Biomedical subjects

W Y Chey

Publications and source records attributed to W Y Chey.

At least 91 records · Page 5Linked to original sources

PubMed1991

The secretin gene: evolutionary history, alternative splicing, and developmental regulation.

The gene encoding the hormone secretin has been isolated and structurally characterized. The transcriptional unit is divided into four exons spanning 813 nucleotides. Comparison of the rat secretin gene to the other members of the glucagon-secretin gene family reveals that similarities are restricted to the exons encoding the biologically active peptides. Analysis of RNA from porcine intestine indicates that at least two transcripts are generated from the porcine secretin gene as a result of differential splicing. The longer and more abundant transcript appears to be identical to a previously isolated cDNA, which encodes a precursor that includes a 72-amino acid C-terminal extension peptide. The shorter transcript does not contain the third exon and, as a result, encodes only 44 residues beyond the C terminus of secretin. The amino acid sequence deduced from the shorter transcript is identical to a precursor form of secretin recently isolated from porcine duodenum [Gafvelin, G., Jornvall, H. & Mutt, V. (1990) Proc. Natl. Acad. Sci. USA 87, 6781-6785]. Developmental studies reveal that both secretin mRNA and peptide levels in the intestine are highest just before birth, prior to the onset of gastric acid secretion and feeding. This observation implies that secretin biosynthesis in developing animals is controlled independently of the principal factors known to regulate secretin release in adult animals.

Amino Acid Sequence↗

PubMed1991

Regulation of pancreatic exocrine secretion.

The exocrine pancreas secretes throughout 24 hours. In both interdigestive and postprandial states, pancreatic secretion is regulated by neural and hormonal actions, and neurohormonal interactions. At the turn of this century, the prevailing theory of Pavlov (1) that pancreatic exocrine secretion was exclusively regulated by secretory fibers in both vagi and splanchnic nerves was refuted by Bayliss and Starling in 1902, who put forward their hypothesis that pancreatic secretion was stimulated by a circulating hormone, "secretin," which was released by hydrochloric acid from the duodenal mucosa (2). Soon, Pavlov conceded to the hypothesis of Bayliss and Starling. Pavlov adopted the theory of a dual mechanism--nervous and hormonal--of the regulation of pancreatic secretion. In recent decades, explosions of new information about old and newly discovered gut hormones or peptides and neuropeptides have resulted in a better understanding of the regulatory mechanism of the exocrine pancreas, and also opened new, exciting frontiers in the investigations of the physiology and pathophysiology of pancreatic secretion.

Animals↗

PubMed1991

Role of cholecystokinin in pancreatic bicarbonate secretion in dogs.

We investigated the effects of endogenous and exogenous cholecystokinin (CCK) on pancreatic exocrine secretion, in particular that of bicarbonate. In six dogs prepared with gastric cannulas and Thomas duodenal cannulas, intraduodenal administration of corn oil (Lipomul) incubated with hog pancreatic enzymes significantly increased pancreatic secretion of both bicarbonate and protein. Increase in pancreatic secretion of both bicarbonate and protein was accompanied by the increase in plasma CCK concentration. However, the increase in bicarbonate as well as protein secretion was blocked by proglumide, a CCK antagonist, given intravenously. In contrast, intraduodenal infusion of undigested Lipomul failed to stimulate the pancreatic exocrine secretion or release of endogenous CCK. These observations indicate that endogenous CCK plays an important role in secretion of both bicarbonate and protein stimulated by digested corn oil. In a group of four dogs with pancreatic fistulas, intravenous infusion of CCK potentiated the stimulatory effect of secretin on pancreatic bicarbonate secretion. The stimulatory effect as well as potentiating effect of CCK on pancreatic bicarbonate secretion was blocked by infusion of proglumide. We conclude that endogenous CCK plays a significant role in fat-stimulated pancreatic secretion, and it is apparent that both endogenous CCK and secretin are equally important for stimulation of pancreatic bicarbonate secretion, which results from potentiation of the action of the two hormones.

