• Korean Journal of Food Science and Technology
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• v.51 no.1
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• pp.64-69
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• 2019

Gluten proteins are key to developing a unique quality of flour because they confer viscosity, cohesiveness, and elasticity in the dough. However, gluten can impede digestion and absorption in gluten-sensitive individuals. In this study, enteritis was induced in mice with dextran sulfate sodium (DSS) salt. The mice later received a diet consisting of 3%, 12%, or 30% fermented noodles with degraded gluten (FNDG) or 30% normal noodle flour for 8 weeks. FNDG did not alter the growth performance or body composition. However, FNDG resulted in increased amylase activity in a dose-dependent manner (p<0.001), and it also improved the digestive capacity. FNDG at 30% concentration increased the level of gastrin (p<0.01) implying increased gut motility. The serotonin receptor levels were significantly reduced by FNDG at 12% (p<0.05) and 30% (p<0.01) concentrations. These findings indicate that a diet containing FNDG could help in the recovery from intestinal inflammation with improving digestive ability and gut motility. Overall, the inclusion of degraded gluten in the diet was found to enhance digestion, gut motility, and absorption in mice.

• Nutrition Research and Practice
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• v.15 no.4
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• pp.411-430
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• 2021

Irritable bowel syndrome (IBS) is a frequently diagnosed gastrointestinal (GI) disorder characterized by recurrent abdominal pain, bloating, and changes in the stool form or frequency without any structural changes and overt inflammation. It is not a life-threatening condition but causes a considerable level of discomfort and distress. Among the many pathophysiologic factors, such as altered GI motility, visceral hypersensitivity, and low-grade mucosal inflammation, as well as other immunologic, psychologic, and genetic factors, gut microbiota imbalance (dysbiosis), which is frequently found in IBS, has been highlighted as an etiology of IBS. Dysbiosis may affect gut mucosal homeostasis, immune function, metabolic regulation, and even visceral motor function. As diet is shown to play a fundamental role in the gut microbiota profile, this review discusses the influence of diet on IBS occurring through the modulation of gut microbiota. Based on previous studies, it appears that dietary modulation of the gut microbiota may be effective for the alleviation of IBS symptoms and, also an effective IBS management strategy based on the underlying mechanism; especially because, IBS currently has no specific treatment owing to its uncertain etiology.

• Journal of Neurogastroenterology and Motility
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• v.24 no.4
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• pp.512-527
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• 2018

This review provides a comprehensive overview of brain imaging studies of the brain-gut interaction in functional gastrointestinal disorders (FGIDs). Functional neuroimaging studies during gut stimulation have shown enhanced brain responses in regions related to sensory processing of the homeostatic condition of the gut (homeostatic afferent) and responses to salience stimuli (salience network), as well as increased and decreased brain activity in the emotional response areas and reduced activation in areas associated with the top-down modulation of visceral afferent signals. Altered central regulation of the endocrine and autonomic nervous responses, the key mediators of the brain-gut axis, has been demonstrated. Studies using resting-state functional magnetic resonance imaging reported abnormal local and global connectivity in the areas related to pain processing and the default mode network (a physiological baseline of brain activity at rest associated with self-awareness and memory) in FGIDs. Structural imaging with brain morphometry and diffusion imaging demonstrated altered gray- and white-matter structures in areas that also showed changes in functional imaging studies, although this requires replication. Molecular imaging by magnetic resonance spectroscopy and positron emission tomography in FGIDs remains relatively sparse. Progress using analytical methods such as machine learning algorithms may shift neuroimaging studies from brain mapping to predicting clinical outcomes. Because several factors contribute to the pathophysiology of FGIDs and because its population is quite heterogeneous, a new model is needed in future studies to assess the importance of the factors and brain functions that are responsible for an optimal homeostatic state.

• Advances in Traditional Medicine
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• v.4 no.2
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• pp.87-90
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• 2004

The efficacy of Arque-Ajeeb (AA), a compound formulation of Unani medicine was investigated for antidiarrhoeal activity against barium sulphate-induced gut motility and castor oil-induced diarrhoea in rats. The control, standard and test groups of experimental animals were administered with distilled water (p.o.), lomotil (p.o.) and AA (0.007 ml and 0.014 ml/100 g, p.o.) respectively. Barium sulphate and castor oil were administered after 15 and 60 min respectively in each group of first and second experiment. The distance traveled by barium sulphate in small intestine was measured after 15 and 30 min of barium sulphate administration and diarrhoea was observed every 30-min for six hour after castor oil administration. Oral administration of AA caused significant reduction in diarrhoea. AA may have the potential to reduce the diarrhoea in rats.

