Duodenal acidification releases cholecystokinin

1985 ◽  
Vol 249 (1) ◽  
pp. G29-G33 ◽  
Author(s):  
Y. F. Chen ◽  
W. Y. Chey ◽  
T. M. Chang ◽  
K. Y. Lee
Keyword(s):  
Small Intestine ◽  
Pancreatic Secretion ◽  
Dependent Manner ◽  
Exocrine Pancreatic Secretion ◽  
Plasma Gastrin ◽  
Proximal Small Intestine ◽  
Duodenal Acidification ◽  
Bicarbonate Output ◽  
Dose Dependent ◽  
Intraduodenal Administration

We studied the effect of hydrochloric acid (HCl) in the proximal small intestine on release of cholecystokinin (CCK) and secretin and on exocrine pancreatic secretion in conscious dogs with gastric cannulas and modified Herrera pancreatic cannulas. Intraduodenal administration of HCl in a concentration of 50 or 100 mM at rates of 0.05, 0.1, 0.2, and 0.4 mmol/min significantly increased plasma concentration of CCK in a dose-dependent manner, whereas plasma gastrin levels decreased. The increased plasma CCK level paralleled a significant increase in pancreatic trypsin output. Plasma secretin concentration and pancreatic bicarbonate output also increased in response to the acid, and the increase was dependent on the acid loads delivered in the duodenum. Thus, in dogs, HCl in the duodenum releases both CCK and secretin to stimulate pancreatic secretion of bicarbonate as well as enzymes.

Effect of glucagon on canine exocrine pancreatic secretion stimulated by a test meal

1978 ◽  
Vol 56 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Manfred V. Singer ◽  
Osvaldo M. Tiscornia ◽  
Joao Paulo Mendes de Oliveiro ◽  
Pierre Demol ◽  
Denis Levesque ◽  
...  
Keyword(s):  
Test Meal ◽  
Pancreatic Secretion ◽  
Gastric Fistula ◽  
Exocrine Pancreatic Secretion ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Bicarbonate Output ◽  
Protein Response ◽  
Protein Output ◽  
Dose Dependent

The effect of glucagon on exocrine pancreatic secretion stimulated by a test meal was studied in three dogs with a chronic gastric fistula and a modified Thomas duodenal fistula which allows easier collection of pure pancreatic juice after a meal. Glucagon was given by continuous intravenous infusion in doses of 5, 10, 15, or 30 μg/kg per hour, before and during a test meal. At each dose level glucagon significantly reduced the water and electrolyte secretion of the pancreas. At 15 and 30 μg/kg per hour glucagon inhibited protein output; this effect was absent at lower doses. These findings demonstrate a dose-dependent inhibition by glucagon of the pancreatic bicarbonate and protein response to a meal. Inhibition of bicarbonate output was more sensitive to glucagon than that of protein output.

Microinjection of exogenous somatostatin in the dorsal vagal complex inhibits pancreatic secretion via somatostatin receptor-2 in rats

2007 ◽  
Vol 292 (3) ◽  
pp. G746-G752 ◽  
Author(s):  
Zhuan Liao ◽  
Zhao-Shen Li ◽  
Yan Lu ◽  
Wei-Zhong Wang
Keyword(s):  
Pancreatic Secretion ◽  
Exocrine Pancreas ◽  
Feedback Inhibition ◽  
Somatostatin Receptor ◽  
Inhibitory Effect ◽  
Receptor Subtype ◽  
Dependent Manner ◽  
Dorsal Vagal Complex ◽  
Somatostatin Receptor Antagonist ◽  
Dose Dependent

Previous studies have suggested that somatostatin inhibits pancreatic secretion at a central vagal site, and the dorsal vagal complex (DVC) is involved in central feedback inhibition of the exocrine pancreas. The aim of this study was to investigate the effect of exogenous somatostatin in the DVC on pancreatic secretion and the somatostatin receptor subtype(s) responsible for the effect. The effects of somatostatin microinjected into the DVC on pancreatic secretion stimulated by cholecystokinin octapeptide (CCK-8) or 2-deoxy-d-glucose (2-DG) were examined in anesthetized rats. To investigate the somatostatin inhibitory action site, a somatostatin receptor antagonist [SRA; cyclo(7-aminoheptanoyl-Phe-d-Trp-Lys-Thr)] was microinjected into the DVC before intravenous infusion of somatostatin and CCK-8/2-DG. The effects of injection of a somatostatin receptor-2 agonist (seglitide) and combined injection of somatostatin and a somatostatin receptor-2 antagonist (CYN 154806) in the DVC on the pancreatic secretion were also investigated. Somatostatin injected into the DVC significantly inhibited pancreatic secretion evoked by CCK-8 or 2-DG in a dose-dependent manner. SRA injected into the DVC completely reversed the inhibitory effect of intravenous administration of somatostatin. Seglitide injected into the DVC also inhibited CCK-8/2-DG-induced pancreatic protein secretion. However, combined injection of somatostatin and CYN 154806 did not affect the CCK-8/2-DG-induced pancreatic secretion. Somatostatin in the DVC inhibits pancreatic secretion via somatostatin receptor-2, and the DVC is the action site of somatostatin for its inhibitory effect.

