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The alimentary tract is an organ of functional diversity. The absorption of water, nutrients, minerals, and vitamins is made possible through the coordinated action of the salivary glands, intestine, stomach, exocrine pancreas and hepatobiliary system. [ABSTRACT FROM AUTHOR]

Bombesin mediates several biological activities in the gastrointestinal (GI) tract and central nervous system in mammals, including smooth muscle contraction, secretion of GI hormones and regulation of homeostatic mechanisms. Here, we report a novel bombesin-like peptide isolated from Boana raniceps. Its amino acid sequence, GGNQWAIGHFM-NH2, was identified and structurally confirmed by HPLC, MS/MS and 454-pyrosequencing; the peptide was named BR-bombesin. The effect of BR-bombesin on smooth muscle contraction was assessed in ileum and esophagus, and its anti-secretory activity was investigated in the stomach. BR-bombesin exerted significant contractile activity with a concentration–response curve similar to that of commercially available bombesin in ileum strips of Wistar rats. In esophageal strips, BR-bombesin acted as an agonist, as many other bombesin-related peptides act, although with different behavior compared to the muscarinic agonist carbachol. Moreover, BR-bombesin inhibited stomach secretion by approximately 50% compared to the untreated control group. This novel peptide has 80% and 70% similarity with the 10-residue C-terminal domain of human neuromedin B (NMB) and human gastrin releasing peptide (GRP10), respectively. Molecular docking analysis revealed that the GRP receptor had a binding energy equal to − 7.3 kcal.mol−1 and − 8.5 kcal.mol−1 when interacting with bombesin and BR-bombesin, respectively. Taken together, our data open an avenue to investigate BR-bombesin in disorders that involve gastrointestinal tract motility and acid gastric secretion. [ABSTRACT FROM AUTHOR]

Pavlov’s seminal observation that sham feeding in dogs stimulates gastric acid secretion through the vagus nerve pioneered the concept of the cephalic phase of digestion. This has been subsequently extended to a wide range of mammals including humans. In the last decades, experimental evidence in rats established that the three amino acid peptide thyrotropinreleasing hormone (TRH) expressed in the brainstem plays a key role in the vagal stimulation of digestive secretory-motor function. The dorsal motor nucleus of the vagus (DMN) neurons expresses TRH receptor subtype 1 (TRH-R1) and receives input of TRH containing fibers arising from TRH synthesizing neurons in medullary raphe nuclei. The activation of TRHTRH-R1 signaling excites the firing of DMN neurons leading to the activation of vagal efferent discharges and gastric myenteric cholinergic neurons. This results in a vagally mediated and atropine-sensitive stimulation of gastric secretory and propulsive motor function, along with duodenal and pancreatic secretion. Importantly, the blockade of TRH or TRH-R1 in the brainstem inhibits the gastric acid response to sham feeding in rats. Collectively, these convergent data support the physiological relevance of medullary TRHTRH-R1 signaling as the end effector of the vagally mediated stimulation of digestive process in the cephalic phase.

The alimentary tract is an organ of functional diversity. The absorption of water, nutrients, minerals, and vitamins is made possible through the coordinated action of the salivary glands, intestine, stomach, exocrine pancreas and hepatobiliary system. [ABSTRACT FROM AUTHOR]

Background and Aim: Gastroesophageal reflux disease (GERD) is a common disease caused by reflux of gastric contents to the esophagus. Proton‐pump inhibitors (PPIs) are recommended as a first‐line therapy to treat GERD. Recently, a new potassium‐competitive acid blocker, vonoprazan, was launched in Japan. We aimed to evaluate the comparative efficacy of vonoprazan and other PPIs in healing GERD. Methods: We used MEDLINE and the Cochrane Central Register of Controlled Trials to search the literature. Double‐blind randomized controlled trials for PPIs and/or vonoprazan that were published in English or Japanese and assessed healing effects in adult GERD patients were included. To estimate the comparative efficacy of treatments, we performed a Bayesian network meta‐analysis to assess the consistency assumption. Results: Of 4001 articles identified in the database, 42 studies were eligible. One study was hand‐searched and added to the analysis. For the main analysis of healing effects at 8 weeks, odds ratios (ORs) of vonoprazan (20 mg daily) to esomeprazole (20 mg), rabeprazole (20 mg), lansoprazole (30 mg), and omeprazole (20 mg) were 2.29 (95% credible interval, 0.79–7.06), 3.94 (1.15–14.03), 2.40 (0.90–6.77), and 2.71 (0.98–7.90), respectively. Subgroup analysis for patients with severe esophagitis at baseline showed significantly higher ORs for vonoprazan versus most of the comparator PPIs. Conclusions: This analysis shows that the GERD healing effect of vonoprazan is higher than that of rabeprazole (20 mg) but not higher than other PPIs. Subgroup analysis indicated that vonoprazan is more effective than most PPIs for patients with severe erosive esophagitis. [ABSTRACT FROM AUTHOR]