Animals↗

PubMed1991

Mechanism of oleic acid-induced inhibition on gastric acid secretion in rats.

We investigated the existence of an enterogastrone in rats induced by duodenal administration of oleic acid. Acid secretion by the luminally perfused stomach was stimulated in anesthetized rats by intravenous infusion of 0.3 micrograms.kg-1.h-1 pentagastrin. Intraduodenal administration of 3 mmol of oleic acid produced a profound inhibition (94%) of pentagastrin-stimulated acid output in 10 rats (P less than 0.01). Of several peptides in plasma including secretin, neurotensin, somatostatin, and peptide YY, only secretin was found to increase significantly (P less than 0.001). A similar degree of inhibition of acid output (93%) was caused by porcine secretin, 5.6 pmol.kg-1.h-1, given intravenously to mimic the plasma level of secretin produced by oleic acid infusion. The inhibitory effect of oleic acid on the acid secretion was completely reversed by intravenous injection of a rabbit antisecretin serum but not by a normal rabbit serum. These observations strongly suggest that the inhibition was mediated via circulating secretin. The inhibition produced by either oleic acid or secretin was completely blocked by indomethacin. The blocking action was completely reversed by intravenous administration of 48 micrograms.kg-1.h-1 prostaglandin E2. We conclude that endogenous secretin is a major enterogastrone released by oleic acid in anesthetized rats and that the inhibitory action of secretin requires endogenous prostaglandins.

Animals↗

PubMed1991

Role of secretin in basal and fat-stimulated pancreatic secretion in conscious rats.

The role of endogenous secretin in basal and fat-stimulated pancreatic exocrine secretion was investigated in conscious rats. Rats were prepared with chronic fistulas draining bile and pancreatic juice, which was collected and returned to the duodenum at all times. Six days postoperative rats were fasted overnight, and pancreatic protein and fluid secretion were monitored for 3 h under basal conditions (0.15 M NaCl, intraduodenally) and during 2 h of intraduodenal infusion of a 20% triglyceride emulsion (Liposyn). Solutions were infused at 4.6 ml/h. Rats received a single bolus injection of 0.1 ml antisecretin serum or normal rabbit serum starting in the second hour of the basal period, and the effect on basal and fat-stimulated pancreatic protein and fluid secretion was determined. Antisecretin serum significantly inhibited basal interdigestive pancreatic protein and fluid secretion by 43% and 36%, respectively. Infusion of 20% fat emulsion stimulated a 2.1-fold increase in pancreatic protein and fluid secretion. The stimulation of both protein and fluid secretion was significantly inhibited by 60% by antisecretin serum. Plasma secretin after 2 h of fat infusion was 17.7 +/- 1.8 pM and was greatly reduced by the presence of secretin antiserum. The results support the hypothesis that secretin released by fatty acids is an important mediator of the pancreatic protein and fluid secretory response to dietary fat in the rat.

Animals↗

PubMed1991

[Ulcerous disease of endocrinal origin caused by a non-gastric substance].

The purpose of this paper is to report on a form of duodenal ulceration associated with a major hypersecretion that we described in 1984. This entity belongs to the group of endocrine duodenal ulcer diatheses of which the Zollinger-Ellison Syndrome (ZES) is the prototype. We have recently in 1989 reported a series of patients with clinical and pathologic features indistinguishable from those of the Zollinger-Ellison syndrome but without hypergastrinemia. We have also found that the plasma and the tumor tissues of these patients contains a potent non-gastrin secretagogue.

Adult↗

PubMed1990

Postprandial levels of prolactin and gut hormones in breast cancer patients: association with stage of disease, but not dietary fat.

