Gastrointestinal motility and Intestinal structure following oral exposure to acrylamide in Wistar rats

Introduction: Acrylamide, a byproduct of the cooking process, has been reported to be a toxicant with likely carcinogenic properties. Its impairment of gastric function has been previously reported. In this study its effects on gastrointestinal motility and intestinal structure was investigated in male Wistar rats.Methods: Forty-five rats (120-180g) were divided into 3 equal groups (n=15) and treated p.o with either 0.2ml distilled-water, or acrylamide (7.5mg/kg and 15mg/kg respectively) for 28days. Thereafter, gastric emptying and intestinal motility was assessed. Intestinal structure (duodenum, jejunum and ileum), mucosal and intestinal cell counts were evaluated using histological techniques.Results: Gastric emptying and intestinal transit time increased (p<0.05) in the experimental (acrylamidetreated; 7.5mg/kg and 15mg/kg) groups compared to control. Mucosal cell counts (duodenum, jejunum and ileum) and ileum intestinal cell counts (p<0.05) were reduced in the experimental groups compared to control. Compared to control, duodenal samples of the experimental groups showed severe coagulative necrosis and sloughing off of the villi, luminal filling with necrotic debris, disruption and necrosis of the crypts of Lieberkühn, moderate polymorphonuclear cell infiltration and vascular congestion. These pathologies albeit with less severity were also observed in the jejunum and ileum of acrylamide treated groups.Conclusion: Increased oral exposure to acrylamide impairs gastric emptying, intestinal motility, mucus secretion and compromises digestive and absorptive functions of the small intestines, especially the duodenum. These observations may be ascribed to acrylamide-induced impaired neuronal signaling, autonomic neuropathy, oxidative stress, inflammation and cell necrosis. Keywords: Acrylamide, gastrointestinal tract, gastric emptying, intestinal motility, small intestines

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Intraluminal lipids modulate avian gastrointestinal motility

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1995.269.2.r445 ◽

1995 ◽

Vol 269 (2) ◽

pp. R445-R452 ◽

Cited By ~ 6

Author(s):

V. Martinez ◽

M. Jimenez ◽

E. Gonalons ◽

P. Vergara

Keyword(s):

Small Intestine ◽

Oleic Acid ◽

Gastric Emptying ◽

Electrical Activity ◽

Transit Time ◽

Gastrointestinal Motility ◽

Phase Iii ◽

Intestinal Transit Time ◽

Speed Of Propagation ◽

Spike Bursts

Infusion of lipids into the ileum delays gastric emptying and intestinal transit time in some species. The aim of this study was to characterize the actions of intraluminal lipid infusion on gastrointestinal electrical activity in chickens. Animals were prepared for electromyography with chronic electrodes in stomach, duodenum, and small intestine. Two catheters were chronically placed in the esophagus and ileum to infuse equimolar doses of either oleic acid (OA) or triolein (TO). Both OA and TO, esophageally infused, inhibited the frequency of the gastroduodenal cycle and increased the frequency of antiperistaltic spike bursts in the duodenum. Ileal infusion of OA, but not of TO, produced the same effects. Both esophageal and ileal OA infusion increased the duration of the migrating myoelectric complex (MMC) and decreased the speed of propagation of phase III. In conclusion, intraluminal infusion of lipids modulates gastrointestinal motility by decreasing the frequency of the gastric cycle, increasing duodenogastric refluxes, and elongating the MMC. These actions could delay gastric emptying and increase transit time, which suggests the presence of an "ileal brake" mechanism similar to that described in mammals.

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NMDA Receptors of Gastric-Projecting Neurons in the Dorsal Motor Nucleus of the Vagus Mediate the Regulation of Gastric Emptying by EA at Weishu (BL21)

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2012/583479 ◽

2012 ◽

Vol 2012 ◽

pp. 1-7 ◽

Cited By ~ 4

Author(s):

Xin Zhang ◽

Bin Cheng ◽

Xianghong Jing ◽

Yongfa Qiao ◽

Xinyan Gao ◽

...

Keyword(s):

Gastric Emptying ◽

Nmda Receptor ◽

Ampa Receptor ◽

Gastrointestinal Motility ◽

Kynurenic Acid ◽

Basic Mechanism ◽

Motor Nucleus ◽

Dorsal Motor Nucleus ◽

Lines Of Evidence

A large number of studies have been conducted to explore the efficacy of electroacupuncture (EA) for the treatment of gastrointestinal motility. While several lines of evidence addressed the basic mechanism of EA on gastrointestinal motility regarding effects of limb and abdomen points, the mechanism for effects of the back points on gastric motility still remains unclear. Here we report that the NMDA receptor (NMDAR) antagonist kynurenic acid inhibited the gastric emptying increase induced by high-intensity EA at BL21 and agonist NMDA enhanced the effect of the same treatment. EA at BL21 enhanced NMDAR, but not AMPA receptor (AMPAR) component of miniature excitatory postsynaptic current (mEPSC) in gastric-projecting neurons of the dorsal motor nucleus of the vagus (DMV). In sum, our data demonstrate an important role of NMDAR-mediated synaptic transmission of gastric-projecting DMV neurons in mediating EA at BL21-induced enhancement of gastric emptying.