Abstract Ethnopharmacological relevance Virola elongata is a tree species belonging to the Myristicaceae family, distributed in the North and Midwest regions of Brazil, in the phytogeographic domain of the Amazon. The aqueous infusion or the hydroethanolic macerate of the stem bark of V. elongata are used in Brazilian and Ecuadorian indigenous folk medicine for several ethnopharmacological purposes, principally, in the treatment of stomach pain, indigestions, and gastric ulcers. This study was aimed to investigate the gastroprotective activity of this plant in order to support its popular use with scientific evidence. Materials and methods The stem bark hydroethanolic extract of the plant (HEVe) was prepared by maceration. Its qualitative and quantitative phytochemical constituents were investigated by classical colorimetric techniques, HPLC, and electrospray ionization-multiple stage fragmentation (ESI-MSn). The gastroprotective and antiulcer activity of HEVe at doses of 100, 300 and 900 mg/kg p.o. were tested using three acute (acidified ethanol, piroxicam, and in-water-restrain stress), and one chronic (acetic acid) animal ulcer models. The probable mode of action of the HEVe was evaluated by analyzing gastric acid secretion, mucus content, nitric oxide effect, and its antioxidant properties (on catalase, myeloperoxidase, and GSH content) in experimental rodents. The direct extract's activity on the growth of Helicobacter pylori was also investigated. Results Total phenolic content in the HEVe was of 146.20 ± 1.07 mg, being flavonoids about 50% (71.79 ± 0.70 mg) of it. Comparative HPLC fingerprint analysis revealed the presence of known phenolic antiulcer compounds, such as gallic acid, catechin, and rutin. Also, methanol/water fractionation and ESI-MSn analysis of the HEVe reveals the presence of quinic acid, 3,3′,4-trihydroxystilbene, juruenolid D, one catechin dimer, one C-glycosyl flavonoid, one polyketide and two neolignans as the major components of the extract. The HEVe attenuated gastric ulceration in all the different models of acute gastric ulcer, by enhancing gastroprotection through its antioxidant properties in vivo, and reducing also considerably the gastric secretion and total acidity. The HEVe also presented healing properties against the induced chronic ulceration process. On the other hand, the HEVe did not exhibit direct activity against H. pylori. Conclusion The HEVe exhibited significant gastroprotective/antiulcer effects and contain a relative high proportion of phenolic compounds, especially flavonoids, that could likely account, at least in part, for its pharmacological properties. The results justify its traditional usage and provided scientific evidence for its potential as a new herbal medicine to treat gastric ulcers. Graphical abstract fx1 [ABSTRACT FROM AUTHOR]

The carrot plant (Daucus carota) and its components are traditionally reported for the management of gastric ulcers. This study was performed to evaluate the role of carrot when administered concurrently with a conventional antiulcer treatment, pantoprazole, in alleviating gastric and duodenal ulcers in female experimental animals. The study involved standard animal models to determine the ulcer preventive effect using pylorus ligation, ethanol, and stress induced acute gastric ulcer models and duodenal ulcer models involving cysteamine. Acetic acid-induced chronic gastric ulcer and indomethacin-induced gastric ulcer models were used to evaluate the ulcer healing effect. Carrot fruit (500 mg/kg) and its co-administration with pantoprazole produced significant protection in an ethanol- and stress-induced acute gastric ulcer and cysteamine-induced duodenal ulcer. The healing of the acetic acid-induced chronic gastric ulcer was also augmented with this combination. Both total proteins and mucin contents were significantly increased in indomethacin-induced gastric ulcers. Similarly, in pylorus ligation, the pepsin content of gastric juice, total acidity, and free acidity were reduced. Overall, both ulcer preventive effects and ulcer healing properties of the pantoprazole were significantly enhanced in animals who received the co-administration of carrot fruit (500 mg/kg).