Previous studies of the relationship between dietary fat and breast cancer have produced conflicting results and have provided no definitive evidence of a mechanistic link between fat and breast tumorigenesis. We conducted a study to compare postprandial levels of prolactin (Prl), a hormone suspected of promoting the growth of some human breast cancer, and several gut hormones, i.e., gastrin (Gs), vasoactive intestinal polypeptide (VIP), neurotensin (Nt), and cholecystokinin (CCK), following high- and low-fat isocaloric test meals. Data were obtained in the posttreatment period from 13 patients with breast cancer (nine stage I and four stage II), who were disease free clinically, and nine healthy controls. Subjects admitted to the research unit on 2 days were given the high-fat meal on day 1 and the low-fat meal on day 2. Blood samples were drawn before (i.e., fasting) and after test meal consumption. All hormone analyses were performed by radioimmunoassay. Results indicated a significant rise in postprandial Prl levels for stage II patients, but not for stage I patients or the controls. Postprandial Gs levels were also elevated, whereas VIP levels were markedly reduced in patients versus controls; these differences were most marked in stage II patients. No significant intergroup differences were noted in postprandial levels of Nt and CCK. Hormone levels of patients and controls did not differ between the test meal situations, which indicated that some other component of the test meals might have been responsible for altered Prl and Gs levels. The differences observed between the stage I and II patients indicated that diet may influence the aggressiveness of tumor behavior and development through alterations in postprandial hormone release.

Breast Neoplasms↗

PubMed1990

Increased volume and decreased emptying of the gallbladder in large (morbidly obese, tall normal, and muscular normal) people.

Impaired gallbladder emptying has been suggested as a possible factor in the pathogenesis of gallstones. Obese people have an increased incidence of gallstones, but there is no evidence of this in nonobese large people. This study was undertaken to determine if abnormal gallbladder motility is present in obese people. Fasting gallbladder volumes were determined using real-time ultrasound in 18 morbidly obese subjects whose weights were in a steady state [45 kg (100 lb) over ideal weight or twice expected weight for age and height; 9 males, 9 females], 18 age- and sex-matched volunteers of average size, and 18 nonobese large normal males (9 tall, 9 muscular). Gallbladder emptying studies with 99mtechnetium-diisopropyliminodiacetic acid were performed using 200 ml of 10% cream as a stimulus. The small-volume liquid fatty meal contained 113indium-diethylenetriaminepentaacetic acid to control for differences in gastric emptying in obesity. The gallbladder emptying rate in large people, both obese and nonobese, was less than that in normals of average size (p = 0.05). Fasting gallbladder volumes in large people were: obese, 41 ml (37-66 ml) (median; 95% confidence limits); nonobese large normal, 40 ml (27-43 ml). These values were greater than in normals of average size [17 ml (14-21 ml) (p = 0.03)]. Postprandial gallbladder volumes were also greater in large people: obese, 15 ml (8-23 ml); nonobese large normal, 20 ml (13-23 ml) compared with 2 ml (1-5 ml) in normals of average size (p less than 0.05). There were no differences between obese and nonobese large people. There were no differences in gastric emptying rates or in cholecystokinin, gastrin, motilin, and secretin release between obese and normal subjects. Gallbladder volume is crudely proportional to body size. Although fasting and postprandial volumes are greater in obesity, this is also present in nonobese, relatively size-matched controls. These data do not support a role for impaired gallbladder emptying in gallstone formation in obese patients whose weights are in a steady state.

Adult↗

PubMed1990

Mechanism of cholecystokinin-induced contraction of the opossum gallbladder.