Effects of ileal infusions of nutrients on motor patterns of canine small intestine

1990 ◽  
Vol 259 (1) ◽  
pp. G78-G85 ◽  
Author(s):  
M. L. Siegle ◽  
H. R. Schmid ◽  
H. J. Ehrlein
Keyword(s):  
Amino Acids ◽  
Small Intestine ◽  
Gastric Emptying ◽  
Motor Pattern ◽  
Inhibitory Effects ◽  
Contraction Force ◽  
Motor Patterns ◽  
Proximal Small Intestine ◽  
Dose Dependent ◽  
Different Doses

In the present study, effects of ileal infusions of nutrients on motor patterns of the proximal small intestine and on gastric emptying were investigated in dogs. An acaloric meal was administered orally, and equicaloric loads of amino acids, oleate, and glucose were infused into the ileum at different doses (0.3, 0.6, and 0.9 kJ/min). The computerized analysis of motor patterns was focused on the differentiation between stationary and propagated contractions recorded by closely spaced extraluminal strain gauges. All three nutrients exerted inhibitory effects on gastric emptying and on contraction force and frequency of the proximal small intestine. Additionally, the propulsive motor pattern induced by the acaloric meal was modulated by reducing the number of contraction waves and their length of spread. All the effects were dose dependent. Among the three nutrients, glucose significantly changed motility at lower doses compared with amino acids and oleate. We conclude that in dogs the ileal brake mechanism is induced by all three nutrients and that it influences not only contraction force and frequency but also the motor patterns of the proximal small intestine.

scholarly journals Dietary chitosan affects metabolism of arachidonic acid in weaned piglets

2017 ◽  
Vol 62 (No. 2) ◽  
pp. 58-66 ◽  
Author(s):  
J.-L. Li ◽  
Y.-Q. Xu ◽  
B.-L. Shi ◽  
D.-S. Sun ◽  
S.-M. Yan ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Small Intestine ◽  
Immune Function ◽  
Mrna Expression ◽  
Basal Diet ◽  
Leukotriene B4 ◽  
Dependent Manner ◽  
Weaned Piglets ◽  
Cox 2 ◽  
Dose Dependent

The effects of chitosan on immune function via arachidonic acid (AA) pathway in weaned piglets were investigated. A total of 180 piglets (Duroc × Yorkshire × Landrace) were randomly assigned to 5 dietary treatments and fed a basal diet supplemented with 0 (control), 100, 500, 1000, and 2000 mg chitosan/kg feed, respectively. Results showed that serum AA, prostaglandin E2 (PGE2), and leukotriene B4 (LTB4) contents in piglets were increased in a linear or quadratic dose-dependent manner with increasing chitosan on day 28 (P < 0.05). Chitosan increased serum cytosolic-phospholipase A2 (cPLA2) activity in a linear or quadratic dose-dependent manner on day 14 or 28, and improved 5-lipoxygenase (5-LOX) activity in a linear manner and cyclooxygenase-2 (COX-2) activity quadratically on day 28 (P < 0.05). Moreover, chitosan elevated gene expression of cPLA2 mRNA quadratically in the small intestine on days 14 and 28, increased the COX-2 mRNA expression in the duodenum or jejunum in a linear or quadratic manner on day 28, and improved the 5-LOX mRNA expression quadratically in the small intestine (P < 0.05). These results implied that the metabolism of AA was regulated by chitosan in a dose-dependent relationship, which may be one reason why chitosan affected immune function via AA pathway in weaned piglets.