Prostaglandins (PGE1 ) 0.1, 0.2 and 0.4 mg/kg and 5-hydroxytryptamine (5-HT) 1, 2.5 and 5 mg/kg dose dependently inhibited gastric secretion in pyloric legated rats model While PGF2 ∝ 0.1, 0.4 and 1mg/kg inhibited gastric acid secretion. Methysergide in the dose 0.05 mg/kg significantly stimulated the gastric secretion. When non-inhibitory dose of PGE1 (0.1 ) and 5-HT (1.0 mg/kg) are injected simultaneously there were potentiation of inhibitory activity on gastric secretary response on volume, acid output, chloride output and pepsin output. The inhibitory activity of both PGE1 (0.4 mg/ kg) and 5-HT (5.0 mg/kg) including the inhibitory potentiating activity could not be modified by the pretreatment of methysergide (0.05 mg/kg). Similarly stimulatory dose of PGF2 ∝ (0.4) mg/kg) and inhibitory dose of PGE1 (0.4 mg/kg) administered together inhibitory response of PGE1 (0.4 mg/kg) were also not modified by methysergide pretreatment.

Correlation of gastric secretion and serotonin status of was studied by adopting different models in human and on experimental animals empowering different aspects. The knowledge base of banana research also shifted to serotonin research. The correlation studies were performed in diseased condition, in neonates and normal adults, conscious and anaesthetized rats and it was used to validate related hypothesis.

Результатом тривалого уведення донатора NO є перебудова періодичної моторної та секреторної активності шлунка. Зменшувались показники моторного індексу на 6-ту добу, суттєво (на 56%) знижувалась міоелектрична активність шлунка на 12-ту добу. Зміни секреторної функції шлунка проявлялися у достовірному зменшенні об’єму виділення шлункового соку в 2,0 та 3,3 раза, зростанні рН, зниженні концентрації глікопротеїнів на 57 та 39%, збільшенні концентрації пепсину в 1,8 та 2,6 раза на 6- та 12-ту добу відповідно. За цих змін спостерігали розбалансування механізмів регуляції секреторної активності шлунка, а вплив натрію нітропрусиду на головні та поверхневі епітеліальні клітини слизової оболонки шлунка був вираженіший у разі збільшення тривалості дії чинника. При уведенні блокатора синтезу NO – L-NNA порушувалась фазова картина міоелектричної активності (МЕА) шлунка, яка ставала подібною до переходу між ІІ та ІІІ фазами. Показники міоелектричного імпульсу (МІ) підвищувались в 1,3 раза на 6-ту добу уведення блокатора. На 12-ту добу спостерігали зміну характеру скорочень у всіх фазах МЕА шлунка та зниження МІ на 28%. Перебудови секреторної функції шлунка проявлялися достовірним збільшенням об’єму шлункового соку на 61 та 17%, у значному зростанні його рН на 6-та 12-ту добу відповідно. Встановлено порушення кислототвірної функції шлунка та активності пілоричного сфінктера, спричинене закиданням дуоденального вмісту до шлунка.

A K + -Cl − cotransport system was documented for the first time during the mid-seventies in sheep and goat red blood cells. It was then described as a Na + -independent and ouabain-insensitive ion carrier that could be stimulated by cell swelling and N -ethylmaleimide (NEM), a thiol-reacting agent. Twenty years later, this system was found to be dispensed by four different isoforms in animal cells. The first one was identified in the expressed sequence tag (EST) database by Gillen et al. based on the assumption that it would be homologous to the Na + -dependent K + -Cl − cotransport system for which the molecular identity had already been uncovered. Not long after, the three other isoforms were once again identified in the EST databank. Among those, KCC4 has generated much interest a few years ago when it was shown to sustain distal renal acidification and hearing development in mouse. As will be seen in this review, many additional roles were ascribed to this isoform, in keeping with its wide distribution in animal species. However, some of them have still not been confirmed through animal models of gene inactivation or overexpression. Along the same line, considerable knowledge has been acquired on the mechanisms by which KCC4 is regulated and the environmental cues to which it is sensitive. Yet, it is inferred to some extent from historical views and extrapolations. [ABSTRACT FROM AUTHOR]

