Postprandial Pancreatic Secretion Research Articles

Effects of porcine pancreastatin on postprandial pancreatic exocrine secretion and endocrine functions in the conscious rat.

The inhibitory effect of a newly discovered polypeptide, pancreastatin, on postprandial pancreatic exocrine secretions and endocrine functions was examined in the conscious rat with a chronic external bile, pancreatic and gastric fistula. The infusion of 100 and 200 pmol/kg/h of pancreastatin significantly inhibited meal-stimulated pancreatic secretion of fluid and protein but not bicarbonate in a dose-dependent manner. The infusion of 100 and 200 pmol/kg/h of pancreastatin increased plasma pancreastatin concentrations (mean +/- SE) up to 133.5 +/- 15.9 and 209.8 +/- 14.5 pM, respectively. However, the same doses of pancreastatin failed to inhibit postprandial insulin and gastrin releases and did not affect blood glucose levels. It is suggested that pancreastatin may be an inhibitor of postprandial pancreatic exocrine secretion. However, the doses used in the present study may not have been high enough to affect endocrine functions.

Effects of non-peptidal CCK receptor antagonist (L-364,718) on pancreatic responses to cholecystokinin, gastrin, bombesin, and meat feeding in dogs.

Postprandial pancreatic secretion results from the interaction of neural and hormonal factors but their contribution to the net postprandial secretion is unknown. Recent description of highly specific and potent cholecystokinin (CCK) receptor antagonists allows the determination of the physiological role of CCK in the postprandial pancreatic secretion. In six dogs with chronic pancreatic fistulae, the blockade of CCK receptors by non-peptidal agent (L-364,718) caused little change in basal pancreatic secretion, but decreased significantly (p less than 0.05) by about 60% the pancreatic protein response to meat feeding and virtually abolished the pancreatic responses to CCK-8 and bombesin. The pancreatic protein responses to pentagastrin, reaching about 37% of CCK maximum, was also significantly reduced but this effect was less pronounced than that observed in tests with CCK-8 or bombesin stimulation. In contrast, cholinergically stimulated pancreatic secretion, reaching about 40% of CCK maximum, was unaffected by L-364,718. Cholecystokinin antagonism also failed to affect the postprandial and bombesin induced increments in plasma CCK and gastrin concentrations, but significantly reduced the PP responses to CCK-8 bombesin and meat feeding possibly as a result of the removal of the CCK mediated release of PP. We conclude that CCK plays a crucial role in the mediation of the postprandial and bombesin induced pancreatic secretion and in the PP release.

Role of pancreatic polypeptide in the regulation of pancreatic exocrine secretion in dogs.

The effect of intravenous infusion of synthetic human pancreatic polypeptide (HPP) or a rabbit anti-PP serum on pancreatic exocrine secretion was studied in 10 dogs with gastric and Thomas duodenal cannulas. The infusion of HPP, at a dose of 1 microgram.kg-1.h-1, achieved a plasma PP concentration that mimicked the peak plasma concentration of PP in both interdigestive and postprandial states. This dose of HPP significantly inhibited pancreatic secretion in the interdigestive state. By contrast, immunoneutralization of circulating PP by a rabbit anti-PP serum resulted in significant increases (P less than 0.05) in both interdigestive and postprandial pancreatic secretion, including water, bicarbonate, and protein. The increase in the pancreatic secretion paralleled a decrease in circulating PP level, which lasted for as long as 5 days. Furthermore, the anti-PP serum blocked the inhibitory action of exogenous HPP on pancreatic exocrine secretion. The present study indicates that endogenous PP plays a significant role in the regulation of the pancreatic exocrine secretion in both interdigestive and digestive states. Thus we conclude that PP is another hormone regulating pancreatic exocrine secretion in dogs.