Gastrin is not a physiological regulator of pancreatic exocrine secretion in the dog

1987 ◽  
Vol 252 (1) ◽  
pp. G40-G44
Author(s):  
E. Kohler ◽  
C. Beglinger ◽  
V. Eysselein ◽  
U. Grotzinger ◽  
K. Gyr
Keyword(s):  
Pancreatic Secretion ◽  
Pancreatic Enzyme ◽  
Exocrine Secretion ◽  
Exocrine Pancreatic Secretion ◽  
Response Curves ◽  
Blood Concentrations ◽  
Pancreatic Enzyme Secretion ◽  
Pancreatic Exocrine ◽  
Bicarbonate Output

The role of gastrin as a regulator of exocrine pancreatic secretion has not been proven adequately. In the present study we therefore compared the relative molar potencies of sulfated and unsulfated gastrin 17 with structurally related CCK peptides (synthetic CCK-8 and natural porcine CCK-33) in stimulating exocrine pancreatic secretion in conscious dogs. Dose response curves were constructed for pancreatic and gastric acid secretion. Plasma gastrin levels after exogenous gastrin 17-I and -II were compared with postprandial gastrin concentrations (meal: ground beef 20 g/kg body wt). The molar potency estimates calculated with synthetic CCK8 as standard (potency = 1.00) for pancreatic protein secretion were natural porcine 50% pure CCK-33 1.60, gastrin 17-I 0.12, and gastrin 17-II 0.16. All four peptides induced a dose-dependent increase in pancreatic bicarbonate output. However, the blood concentrations needed to stimulate pancreatic secretion were above the postprandial gastrin levels. Our data indicate that both gastrin 17 peptides are not physiological regulators of pancreatic enzyme secretion in dogs.

Endogenous cholecystokinin drives gallbladder emptying in dogs

1986 ◽  
Vol 251 (4) ◽  
pp. G553-G558
Author(s):  
K. Shiratori ◽  
S. Watanabe ◽  
W. Y. Chey ◽  
K. Y. Lee ◽  
T. M. Chang
Keyword(s):  
Corn Oil ◽  
Venous Blood ◽  
Gallbladder Emptying ◽  
Dependent Manner ◽  
Gallbladder Volume ◽  
Dose Dependent ◽  
Intraduodenal Administration ◽  
Different Doses ◽  
Cck Release

We investigated the effect of fat in the duodenum on the gallbladder emptying in seven dogs prepared with gastric, duodenal, and gallbladder cannulas. Gallbladder volume was measured at 15-min intervals, and venous blood samples were obtained at regular intervals for 2.5 h. Intraduodenal administration of Lipomul (pH 5.0, corn oil) in three different doses (1.1, 2.2, and 4.4 mmol/10 min) resulted in significant increases in gallbladder emptying in a dose-dependent manner (r = 0.8668, P less than 0.001). Likewise, the increase in integrated cholecystokinin (CCK) release in response to Lipomul was also dose dependent (r = 0.7334, P less than 0.001). A statistically significant correlation was found between integrated CCK release and gallbladder emptying in response to Lipomul (P less than 0.001). To determine the role of circulating endogenous CCK on gallbladder emptying effects of intravenous administration of proglumide and a rabbit anti-CCK serum on gallbladder emptying were studied. Gallbladder emptying was virtually abolished by the antiserum. Proglumide not only abolished the emptying but also increased gallbladder volume. Thus we conclude that in dogs the gallbladder emptying in response to fat in the upper small intestine depends on increased circulating endogenous CCK.

Thyroid hormone regulates the activity and expression of the peptide transporter PEPT1 in Caco-2 cells

2002 ◽  
Vol 282 (4) ◽  
pp. G617-G623 ◽  
Author(s):  
Kayoko Ashida ◽  
Toshiya Katsura ◽  
Hideyuki Motohashi ◽  
Hideyuki Saito ◽  
Ken-Ichi Inui
Keyword(s):  
Small Intestine ◽  
Thyroid Hormone ◽  
Kinetic Analysis ◽  
Apical Membrane ◽  
Peptide Transporter ◽  
Dependent Manner ◽  
Small Peptides ◽  
Control Value ◽  
Dose Dependent ◽  
Pept1 Mrna

An oligopeptide transporter (PEPT1) in the small intestine plays an important role in the absorption of small peptides and peptide-like drugs. We examined the effect of thyroid hormone 3,5,3′-l-triiodothyronine (T3) on the activity and expression of PEPT1 in human intestinal Caco-2 cells. Treatment of Caco-2 cells with T3 inhibited [14C]glycylsarcosine uptake in a time- and dose-dependent manner. [14C]glycylsarcosine uptake was reduced by pretreatment of the cells with 100 nM T3 for 4 days (67% of control value), whereas methyl-α-d-[U-14C]glucopyranoside and [3H]threonine uptake were not decreased. Kinetic analysis showed that T3 treatment significantly decreased the maximum uptake (Vmax) value for [14C]glycylsarcosine uptake but had no effect on the K m value. Moreover, T3 treatment caused a significant decrease in the amount of PEPT1 mRNA (25% of the control). Western blotting indicated that the amount of PEPT1 protein in the apical membrane was decreased (70% of the control). These findings indicate that T3 treatment inhibits the uptake of [14C]glycylsarcosine by decreasing the transcription and/or stability of PEPT1 mRNA.