A comprehensive mathematical model of the digestive processes in humans could allow for better design of functional foods which may play a role in stemming the prevalence of food related diseases around the world. This work presents a mathematical model for a nutrient based feedback mechanism controlling gastric emptying, which has been identified in vivo by numerous researchers. The model also takes into account the viscosity of nutrient meals upon gastric secretions and emptying. The results show that modelling the nutrient feedback mechanism as an on/off system, with an initial emptying rate dependent upon the secretion rate (which is a function of the gastric chyme viscosity) provides a good fit to the trends of emptying rate for liquid meals of low and high nutrient content with varying viscosity. [ABSTRACT FROM AUTHOR]

Background and Aim Proton pump inhibitors (PPIs) are among the most widely used medications worldwide. Dementia is an increasingly common cause of disability in older populations. Recent studies have suggested an increased risk of cognitive impairment and dementia diagnosis among people who consume PPIs. This systematic review explores dementia, cognitive impairment, and the use of PPIs. Methods Systematic searches were conducted in the databases of MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials (CENTRAL), PSYCinfo, Scopus, Web of Science, and for articles published from inception to June 30, 2016. Primary outcomes of interest were the use of PPIs and diagnosis of dementia or acute cognitive impairment. Studies conducted on people aged less than 18 years old were excluded. All study designs were eligible for inclusion. Two reviewers independently assessed study quality and extracted data from included studies. Results The systematic search strategy and screening process yielded 11 studies for inclusion in the systematic review. Four studies explored PPI use and dementia, and seven studies explored PPI use and acute cognitive impairment. Three of the four studies exploring dementia identified a positive association with PPI use. A positive association was also observed in the majority of studies exploring acute cognitive impairment. Conclusions Based on the current published literature, this systematic review has identified that the reported association between PPI use and dementia is limited by methodological issues and conflicting results. Further longitudinal studies with robust bias limitation are required to explore the use of PPIs and dementia or acute cognitive impairment, and to ascertain the existence of any causal relationships. [ABSTRACT FROM AUTHOR]

The alimentary tract is an organ of functional diversity. The absorption of water, nutrients, minerals, and vitamins is made possible through the coordinated action of the salivary glands, intestine, stomach, exocrine pancreas and hepatobiliary system. [ABSTRACT FROM AUTHOR]

Nano TiO 2 has been widely used in food industry as a coloring agent, whether the application has adverse effects on stomach for humans and animals is rarely concerned. This study determined whether intragastric administration with nano TiO 2 every day for nine months cause gastric damages and dysfunction, and is associated with changes of stomach damage-related protein expression in mice. Our results suggested that nano TiO 2 exposure resulted in significant titanium accumulation in the stomach, reductions in daily food intake and water intake, stomach weight, and stomach indices. Importantly, mice exhibited severe gastric damages such as gastric mucosa atrophy, erosion, inflammatory cell infiltration and cell morphologic damages including apoptosis, and coupled with reductions of serum pepsin activity, stomach total acidity and H + concentration, and increases of serum gastrin concentration and gastric pH. Furthermore, these are associated with decreased expression of IκB, TFF 1, 2, and increased expression of NF-κB, TNF-α, IL-lβ, -6, -8, COX-2, and PGE2 in the stomach. The findings showed that gastric toxicity of mice induced by chronic exposure to nano TiO 2 may be associated with alterations of gastritis-related protein expression in mice. It implies that the potential adverse effects to digestive system health should be concerned. [ABSTRACT FROM AUTHOR]