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Effect of Dai-kenchu-to on gastrointestinal motility and gastric emptying

International Journal of Surgery ◽

10.1016/j.ijsu.2009.03.008 ◽

2009 ◽

Vol 7 (3) ◽

pp. 218-222 ◽

Cited By ~ 4

Author(s):

Naruo Kawasaki ◽

Koji Nakada ◽

Yutaka Suzuki ◽

Yoshiyuki Furukawa ◽

Nobuyoshi Hanyu ◽

...

Keyword(s):

Gastric Emptying ◽

Gastrointestinal Motility

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▾ Cisapride – more selective than metoclopramide

Drug and Therapeutics Bulletin ◽

10.1136/dtb.28.23.89 ◽

1990 ◽

Vol 28 (23) ◽

pp. 89-90

Keyword(s):

Gastric Emptying ◽

Gastrointestinal Motility ◽

Chemical Structure ◽

Sphincter Pressure ◽

Antiemetic Effect ◽

Gut Motility ◽

Prokinetic Drugs ◽

Similar Chemical ◽

Non Ulcer Dyspepsia ◽

Product Licence

Metoclopramide (Maxolon; Primperan), has been around for over 20 years and domperidone (Motilium - Sterling Winthrop) for eight years. Both are prokinetic drugs which speed gastric emptying, increase oesophageal sphincter pressure, stimulate gut motility and in addition have a central antiemetic effect. Cisapride (Prepulsid - Janssen; Alimix - Cilag) has a similar chemical structure to metoclopramide and is intended for the reduction of oesophageal reflux and relief of symptoms caused by impaired gastrointestinal motility. The product licence has recently been extended to include treatment of non-ulcer dyspepsia.

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Role of gut-brain axis in persistent abnormal feeding behavior in mice following eradication of Helicobacter pylori infection

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.90752.2008 ◽

2009 ◽

Vol 296 (3) ◽

pp. R587-R594 ◽

Cited By ~ 40

Author(s):

Premysl Bercik ◽

Elena F. Verdú ◽

Jane A. Foster ◽

Jun Lu ◽

Angela Scharringa ◽

...

Keyword(s):

Gastric Emptying ◽

Feeding Behavior ◽

Computer Assisted ◽

Bacterial Eradication ◽

Cell Counts ◽

Tnf Α ◽

Gastric Sensitivity ◽

H Pylori ◽

The Brain

Bacterial infection can trigger the development of functional GI disease. Here, we investigate the role of the gut-brain axis in gastric dysfunction during and after chronic H. pylori infection. Control and chronically H. pylori-infected Balb/c mice were studied before and 2 mo after bacterial eradication. Gastric motility and emptying were investigated using videofluoroscopy image analysis. Gastric mechanical viscerosensitivity was assessed by cardioautonomic responses to distension. Feeding patterns were recorded by a computer-assisted system. Plasma leptin, ghrelin, and CCK levels were measured using ELISA. IL-1β, TNF-α, proopiomelanocortin (POMC), and neuropeptide Y mRNAs were assessed by in situ hybridizations on frozen brain sections. Gastric inflammation was assessed by histology and immunohistochemistry. As shown previously, H. pylori-infected mice ate more frequently than controls but consumed less food per bout, maintaining normal body weight. Abnormal feeding behavior was accompanied by elevated plasma ghrelin and postprandial CCK, higher TNF-α (median eminence), and lower POMC (arcuate nucleus) mRNA. Infected mice displayed delayed gastric emptying and visceral hypersensitivity. Eradication therapy normalized gastric emptying and improved gastric sensitivity but had no effect on eating behavior. This was accompanied by persistently increased TNF-α in the brain and gastric CD3+ T-cell counts. In conclusion, chronic H. pylori infection in mice alters gastric emptying and mechanosensitivity, which improve after bacterial eradication. A feeding pattern reminiscent of early satiety persists after H. pylori eradication and is accompanied by increased TNF-α in the brain. The results support a role for altered gut-brain pathways in the maintenance of postinfective gut dysfunction.

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Xenin-25 increases cytosolic free calcium levels and acetylcholine release from a subset of myenteric neurons

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00116.2012 ◽

2012 ◽

Vol 303 (12) ◽

pp. G1347-G1355 ◽

Cited By ~ 13

Author(s):

Sheng Zhang ◽

Krzysztof Hyrc ◽

Songyan Wang ◽

Burton M. Wice

Keyword(s):