Effect of cholecystokinin receptor antagonist on pancreatic responses to exogenous gastrin and cholecystokinin and to meal stimuli

Exocrine pancreatic response to food is believed to result from the interaction of neural and hormonal factors, but their contribution in the net postprandial secretion is unknown. Recent description of a highly specific and potent Cholecystokinin (CCK)-receptor antagonist permitted the evaluation of the physiologic role of CCK in postprandial pancreatic secretion. In dogs with chronic pancreatic fistula, CCK antagonism caused little alteration in sham feeding- or urecholine-induced pancreatic protein secretion, but reduced by ~60% the pancreatic protein response to a gastrointestinal meal and virtually abolished the pancreatic responses to duodenal perfusion with amino acids or oleate and to exogenous CCK, but not to secretin or neurotensin. The pancreatic protein responses, particularly to lower doses of gastrin, were also reduced by CCK-receptor antagonist, but no changes in the responses to secretin or neurotensin were detected. Cholecystokinin antagonism also significantly reduced the pancreatic polypeptide responses to CCK, gastrin, and the gastrointestinal meal, possibly due to removal of the CCK-mediated release of pancreatic polypeptide. We conclude that CCK plays a crucial role in the mediation of the gastrointestinal phase, but not the cephalic phase, of pancreatic secretion.

Adrenergic pathway in the inhibition of pancreatic secretion by peptide YY in dogs

Peptide YY (PYY) is released by perfusion of an ileocolonic segment with oleate and inhibits exocrine pancreatic secretion. This study was designed to determine the role of the adrenergic pathway in the PYY-induced inhibition of pancreatic secretion. After intravenous administration of PYY, there was a dose-dependent inhibition of pancreatic HCO3 and protein responses to secretin, cholecystokinin, and feeding in conscious dogs and a reduction in pancreatic blood flow in anesthetized animals. These inhibitory effects of PYY on pancreatic secretion and blood flow were abolished in the presence of combined phentolamine and propranolol. Ileal perfusion with oleate caused a rise in plasma PYY levels similar to that observed after intravenous infusion of exogenous PYY. Combined α- and β-adrenergic blockade also antagonized the effects of ileal perfusion with oleate on hormonal and postprandial pancreatic secretion. We conclude that exogenous PYY or endogenous PYY released by ileal oleate inhibits pancreatic secretory responses to exogenous secretin, cholecystokinin, or a meal and causes pancreatic vasoconstriction. Both these effects are mediated, at least in part, by the adrenergic pathway.

Meal-stimulated cholecystokinin release and exocrine pancreatic secretion in dogs.

To confirm the role of cholecystokinin (CCK) and secretin in digestion, exocrine pancreatic secretion, plasma CCK, and secretin were measured simultaneously in six dogs prepared with gastric and pancreatic fistulas after feeding a solid meal. Plasma CCK concentration determined by radioimmunoassay increased significantly from the basal level, reached a peak 35 min after meal ingestion, and after a dip it further increased toward the end of the 3-h observation. Pancreatic protein output increased significantly, peaked at the fifth 10-min period, and then declined progressively. Plasma CCK concentration and pancreatic protein output correlated significantly during the first postprandial hour. Plasma secretion demonstrated significant elevation at 15 min and a peak at 25 min after a meal. Plasma secretin correlated significantly with both bicarbonate output and flow rate during the 3 h. Simultaneous measurements of plasma CCK and secretin and of pancreatic secretion suggested that postprandial pancreatic secretion is primarily mediated by releases of CCK and secretin, but these hormones do not seem to be the only factors responsible for the secretion.

Pancreatic secretory response to intestinal stimulants: a review.

In humans and many laboratory animals, protein digestion products such as peptides and amino acids and fat digestion products such as fatty acids and monoglycerides are potent intestinal stimulants of pancreatic enzyme secretion. The pancreatic enzyme response to these intestinal stimulants is related to the perfused load (amount per unit time) rather than to concentration. Both neural and hormonal pathways mediate the enzyme response to these intestinal stimulants. Enteropancreatic, cholinergic, vago-vagal reflexes are probably the most important mediators of the enzyme response to low loads of amino acids and fatty acids; hormones, such as cholecystokinin, seem to be the major mediators of the response to high loads of amino acids and fatty acids. Under physiological conditions it is probably the interplay of neural and hormonal mechanisms which regulates the pancreatic response to these stimulants. Gastric acid is the major regulator of postprandial pancreatic bicarbonate secretion. Secretion released by HCl is probably the most important physiological hormonal mediator of postprandial pancreatic bicarbonate secretion; its effect being potentiated by extrinsic (vagal) and intrinsic (intrapancreatic) cholinergic nerves and release of other hormones, such as cholecystokinin.

