystokinin release and biliopancreatic secretion in response to selective perfusion of the duodenal loop with aminoacids in man.

Abstract

SUMMARY The aim of this study was to measure the role of the duodenal loop in biliopancreatic secretion in man by infusing various stimuli at the ampulla of Vater and collecting duodenal contents at the ligament of Treitz, above an occluding balloon. Perfusion at 10 mVmin of a first mixture of aminoacids -phenylalanine (47.2 mmol), methionine (38.2 mmol), tryptophan (11 mmol), valine (61-6 mmol) -increased cholecystokinin (CCK) plasma concentrations and duodenal bile salt output (p<O.005) as compared with a control electrolyte solution, but did not change pancreatic enzyme secretion significantly; duodenal infusion of another aminoacid mixture -arginine (32.4 mmol), histidine (14.1 mmol), leucine (36 mmol), isoleucine (21-5 mmol), lysine (31 mmol), threonine (23 mmol) -did not change CCK plasma concentrations, bile salt or pancreatic enzyme output. The respective role of duodenal distension and endogenous CCK was investigated by perfusing the first aminoacid solution and the control solution at 2, 5, and 10 ml/min. Changing the perfusion rate of control solution from 2 to 5 mImin led to a significant increase (p<0O01) in pancreatic secretion with no further increase at 10 ml/min. Bile salt output was not influenced by the perfusion rate of control solution. During the perfusion of the aminoacid solution, despite a stepwise increase in CCK release, the only significant change in pancreatic secretion was an increase of lipase output (p<005) when the infusion rate was raised from 2 to 5 mllmin. Our results suggest that duodenal CCK release (1) depends on the nature of aminoacids (2) has a predominant role in the regulation of pancreatic secretion at low perfusion rate but is less effective when superimposed on a mechanical stimulus caused by duodenal distension (3) is a major stimulus for gall bladder contraction which is not influenced by duodenal distension.Infusion of aminoacids (AA) intraduodenally stimulates pancreatic enzyme secretion and gall bladder contraction. '' These effects are mediated by hormonal (essentially cholecystokinin (CCK) release) and neural pathways.'' It is accepted that stimulation of pancreatic enzyme production depends on the length of small intestine exposed to nutrients' but it has also been shown in man that, when a meal was infused into the stomach, the gastroduodenal segment was sufficient to elicit the entire postprandial enzyme output, with the more distal bowel not modifying this output in any way. 1158The role of the duodenal loop itself in biliopancreatic secretion has never been directly assessed in man but it was reported in canine experiments that perfusing the proximal 10 cm of intestine with phenylalanine did not induce any pancreatic secretory response. ' The aim of this work was to evaluate the role of the duodenal loop, separated from the rest of the bowel by a balloon, in biliopancreatic secretion in man.

Effect of L-Tryptophan and L-Leucine on Gut Hormone Secretion, Appetite Feelings and Gastric Emptying Rates in Lean and Non-Diabetic Obese Participants: A Randomized, Double-Blind, Parallel-Group Trial

“…For example, an intraduodenal infusion of a mixture of tryptophan, valine, methionine and phenylalanine dose-dependently stimulated CCK release and bile salt secretion, whereas an intraduodenal administration of a mixture of arginine, histidine, leucine/isoleucine, lysine and threonine did not change CCK concentrations or bile salt secretion [3]. This finding supports the hypothesis that gut peptide release is dependent upon the nature of the specific nutrient.…”

“…Early studies from the end of the last century provided experimental evidence that, through the release of CCK, L-trp modulates various digestive functions, including bile salt and pancreatic enzyme secretion, as well as appetite [3, 7, 26]. Along these lines, it has been proposed that CCK plays a role in the regulation of GLP-1 release which, in turn, could modulate digestive and metabolic processes [20].…”

Calcium‐sensing receptor mediates phenylalanine‐induced cholecystokinin secretion in enteroendocrine STC‐1 cells

“…1) at normal extracellular Ca 2+ concentrations (1.2 m m ). The effective concentration of Phe (20 m m ) in these cells corresponds to the Phe concentrations (8–50 m m ) that were found to stimulate CCK or pancreatic secretion in human and dog studies [2–5]. CCK secretion induced by 10 and 20 m m Phe was significantly enhanced by increasing the extracellular Ca 2+ concentration from 1.2 to 3.0 m m .…”

“…Fatty acids, dietary protein and peptides are potent stimulants [1]. Aromatic amino acids (phenylalanine and tryptophan) are also known to stimulate CCK and pancreatic secretion in humans and dogs [2–5]. The cellular mechanism by which these amino acids stimulate CCK secretion in enteroendocrine cells is still unclear.…”

Effects of Intraduodenal Infusions of L-phenylalanine and L-glutamine on Antropyloroduodenal Motility and Plasma Cholecystokinin in Healthy Men

“…This is in line with earlier studies showing that aromatic amino acids modulate upper GI function including biliopancreatic secretion, upper intestinal motility and gastrin and gastric acid secretion. 18,[31][32][33][34][35][36] Whether the different secretory responses are related to different amino acids transport mechanisms or luminal amino acids receptors, however, requires further research. We also evaluated the effect of L-Phe and L-Gln on APD motility.…”