The present study evaluated the mechanism of cholecystokinin-induced gallbladder contraction in awake opossums. Each of 19 chronic animal preparations had an indwelling gallbladder cannula for monitoring changes in gallbladder volume and a jugular catheter for administration of cholecystokinin octapeptide and drugs. An intraduodenal catheter allowed intraduodenal infusion of Isocal (Mead Johnson Laboratories, Evansville, Ind.). Bipolar electrodes in the stomach, duodenum, and jejunum enabled monitoring of the duodenal migratory myoelectric complex cycle. One-hour infusions of cholecystokinin octapeptide (10 ng/kg/min), intraduodenal Isocal (0.4 ml/min), or feeding were started 20 min after cessation of phase 3 duodenal migratory myoelectric complex activity. Bolus intravenous doses of potential pharmacological antagonists were given 10 min before and 20 min after the onset of cholecystokinin octapeptide infusion, Isocal infusion, or feeding. Each test challenge induced about 60% gallbladder emptying at 30 min and 70% at 60 min. Cholecystokinin octapeptide-induced gallbladder emptying was converted to filling by hexamethonium and nearly abolished by atropine. Similar results were obtained for gallbladder emptying induced by feeding or duodenal infusion of Isocal. Phentolamine caused a modest decrease of cholecystokinin octapeptide-induced gallbladder contraction at 30 min, whereas postprandial or Isocal-induced gallbladder contraction was unaffected. Cholecystokinin octapeptide-induced gallbladder contraction was not affected by pirenzepine, 4-diphenylacetoxy-N-methylpiperidine methiodide, prazosin, pyrilamine, cimetidine, methysergide, naloxone, or propranolol. In acute studies of anesthetized animals, gallbladder contraction induced by a D100 intravenous bolus of cholecystokinin octapeptide (800 ng/kg) was not antagonized by hexamethonium, atropine, or tetrodotoxin. It is concluded (a) that cholecystokinin-induced physiologic contraction of the opossum gallbladder occurs through neural mechanisms rather than by a direct action of cholecystokinin on gallbladder smooth muscle, and (b) that studies using pharmacologic bolus doses of cholecystokinin octapeptide and tetrodotoxin indicate that cholecystokinin receptors exist on the gallbladder smooth muscle which do not seem to have any physiological role in gallbladder emptying.

Animals↗

PubMed1990

Effect of pancreatic proteases on plasma cholecystokinin, secretin, and pancreatic exocrine secretion in response to sodium oleate.

The effect of pancreatic proteases or juice on the sodium oleate-stimulated pancreatic secretion and plasma concentrations of secretin and cholecystokinin in anesthetized rats was investigated. Each rat received sodium oleate in a dose of 0.12 mmol.h-1 via a duodenal tube. Sodium oleate infusion significantly increased pancreatic secretion (volume and protein output) compared with the saline given the control group. The increase in pancreatic secretion paralleled significant elevations of plasma concentrations of secretin and cholecystokinin. To determine a possible role of pancreatic proteases on the responses induced by sodium oleate, saline, chymotrypsin, and trypsin, a combination of chymotrypsin and trypsin or pancreatic juice was infused into the duodenum. The pancreatic secretion was significantly reduced by pancreatic proteases or pancreatic juice, and the reduction paralleled the decreases in plasma concentrations of the two hormones. These agents suppressed both pancreatic secretion and plasma hormone levels in the following order of magnitude: (pancreatic juice or chymotrypsin + trypsin) greater than (trypsin) greater than (chymotrypsin). The reduction of pancreatic secretion by pancreatic proteases was reversed by intravenous administration of secretin and cholecystokinin in physiological doses. It is concluded that negative-feedback regulation of pancreatic secretion is operative in the intestinal phase in rats and that both secretin and cholecystokinin are involved in the regulation.

Animals↗

PubMed1990

An epidemiologic study of inflammatory bowel disease in Rochester, New York. Hospital incidence.