Effect of rabbit anti-pancreatic polypeptide serum on postprandial pancreatic exocrine secretion in dogs

To determine whether pancreatic polypeptide (PP) is a physiologic inhibitor of pancreatic secretion, we have studied the effects of normal rabbit serum and anti-PP serum on pancreatic secretion during infusion of a physiologic dose of PP or intragastric food instillation in dogs. Infusion of 180 pmol/kg · h of PP, previously incubated with normal rabbit serum, induced increases in plasma PP (220 ± 21 pmol/L) similar to those after the meal (213 ± 51 pmol/L) and was accompanied by significant inhibition of pancreatic flow rate, bicarbonate output, and protein output (p < 0.05) stimulated by secretin and cholecystokinin (n = 6). However, when the effect of exogenous PP was studied after in vivo administration of anti-PP serum or after previous in vitro incubation with anti-PP serum, no inhibition of pancreatic secretion was found, indicating that immunoneutralization of PP blocks the biologic activity of the hormone. Intragastric instillation of 400 ml of liver extract resulted in significant increases in pancreatic flow rate and outputs of protein and bicarbonate (p < 0.01; n = 8), both during administration of normal rabbit serum and anti-PP serum. The postprandial increase in pancreatic secretion during administration of anti-PP serum was not significantly different from that during administration of normal rabbit serum. We, therefore, conclude that PP is not a physiologic inhibitor of postprandial pancreatic secretion.

Effects of amino acids on pancreatic polypeptide before and after vagotomy in the dog.

We have previously indicated a marked influence of the vagus nerve on postprandial pancreatic polypeptide secretion. The present study was designed to determine whether the vagus nerve also plays a role in the regulation of pancreatic polypeptide secretion by absorbed nutrients. The pancreatic polypeptide responses to 17 intravenously administered amino acids, as well as arginine and glucose, were measured and compared with those 1 year after truncal vagotomy in conscious dogs. In response to the infusion of a mixture of amino acids (20 g during 60 min), plasma pancreatic polypeptide concentrations decreased in normal dogs. The effect was, however, completely reversed by vagotomy, with a significant pancreatic polypeptide release being observed (p less than 0.05). Arginine (5 g during 60 min) also showed a similar, although not statistically significant, effect. After intravenous bolus-injection of glucose (0.5 g/kg body weight), a transient decrease of pancreatic polypeptide secretion was found; vagotomy abolished this response. These results suggest that the vagus nerve may have a suppressive role in the process of pancreatic polypeptide secretion induced by intravenous amino acid(s) and glucose.

Cimetidine and postprandial pancreatic exocrine secretion in dogs

In dogs fitted with a pancreatic cannula and a duodenal cannula the intake of a standard meal induced a significant increase in the flow of pancreatic secretion and in the output of amylase, total protein, bicarbonate and chloride. The oral administration (200 mg/day) of cimetidine to dogs was seen to elicit a marked decrease in postprandial flow increase and bicarbonate output, coinciding with a significant increase in amylase and total protein output. At the same time the postprandial duodenal pH remained at levels similar to those obtained in basal periods. The implications of secretin, gastrin and cholecystokinin (CCK) on these effects are discussed.

Pancreatic enzyme response to a liquid meal and to hormonal stimulation. Correlation with plasma secretin and cholecystokinin levels.

Pancreatic trypsin output and plasma secretin and cholecystokinin (CCK) levels were measured in five healthy volunteers to investigate the mechanisms involved in regulating postprandial pancreatic secretion. The pancreas was stimulated by a liquid test meal or by either intravenous secretin (1-82 pmol/kg-1 per h-1) or caerulein, a CCK analogue (2.3-37 pmol/kg-1 per h-1), or by a combination of secretin and caerulein. Pancreatic secretion was assessed by a marker perfusion technique (polyethylene glycol [PEG 4000]), plasma secretin, and CCK by specific radioimmunoassays. Increasing doses of secretin produced increasing bicarbonate output (P less than 0.01), whereas trypsin was not stimulated over basal. Graded caerulein produced a stepwise increase in trypsin and bicarbonate output (P less than 0.01). Potentiation occurred for bicarbonate secretion between secretin and caerulein, but not for trypsin output. Postprandial trypsin secretion averaged 29.1 IU/min-1 over 150 min (equal to 55% of maximal response to caerulein). The peak trypsin response amounted to 90% of maximal caerulein. Significant increases of plasma secretion (P less than 0.05) and CCK (P less than 0.01) were observed after the meal. Comparison of enzyme and CCK responses to the testmeal or to exogenous caerulein suggested that the amount of CCK released after the meal could account for the postprandial trypsin secretion. We conclude that (a) the postprandial enzyme response in man is submaximal in comparison to maximal exogenous hormone stimulation; (b) CCK is a major stimulatory mechanism of postprandial trypsin secretion, whereas secretin is not involved; and (c) Potentiation of enzyme secretion is not a regulatory mechanism of the postprandial secretory response.