Gastric Emptying ◽

Exocrine Pancreas ◽

Acetylcholine Release ◽

Free Calcium ◽

Cytosolic Free Calcium ◽

Myenteric Neurons ◽

Neuronal Markers ◽

Central Neurons ◽

Small Intestines ◽

Neurotensin Receptor 1

Xenin-25 (Xen) is a 25 amino acid neurotensin-related peptide reportedly produced with glucose-dependent insulinotropic polypeptide (GIP) by a subset of K cells in the proximal gut. We previously showed exogenously administered Xen, with GIP but not alone, increases insulin secretion in humans and mice. In mice, this effect is indirectly mediated via a central nervous system-independent cholinergic relay in the periphery. Xen also delays gastric emptying, reduces food intake, induces gall bladder contractions, and increases gut motility and secretion from the exocrine pancreas, suggesting that some effects of Xen could be mediated by myenteric neurons (MENs). To determine whether Xen activates these neurons, MENs were isolated from guinea pig proximal small intestines. Cells expressed neuronal markers and exhibited typical neuron-like morphology with extensive outgrowths emanating from cell bodies. Cytosolic free Ca2+ levels ([Ca2+]i) were measured using Fura-2. ATP/UTP, KCl, and forskolin increased [Ca2+]i in 99.6%, 92%, and 23% of the MENs imaged, respectively, indicating that they are functional and activated by nucleotide receptor signaling, direct depolarization, and cAMP. [Ca2+]i increased in only 12.7% of MENs treated with Xen. This rise was blocked by pretreatment with EGTA, diazoxide, SR48692, and neurotensin. Thus the Xen-mediated increase in [Ca2+]i involves influx of extracellular Ca2+ and activation of neurotensin receptor-1 (NTSR1). Xen also increased acetylcholine release from MENs. Amylin, produced by β-and enteroendocrine cells, delays gastric emptying and increased [Ca2+]i almost exclusively in Xen-responsive MENs. Immunohistochemistry demonstrated NTSR1 expression in human duodenal MENs. Thus myenteric rather than central neurons could mediate some effects of Xen and amylin.

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The control mechanisms of gastric emptying are not overridden by motor stimulants

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1986.251.6.g744 ◽

1986 ◽

Vol 251 (6) ◽

pp. G744-G751 ◽

Cited By ~ 2

Author(s):

S. Wulschke ◽

H. J. Ehrlein ◽

C. Tsiamitas

Keyword(s):

Gastric Emptying ◽

Gastrointestinal Motility ◽

Control Mechanisms ◽

Wall Tension ◽

Physiological Conditions ◽

Duodenal Motility ◽

Antral Motility

We wanted to determine if an acceleration of the normal emptying rate by motor stimulants interfers with control mechanisms limiting gastric emptying. Therefore, we studied the effects of 5-hydroxytryptophane (5-HTP) and cisapride on canine gastrointestinal motility and gastric emptying after ingestion of viscous acaloric and nutritive meals. Prolonged contractions and relaxations that change lumen size (isotonic component) and wall tension (isometric component) are defined as “basal contractions” and “basal relaxations”, respectively. The nutrient meal emptied much slower than the acaloric meal due to several alterations of gastric, pyloric, and duodenal motility. Both drugs stimulated antral motility but failed to accelerate gastric emptying of the nutrient meal. The main causes for the failure were a basal relaxation of the proximal antrum and a basal contraction of the duodenum. In conclusion, basal contractions of the proximal antrum and duodenum play an important role in the process of gastric emptying, and under physiological conditions the control mechanisms of gastric emptying provide an optimal emptying rate that cannot be markedly accelerated by 5-HTP and cisapride.

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Osmoltye and tryptophan receptors controlling gastric emptying in the dog

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1976.231.3.848 ◽

1976 ◽

Vol 231 (3) ◽

pp. 848-853 ◽

Cited By ~ 13

Author(s):

Stephens ◽

RF Woolson ◽

AR Cooke

Keyword(s):

Amino Acids ◽

Amino Acid ◽

Gastric Emptying ◽

Brush Border ◽

Inhibitory Effect ◽

Intestinal Cell ◽

Acid Transport ◽

Transport Pathway ◽

Molar Basis ◽

Intestinal Receptors

The effect of three monosaccharides, three disaccharides, two dipeptides, combinations of tryptophan with two hexoses, one hexitol, and two amino acids ongastric emptying was studied in dogs to further define the samll intestinal receptors responsive to osmolytes and tryptophan. On a molar basis the disacchardies and dipeptides were almost twice as potent as their respective constituent monosaccharides or amino acids implying that the osmoreceptor is deep to the brush border disaccharidases and cytosol dipeptidases. Tryptophan probably acts by a mechanism different from the osmoreceptor since slowing of gastric emptying by tryptophan was inhibited by methionine which has no effect on a stimulant of the osmoreceptor mechanism. Lysine unlike methionine does not share the neutral amino acid transport pathway with tryptophan. Lysine did not change the inhibitory effect of tryptophan on gastric emptying. This imples that transport of tryptophan into the intestinal cell is necessary for its slowing effect. Glucose and galactose also inhibited the tryptophan effect whereas a nonabsorbed hexitor, mannitol, was without effect. Interference by the hexoses was also probably by competition with tryptophan for transport into the cell. These studies further indicate that the tryptophan receptor is different from the osmoreceptor.

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