The epidemiological understanding of inflammatory bowel disease has been limited by the referral bases of most inflammatory bowel disease studies. The Colitis-Ileitis Study Group of Rochester, N.Y., developed a community-wide, computerized cumulative registry of all inflammatory bowel disease patients hospitalized at the 8 community hospitals for 1973-86. Clinical data were abstracted from each of the 1651 identified hospital charts. All of these patients resided in Monroe County (city and suburbs) and the 5 contiguous counties (Genesee/Finger Lakes Region, population 1,030,640). Of the 1651 hospital patients identified in the study, 1358 resided in Monroe County (Rochester and its immediate suburbs, population 702,238). Incidence, defined as time of onset of symptoms of inflammatory bowel disease, rose from baseline rates in the 1930s to peak in 1980 (Crohn's disease = 50.29/10(5) per decade, ulcerative colitis = 35.12/10(5) per decade) and declined through 1986. For Crohn's disease, the age-specific incidence rates peaked in the 20-29-yr-old group in each of the 5 decades studied. Ulcerative colitis seems to occur at all ages and may have a bimodal distribution. There was a period effect, with the 1970s having the highest incidence of Crohn's disease and ulcerative colitis for each age group. However, the age-specific incidence rate for Crohn's disease showed a 40% decrease in the 1980s compared with the 1970s in the 10-39-yr-old group (p less than 0.001). The age-specific incidence rate for ulcerative colitis showed a 50% decrease in the 1980s compared with the 1970s in the 10-49-yr-old group (p less than 0.001).

Age Factors↗

PubMed1990

A nongastrin malignant ampullary tumor causing gastric acid and pepsin hypersecretion. A case report.

We report a case of multiple duodenal ulcers with gastric hypersecretion due to a nongastrin secretagogue produced by a malignant tumor of the pancreas in a 78-year-old man. The case resembled a Zollinger-Ellison syndrome (ZES) with high acid output (basal acid output 27, sham meal-stimulated 37, maximum acid output 47 mEq/h), but with fasting gastrin 43 pg/ml, nonresponsive to secretin. As in ZES, pepsin output was comparatively low, and secretion was inhibitable by atropine (50% inhibited by 1 microM). The tumor removed at surgery contained less than 1 ng gastrin per gram, but was many times more potent than pentagastrin in stimulating acid from a lumen-perfused rat stomach. The tumor also contained cholecystokinin (CCK-8 and CCK-33), motilin, insulin, and somatostatin, which were also present in adjacent normal pancreas; in addition, the tumor contained pancreatic polypeptide and pancreatic cancer-associated antigen. This case represents a rare syndrome due to an as yet undefined peptide secreted by a (frequently malignant) pancreatic endocrine tumor and masquerading as ZES. This is the first report of studies of pepsin secretion and of the effect of atropine, suggesting that the physiologic effects of the secretagogue resemble that of gastrin.

Adenoma↗

PubMed1990

An important role of endogenous insulin on exocrine pancreatic secretion in rats.

We have investigated a physiological role of endogenous insulin on exocrine pancreatic secretion stimulated by a liquid meal as well as exogenous secretin and cholecystokinin octapeptide (CCK-8) in conscious rats. Each rat was prepared with a chronic pancreatic fistula and an indwelling catheter in a jugular vein. Oral ingestion of a liquid meal (5 ml) resulted in significant increases in pancreatic secretion, including volume, bicarbonate, and amylase output, in these rats. A rabbit anti-insulin serum (1.0 ml) given intravenously completely blocked the postprandial exocrine pancreatic secretion, whereas a normal rabbit serum did not influence the pancreatic secretion in the same rats. When pancreatic secretion was stimulated by intravenous administration of both secretin and CCK-8 in three different doses, including 0.015, 0.03, and 0.06 clinical unit and microgram.kg-1.h-1, respectively, volume, bicarbonate, and amylase output increased significantly in a dose-dependent manner. This increase in pancreatic secretion was also completely blocked by a rabbit anti-insulin serum, whereas it was not influenced by a normal rabbit serum. The amount of the antiserum employed abolished the postprandial increases in plasma insulin concentration. We conclude that endogenous insulin plays an important role on the regulation of postprandial pancreatic secretion in rats. Furthermore, for the stimulatory action of the two intestinal hormones secretin and CCK-8 on the pancreatic exocrine secretion, endogenous insulin is need.

Amylases↗

PubMed1990

Hormonal mechanism of sodium oleate-stimulated pancreatic secretion in rats.