Pancreatic polypeptide inhibits exocrine pancreatic responses to six stimulants.

We determined the effects of three different doses of pancreatic polypeptide (50, 200, and 800 pmol X kg-1 X h-1) on pancreatic responses to graded doses of intravenous secretin, caerulein, and bethanechol and intraduodenal HCl, L-phenylalanine, and sodium oleate in dogs. The two lowest doses of pancreatic polypeptide (PP), which produced blood levels lower than measured after a meal, significantly inhibited the pancreatic responses to secretin, caerulein, HCl, and L-phenylalanine; the highest dose of PP inhibited the responses to bethanechol and sodium oleate. There was no difference in the degree of inhibition of bicarbonate or protein secretion caused by pancreatic polypeptide. With secretin, caerulein, bethanechol, and sodium oleate, inhibition was most pronounced against lower doses and was surmountable with higher doses of these stimulants. Inhibition of responses to HCl and L-phenylalanine was observed at all doses of these stimulants. Inhibition of the exocrine pancreatic secretory responses to six different stimulants by PP suggests that this hormone may play an important role in regulation of postprandial pancreatic secretion.

The Intestinal Phase of Pancreatic Polypeptide Release

The purpose of this study was to determine whether nutrients in the small intestine cause a change in plasma pancreatic polypeptide concentration and, if so, the relative potencies of the major nutrient stimuli at different levels of the small intestine. We first compared the pancreatic polypeptide response to gastric and duodenal instillation of a test meal with that to ingestion of the same meal and modified sham feeding, in 10 healthy subjects. Intragastric feeding accounted for 70%, intraduodenal feeding accounted for 60%, and modified sham feeding accounted for 16% of the integrated pancreatic polypeptide response to meal ingestion. In separate experiments using a double-balloon intestinal perfusion technique, we examined the effects on plasma pancreatic polypeptide concentrations of 60-min infusions of isocaloric and isosmolar solutions of essential amino acids, oleic acid, and glucose in the upper, middle, and distal small intestine in random order in 7 healthy subjects. In the proximal small intestine, all three nutrients produced a significant rise in plasma pancreatic polypeptide concentrations, with a sequence of potency of: amino acids mixture (response = 3.04 ± 0.64 ng·min/ml), oleic acid (response = 1.25 ± 0.29 ng·min/ml), and glucose (response = 0.52 ± 0.14 ng·min/ml). The three nutrients retained their relative potencies in the middle small intestine, but were less effective than in the proximal segment (responses = 1.20 ± 0.26, 0.64 ± 0.12 and 0.39 ± 0.10 ng·min/ml for amino acids, oleic acid, and glucose, respectively). None of the nutrients perfused into the distal small intestine elicited a pancreatic polypeptide response. Thus, this study shows that the small intestine plays an important role in pancreatic polypeptide secretion which is dependent upon the nature of the nutrient and diminishes in effectiveness with distal progression. The demonstration of the existence of an enteropancreatic mechanism for the release of pancreatic polypeptide supports a possible physiologic role of pancreatic polypeptide as an inhibitor of postprandial pancreatic and biliary secretion.

Inhibition of postprandial pancreatic and biliary secretion by loperamide in patients with short bowel syndrome.

Patients with the short bowel syndrome are usually afflicted by chronic diarrhoea and treated with opiate drugs, yet little documentation of the effects of such drugs on digestive function is available. In the present study we found that acute oral administration of loperamide resulted in 50% inhibition of postprandial trypsin and bilirubin output in patients with short bowel syndrome. These changes are consistent with an opiate effect.