scholarly journals Biofilm Formation and Virulence of Shigella flexneri is Modulated by pH of Gastrointestinal Tract

2020 ◽  
Author(s):  
I-Ling Chiang ◽  
Yi Wang ◽  
Satoru Fujii ◽  
Brian D. Muegge ◽  
Qiuhe Lu ◽  
...  
Keyword(s):  
Small Intestine ◽  
Epithelial Cells ◽  
Shigella Flexneri ◽  
Public Health Issue ◽  
Dependent Manner ◽  
Specific Amino Acid ◽  
Major Public Health Issue ◽  
Cellular Invasion ◽  
Ph Conditions ◽  
Dose Dependent

AbstractShigella infections remain a major public health issue in developing countries. One model of Shigella pathogenesis suggests that the microfold epithelial cells in the small intestine are the preferred initial site of infection. However, a growing body of evidence supports an alternative model whereby Shigella primarily infects a much wider range of epithelial cells that reside primarily within the colon. Here, we investigated whether the luminal pH difference between the small intestine and colon could provide evidence in support of either model of Shigella flexneri pathogenesis. As virulence factors leading to cellular invasion are linked to biofilms in S. flexneri, we examined the effect of pH on S. flexneri’s ability to form and maintain adherent biofilms when induced by deoxycholate. We showed that a basic pH inhibited formation and dispersed pre-assembled mature biofilms while an acidic pH (similar to the colonic environment) did not have either of these effects. To further elucidate this phenomenon at the molecular level, we probed the transcriptomes of biofilms and S. flexneri grown in different pH conditions. We identified specific amino acid metabolic pathways (cysteine and arginine) that were enriched in the bacteria that formed the biofilms, but decreased upon pH increase. We then utilized a type III secretion system reporter strain to show that increasing pH reduced deoxycholate-induced virulence of S. flexneri in a dose dependent manner. Taken together, these experiments support a model whereby Shigella infection is favored in the colon because of the local pH differences in these organs.

Biofilm Formation and Virulence of Shigella flexneri is Modulated by pH of Gastrointestinal Tract

2021 ◽  
Author(s):  
I-Ling Chiang ◽  
Yi Wang ◽  
Satoru Fujii ◽  
Brian D. Muegge ◽  
Qiuhe Lu ◽  
...  
Keyword(s):  
Small Intestine ◽  
Epithelial Cells ◽  
Type Iii Secretion ◽  
Shigella Flexneri ◽  
Public Health Problem ◽  
Dependent Manner ◽  
Specific Amino Acid ◽  
Cellular Invasion ◽  
Ph Conditions ◽  
Dose Dependent

Shigella infection remains a public health problem in much of the world. Classic models of Shigella pathogenesis suggest that microfold epithelial cells in the small intestine are the preferred initial site of invasion. However, recent evidence supports an alternative model whereby Shigella primarily infects a much wider range of epithelial cells that reside primarily in the colon. Here, we investigated whether the luminal pH difference between the small intestine and colon could provide evidence in support of either model of Shigella flexneri pathogenesis. As virulence factors culminating in cellular invasion are linked to biofilms in S. flexneri , we examined the effect of pH on S. flexneri ’s ability to form and maintain adherent biofilms when induced by deoxycholate. We showed that a basic pH (as expected in the small intestine) inhibited formation and dispersed pre-assembled mature biofilms while an acidic pH (similar to the colonic environment) did not permit either of these effects. To further elucidate this phenomenon at the molecular level, we probed the transcriptomes of biofilms and S. flexneri grown in different pH conditions. We identified specific amino acid metabolic pathways (cysteine and arginine) that were enriched in the bacteria that formed the biofilms, but decreased when pH increased. We then utilized a type III secretion system reporter strain to show that increasing pH reduced deoxycholate-induced virulence of S. flexneri in a dose dependent manner. Taken together, these experiments support a model whereby Shigella infection is favored in the colon because of the local pH differences in these organs.

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

1990 ◽  
Vol 258 (2) ◽  
pp. G268-G274 ◽  
Author(s):  
K. Y. Lee ◽  
L. Zhou ◽  
X. S. Ren ◽  
T. M. Chang ◽  
W. Y. Chey
Keyword(s):  
Pancreatic Secretion ◽  
Physiological Role ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Dependent Manner ◽  
Exocrine Pancreatic Secretion ◽  
Liquid Meal ◽  
Amylase Output ◽  
Endogenous Insulin

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.

Sign in / Sign up

Export Citation Format

Share Document