We have investigated the role of two intestinal hormones, secretin and cholecystokinin (CCK), on the pancreatic exocrine secretion stimulated by sodium oleate in anesthetized rats. Each rat was prepared with a polyethylene tube in the proximal duodenum and ligation of the pylorus. To collect pancreatic juice, the common bile-pancreatic duct was cannulated near the duodenal wall while bile was diverted to the exterior. Intraduodenal infusion of sodium oleate at doses of 0.03, 0.06, 0.12, and 0.24 mmol/h resulted in significant increases in pancreatic secretion including fluid, bicarbonate, and protein output. The increases of the three parameters were dose dependent and were correlated well with the increases in plasma secretin and CCK concentrations. To further clarify their hormonal roles, we have repeated identical experiments under intravenous administration of a rabbit anti-secretin serum (0.1 ml) or CR 1409 (4 mg.kg-1.h-1), a CCK-receptor antagonist, or a combination of both the antiserum and CR 1409. The antiserum significantly suppressed volume flow and bicarbonate secretion with a minor inhibitory effect on protein secretion, whereas a normal rabbit serum did not. CR 1409 significantly suppressed all three parameters. The combined treatment with both the antiserum and CR 1409 almost completely abolished the pancreatic secretion. Atropine given intravenously significantly inhibited the protein output but did not influence volume flow or bicarbonate output in response to sodium oleate. We thus conclude that, in rats, fat-stimulated pancreatic secretion of volume flow and bicarbonate depends entirely on the circulating endogenous secretin and CCK but that the protein output appears to be under control of both hormonal and cholinergic controls.

Animals↗

PubMed1990

Mechanism of acid-induced release of secretin in rats. Presence of a secretin-releasing peptide.

In fasting rats, intraduodenal infusion of dilute hydrochloric acid results in significant increases in both pancreatic exocrine secretion and plasma concentration of secretin. To test the hypothesis that acid-induced release of secretin is mediated by a secretin-releasing factor (S-RF), anesthetized rats were prepared with pyloric ligation, duodenal and jejunal cannulas, and pancreatic duct cannulas. Donor rats were infused intraduodenally with 0.01 N HCl, 0.15 M NaCl, or a combination of 0.01 N HCl and 0.05 N NaHCO3 at 0.3 ml/min for 1.5 h, and the perfusates were collected via jejunal cannulas. The perfusates with pH adjusted to 6.0 were concentrated threefold and infused into the duodena of recipient rats. The concentrate of acid perfusate (CAP) significantly increased both pancreatic volume flow and bicarbonate output and plasma concentration of secretin, whereas concentrates of the saline perfusate (CSP) or the perfusate of a combination of 0.01 N HCl and 0.05 N NaHCO3 (CABP) did not influence pancreatic secretion or plasma concentration of secretin. The increased pancreatic secretion by CAP was attributed to increased circulating secretin because when secretin was immunoneutralized by a rabbit antisecretin serum, CAP-stimulated pancreatic secretion was abolished. The bioactivity of CAP was trypsin-sensitive and heat stable. The active substance in CAP had a molecular weight of less than 5,000 and greater than 1,000, as determined by ultrafiltration and bioassay. In conclusion, dilute HCl releases an S-RF into the upper small intestinal lumen to stimulate release of secretin. This substance, with molecular weight of less than 5,000, is heat stable and trypsin sensitive. Thus, the acid-stimulated release of secretin is mediated by a secretin-releasing peptide in the upper small intestinal lumen.

Animals↗

PubMed1990

Geranyl-geranyl acetone: a novel stimulant of secretin release in the dog.