• Korean Journal of Veterinary Research
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• v.44 no.2
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• pp.171-177
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• 2004

The regional distributions and frequencies of argentaffin endocrine cells in gastrointestinal (GI) tract of osteoporotic Sprague-Dawley rat induced by ovariectomy were studied by Masson-Hamperl silver stain. The experimental animals were divided into two groups, one is non-ovariectomized group (Sham) and the other is ovariectomized group (OVX). Samples were collected from each part of GI tract (fundus, pylorus, duodenum, jejunum, ileum, cecum, colon and rectum) at 10th week after ovariectomy or sham operation. Argentaffin cells were detected throughout the entire GI tract with various frequencies regardless of ovariectomy except for the rectum of OVX in which no cells were detected. Most of these argentaffin cells in the mucosa of GI tract were generally spherical or spindle in shape (open type cell) while cells showing round in shape (close type cell) were rarely found in gland regions. Significant decrease of argentaffin cells was detected in OVX compared to that of Sham except for the fundus and jejunum. However, in the fundus and jejunum, argentaffin cells in OVX showed similar frequency compared to that of Sham. In conclusion, the endocrine cells are the anatomical units responsible for the production of gut hormones that regulate gut motility and digestion including absorption, and a change in their density would reflect the change in the capacity of producing these hormones and regulating gut motility and digestion. Ovariectomy induced severe quantitative changes of GI argentaffin endocrine cell density, and the abnormality in density of GI endocrine cells may contribute to the development of gastrointestinal symptoms in osteoporosis such as impairments of calcium and some lipids, frequently encountered in patients with postmenopausal osteoporosis.

• Molecules and Cells
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• v.46 no.11
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• pp.672-674
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• 2023

Schematic diagram of the interaction between the intestinal muscularis externa (MMΦ) macrophages and the enteric nervous system (ENS) neurons during different developmental periods. At the early postnatal stage, MMΦs play a critical role in ENS maturation and refinement through synaptic pruning and enteric neuron phagocytosis. In addition, during the adult stage, a specific MMΦ subset named neuron-associated (NA)-MMΦ, supports enteric neuronal survival and functions. Conversely, enteric neurons promote the phenotypic MMΦ changes by secreting transforming growth factor-β (TGFβ), transitioning them from a phagocytic phenotype in the early postnatal period to a neuroprotective and immune-surveillant phenotype in the young adult period. Disruptions in these interactions could lead to alterations in the enteric neuron numbers, ultimately resulting in reduced gut motility.

• Journal of Microbiology and Biotechnology
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• v.29 no.1
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• pp.30-36
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• 2019

Numerous studies have reported that enteric neurons involved in controlling neurotransmitter secretion and motility in the gut critically contribute to the progression of gut inflammation. Clostridium difficile toxins, which cause severe colonic inflammation, are also known to affect enteric neurons. Our previous study showed that C. difficile toxin A directly induces neural cell toxicities, such as viability loss and apoptosis. In the current study, we attempted to identify a potent inhibitor of toxin A-induced neural cell toxicity that may aid in managing toxin A-induced gut inflammation. In our recent study, we found that the Korea dung beetle-derived antimicrobial peptide CopA3 completely blocked neural cell apoptosis caused by okadaic acid or 6-OHDA. Here, we examined whether the antimicrobial peptide CopA3 inhibited toxin A-induced neural cell damage. In neuroblastoma SH-SY5Y cells, CopA3 treatment protected against both apoptosis and viability loss caused by toxin A. CopA3 also completely inhibited activation of the pro-apoptotic factor, caspase-3. Additionally, CopA3 rescued toxin A-induced downregulation of neural cell proliferation. However, CopA3 had no effect on signaling through ROS/p38 $MAPK/p27^{kip1}$, suggesting that CopA3 inhibits toxin A-induced neural cell toxicity independent of this well-characterized toxin A pathway. Our data further suggest that ability of CopA3 to rescue toxin A-induced neural cell damage may also ameliorate the gut inflammation caused by toxin A.