Output of bile and pancreatic enzymes after test meals with different fat content. Influence of body weight on pancreatic enzyme composition.

The output of bile and pancreatic enzymes after two mixed meals with different fat content was studied in 16 healthy volunteers of normal body-weight. A quantitative multiple indicator dilution method was used. The delivery of more fat per time to the duodenum after the fat rich compared to the low fat meal was followed by the emptying of more bile but did not significantly increase the pancreatic response. The ratio between amylase and lipase was constant throughout the course of a single experiment but differed between the subjects. The ratio decreased with an increasing body weight, indicating a relative dominance of amylase over lipase in the lighter and the reverse in the heavy subjects. The same correlation was found when results from a previously reported series with a glucose containing mixed meal were reexamined. It is proposed that long time dietary differences might influence the enzyme composition of the postprandial pancreatic secretion.

Gastrin-related peptides as stimulants of pancreatic and gastric secretion.

Gastrin-related peptides as stimulants of pancreatic and gastric secretion.

A new cannula for the study of pancreatic function.

A new cannula for the study of pancreatic function.

Diversion of pancreatic juice on gastric and pancreatic response to a meal stimulus.

ARTICLESDiversion of pancreatic juice on gastric and pancreatic response to a meal stimulusAR Cooke, DL Nahrwold, and MI GrossmanAR Cooke, DL Nahrwold, and MI GrossmanPublished Online:01 Sep 1967https://doi.org/10.1152/ajplegacy.1967.213.3.637MoreSectionsPDF (539 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByRegulation of Pancreatic SecretionA secretin releasing peptide exists in dog pancreatic juiceLife Sciences, Vol. 66, No. 14Feedback Regulation of Pancreatic Exocrine Secretion in Minipigs8 July 2009 | Scandinavian Journal of Gastroenterology, Vol. 32, No. 4Gastrin-releasing peptide and CCK after intraduodenal inhibition of proteases in dogsInternational journal of pancreatology, Vol. 15, No. 3Role of secretin in negative feedback regulation of postprandial pancreatic secretion in dogsGastroenterology, Vol. 105, No. 2The importance of gastric secretion in the feedback control of interdigestive and postprandial pancreatic secretion in ratsRegulatory Peptides, Vol. 36, No. 1Is there a duodenum-pancreas negative feedback?International journal of pancreatology, Vol. 8, No. 4Alterations in Digestive Function Caused by Pancreatic DiseaseSurgical Clinics of North America, Vol. 69, No. 3Effect of Pancreatic juice and Trypsin on Oleic Acid-Stimulated Pancreatic Secretion and Plasma Secretin in DogsGastroenterology, Vol. 96, No. 5Pancreatic Secretion and the Release of Cholecystokinin after a Meal in Dogs with and without Exclusion of Pancreatic Juice8 July 2009 | Scandinavian Journal of Gastroenterology, Vol. 24, No. 4Pancreatic secretory response to ordinary meals: Studies with pure pancreatic juiceGastroenterology, Vol. 94, No. 2Bile exclusion from the duodenumDigestive Diseases and Sciences, Vol. 30, No. 10Effect of intraluminal bile on the feedback regulatory mechanism of pancreatic enzyme secretion in conscious ratsGastroenterologia Japonica, Vol. 20, No. 3Pancreatic bicarbonate response to food-bound hydrogen ion along the gutGastroenterology, Vol. 87, No. 3Regulation of Pancreatic SecretionClinics in Gastroenterology, Vol. 13, No. 3Morton I. 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Effect of excluding pancreatic juice from duodenum on secretory response of pancreas to a meal.

Conclusion1. When canine pancreatic juice secreted in response to a meal was permanently removed by the method used in these experiments, the total volume of juice secreted was significantly greater than was the case when the juice was replaced in the duodenum. 2. A similar reduction in the volume of postprandial pancreatic secretion occurred when tenth normal sodium bicarbonate solution was instilled into the duodenum in place of pancreatic juice. 3. No similar reduction in secretion occurred when equivalent volumes of isotonic saline solution were substituted for pancreatic juice.