Geranyl-geranyl acetone (GGA), a new acyclic polyisoprenoid, anti-ulcer drug appears to exert its beneficial effect by stimulating bicarbonate secretion from the stomach and pancreas. Its efficacy in stimulating pancreatic bicarbonate is particularly striking, and this study was designed to examine the mechanism for this action. Since it is structurally similar to the side chain of the prostaglandin molecule, its ability to stimulate bicarbonate secretion could be a direct one. On the other hand, the magnitude of pancreatic bicarbonate response (about 50% of maximal response to secretin) suggests it might act by releasing secretin. Two types of experiments were performed in dogs with pancreatic fistulas: first, secretagogue interactions were examined by studying the effect of intraduodenal GGA (8 mg/kg) or its carrier (control) on the dose-response curves to exogenous secretin and cholecystokinin octapeptide (CCK-8); second, the effect of graded doses of intraduodenal GGA on pancreatic bicarbonate and plasma secretin-like immunoreactivity (SLI) responses was tested directly. Pancreatic bicarbonate responses (micromoles per 30 min) were to secretin doses of 32, 125, and 500 ng/kg/h. Without and with GGA, responses were 74 +/- 27, 952 +/- 215, and 2,000 +/- 425 and 599 +/- 110, 1,624 +/- 472, and 2,129 +/- 398 ng/kg/h, respectively. Similarly, the bicarbonate responses to CCK-8 were augmented. Basal plasma SLI was 1.5 +/- 0.6 pM/ml. Peak plasma SLI in response to 2, 4, and 8 mg of GGA intraduodenally were 6.8 +/- 0.7, 8.9 +/- 3.1, and 19.6 +/- 2.7 pM/ml, respectively. It is concluded that GGA is a potent stimulant of pancreatic bicarbonate secretion, and this action appears to be mediated by the release of duodenal secretin.

Animals↗

PubMed1989

Effect of pancreatic juice diversion on secretin release in rats.

We investigated a possible role of secretin in the mechanism of exocrine pancreatic secretion after exclusion of pancreatic juice from the intestine in anesthetized rats. Diversion of pancreatic juice from the duodenum resulted in a significant increase in plasma secretin concentration from 0.76 +/- 0.39 pM at 0 time to 3.09 +/- 0.30 pM at 4 h after diversion. This increase in secretin coincided with a steady but significant increase in pancreatic secretion of volume and bicarbonate. Intraduodenal administration of fresh pancreatic juice completely reversed the diversion-induced increases in both plasma secretin and pancreatic secretion. Intravenous injection of a rabbit-antisecretin serum blocked the increase of pancreatic secretion during diversion of pancreatic juice from the duodenum. Thus, we conclude that endogenous secretin is involved in a hormonal mechanism regulating increased pancreatic exocrine secretion in pancreatic juice-diverted rats.

Animals↗

PubMed1989

Effect of pancreatic juice and trypsin on oleic acid-stimulated pancreatic secretion and plasma secretin in dogs.

We have investigated a negative feedback mechanism in the intestinal phase of pancreatic exocrine secretion in dogs with gastric cannulas and Thomas duodenal cannulas in whom pancreatic juice was collected by cannulation of the main pancreatic duct. Intraduodenal infusion of oleic acid emulsion in a dose of 18 mmol/h resulted in a significant increase in pancreatic secretion of water, bicarbonate, and protein, which was accompanied by increased plasma concentrations of both secretin and cholecystokinin. Infusion of pancreatic juice or bovine trypsin into the duodenum significantly inhibited the oleic acid-stimulated pancreatic secretion. This inhibition coincided with a significant decrease in plasma secretin level, whereas plasma cholecystokinin concentration was not affected by either pancreatic juice or trypsin. Neither pancreatic secretion nor plasma secretin concentration was affected by intraduodenal administration of NaHCO3 solution. The trypsin-induced suppression of pancreatic secretion was prevented by intravenous administration of secretin in a dose that achieved a plasma secretin level comparable to that during the oleic acid administration. This study indicates that a negative feedback mechanism is operative in the intestinal phase of pancreatic exocrine secretion in dogs, and endogenous secretin plays a significant role in the mechanism.

Animals↗