• Journal of Microbiology and Biotechnology
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• v.27 no.6
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• pp.1163-1170
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• 2017

Clostridium difficile releases two exotoxins, toxin A and toxin B, which disrupt the epithelial cell barrier in the gut to increase mucosal permeability and trigger inflammation with severe diarrhea. Many studies have suggested that enteric nerves are also directly involved in the progression of this toxin-mediated inflammation and diarrhea. C. difficile toxin A is known to enhance neurotransmitter secretion, increase gut motility, and suppress sympathetic neurotransmission in the guinea pig colitis model. Although previous studies have examined the pathophysiological role of enteric nerves in gut inflammation, the direct effect of toxins on neuronal cells and the molecular mechanisms underlying toxin-induced neuronal stress remained to be unveiled. Here, we examined the toxicity of C. difficile toxin A against neuronal cells (SH-SY5Y). We found that toxin A treatment time- and dose-dependently decreased cell viability and triggered apoptosis accompanied by caspase-3 activation in this cell line. These effects were found to depend on the up-regulation of reactive oxygen species (ROS) and the subsequent activation of p38 MAPK and induction of $p21^{Cip1/Waf1}$. Moreover, the N-acetyl-$\text\tiny L$-cysteine (NAC)-induced down-regulation of ROS could recover the viability loss and apoptosis of toxin A-treated neuronal cells. These results collectively suggest that C. difficile toxin A is toxic for neuronal cells, and that this is associated with rapid ROS generation and subsequent p38 MAPK activation and $p21^{Cip1/Waf1}$ up-regulation. Moreover, our data suggest that NAC could inhibit the toxicity of C. difficile toxin A toward enteric neurons.

• Advances in pediatric surgery
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• v.8 no.2
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• pp.113-118
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• 2002

The etiology of several motility disorders, including persistent megacolon after definitive surgery for Hirschsprung's disease, meconium ileus which is not associated with cystic fibrosis and idiopathic megacolon, is still unclear. Interstitial cells of Cajal (ICC) are thought to modulate gut motility as gastrointestinal pace maker cells. The aim of this study was to evaluate the role of ICC in the bowel walls of the patients (n=15) who had variable motility disorders. The ICC were identified by immunohistochemical staining using an anti-C-Kit antibody and the results were compared with control specimens (n=2). The control group (G1) showed evenly distributed ICC in their bowel walls. The second group (G2, n=5) who had normal bowel movements after Duhamel procedures and the third group (G3, n=4) who had persistent megacolon after Duhamel procedures showed absent or scarcely distributed ICC in their aganglionic bowels. The ICC were immunohistochemical staining using an anti-C-Kit antibody and the results were compared with control specimens (n=2). The control group (G1) showed evenly distributed ICC in their bowel walls. The second group (G2, n=5) who had normal bowel movements after Duhamel procedures and the third group (G3, n=4) who had persistent megacolon after Duhamel procedures showed absent or scarcely distributed ICC in their aganglionic bowels. Whereas ICC were evenly distributed in the ganglionic bowels of G2, they were not seen or scarecely distributed in the ganglionic bowels of G3. Two patients (G4) who suffered from idiopathic megacolon showed absence or decrease of ICC in spite of presence of ganglion cells in their colons. Four neonates (G5) who underwent ileostomy because of meconium obstruction showed absent or markedly decreased ICC in the the colon at the time of ileostomy and the distribution of ICC was changed to a normal pattern at the time of ileostomy closure between 39-104 days of age and their bowel motility were restored after that. The results suggest that lack of ICC caused reduce motility in the ganglionic colons and it may be responsible for the development of various motility disorders. Delayed maturity of ICC may also playa role in the meconium obstruction of neinates.

• Journal of Life Science
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• v.23 no.10
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• pp.1295-1303
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• 2013

According to facts revealed up until the present, there are a total of 68 known phyla on earth, including 55 phyla of bacteria and 13 phyla of archaea. The human large intestine has 9 phyla of microorganisms, which is a relatively lower diversity compared to the general environments of soil or sea. The diversity of intestinal microorganisms is affected by the characteristics of the host (genetic background, sex, age, immune system, and gut motility), the diet (non-digestible carbohydrates, fat, prebiotics, probiotics), and the intake of antibiotics, which in turn have an effect on energy storage processes, gene expressions, and even metabolic diseases like obesity. Probiotics are referred to as living microorganisms that improve the intestinal microbiota and contribute to the health of the host; in addition, probiotics usually comprise lactic acid bacteria. Recently, bacteriotherapy using probiotics has been utilized to treat sicknesses like diarrhea and irritable bowel syndrome. Prebiotics are a food ingredient which can selectively adjust intestinal microorganisms and which comprise inulin, fructooligosaccharides, galactooligosaccharides, and lactulose. In recent days, attention has been paid to the use of dietary cellulose in the large intestine and the production of short chain fatty acids (short-chain fatty acids) in relation to obesity and anticancer. More research into microorganisms in the large intestine is necessary to identify specific microorganism species, which are adjusted by diverse non-digestible carbohydrates, prebiotics, and probiotics in the large intestine and to understand the connection between sicknesses and metabolites like short chain fatty acids produced by these microorganism species.