[Objectives] Deoxynivalenol (DON) is a common mycotoxin in feed and its row materials in the world. This study aimed to explore the influence of DON on the composition of gastric juice in rats. [Methods] 24 Wistar rats were gavaged at the dose of 0, 1, 5 and 25 mg·kg-1 DON after fasting for 24 h, and 0.5 h later pylori ligation was used to collect gastric juice within 4 h. The composition of gastric juice was detected, including volume, pH value, pepsin content and activities, mucin and metal ions. [Results] The results showed that the DON exposure resulted in a decrease by 24.88%, 51.39% and 60.88%, respectively, compared to the control, and the differences were significant (P < 0.05). In addition, pH value reached 3.20, 3.81 and 6.70 in DON exposed rats, with control group at 1.93. Similarly, the mucin decreased by 8.42%, 10.02% and 12.30%, respectively. The contents of pepsin decreased by 7.96%, 18.33% and 50.83%, and the activities decreased by 27.97%, 55.36% and 67.82% at 1, 5 and 25 mg·kg-1 DON group, respectively. The dry weight was significantly higher than the control, with 42.97%, 250.16% and 2 460.32% at 1, 5 and 25 mg·kg-1 DON, respectively. The results of inductively coupled plasma atomic emission spectrometry (ICP-AES) assay showed that DON exposure also disrupted the composition of K+, Na+, Ca2+, Zn2+ of gastric juice. [Conclusions] These results suggest that DON exposure influences the composition of gastric juice in Wistar rats, and causes the disorder of gastric secretion in rats. [ABSTRACT FROM AUTHOR]

Background/Aims: Paraoxon, an organophosphate metabolite of the insecticide parathion inhibits the enzyme, acetylcholinesterase (Achase). Organophosphates affect the heart, visual system, nervous system and muscles. In this present study, we investigate the effects of the chronic consumption of paraoxon on gastric acid and pepsin secretion in N-mari rats. Materials and Methods: This study was performed from April 2003 to May 2004 in the Physiology department of Baghiatalah University of Medical Sciences, Tehran, Iran. It was performed on three groups of female N-mari rats (10 /group) each weighing 200-250 g. The first group received 0.05 mg/kg/day paraoxon subcutaneously for one month. The second group received the same chronic doses of ethyl alcohol (96%) (solvent of paraoxon) and the third group (control) received no drugs. After tracheostomy and laparatomy, gastric secretions were collected with a tube via the duodenum. Pentagastrin (25 µg/kg, i.p.) was used as a gastric stimulator. Acid and pepsin secretions were measured by titration and the Anson method, respectively. The stages of the measurements were basal (first and second), stimulated and returned-basal. Results: Basal acid secretion in the paraoxon group was greater than those in the alcohol and control groups (14.61 ± 1.46, 7.18 ± 0.28 and 7.88 ± 0.26 µmol/15 min, respectively, P < 0.001)). Although pentagastrin-stimulated acid secretion in all the three groups was greater than that of the basal state, there were no significant differences among the three groups. Basal pepsin secretions in the paraoxon group were greater than those in the alcohol and control groups (2.97 ± 0.32, 1.19 ± 0.25 and 0.55 ± 0.06 µg/15 min, respectively). Pentagastrin-stimulated pepsin secretion in the paraoxon group was significantly greater than those in the alcohol and control groups (3.22 ± 0.38, 2.22 ± 0.46 and 1.09 ± 0.66 µg/15 min, respectively, P < 0.001). Conclusion: Chronic exposure to paraoxon results in the increased secretion of gastric acid and pepsin.

Background: We previously described the gastroprotective effect of 2-phenylquinoline (2-PQ), the main alkaloid isolated from the bark of Galipea longiflora (Rutaceae). However, despite the significant and promising results, the pharmacological mechanisms of the gastroprotection induced by 2-PQ have not been investigated.Purpose: To evaluate the mechanisms underlying the gastroprotective effects of 2-PQ.Study Design: We used an in vivo mouse ulcer model and in vitro methodologies involving H⁺/K⁺-ATPase and L929 murine fibroblasts.Methods: The gastroprotective activity of 2-PQ (10-100 mg/kg, orally, p.o) was assessed against gastric ulcer induced by 60% ethanol/0.03 M hydrochloric acid (HCl) in mice or that induced by indomethacin (80 mg/kg, p.o) in rats. The cytotoxicity was assessed in L929 murine fibroblasts. Ulcerated tissues were analyzed histologically, histochemically, and biochemically. The antisecretory activity of 2-PQ was evaluated in vivo and in vitro.Results: 2-PQ showed no cytotoxicity, reduced the lesion area induced by ethanol/HCl (log half-maximal effective dose, ED50 = 1.507), and the histological evaluation supported these results. Furthermore, 2-PQ reduced indomethacin-induced gastric ulceration. The gastroprotection was accompanied by normalization of superoxide dismutase (SOD) and glutathione-S-transferase (GST) activity, an intense increase in reduced glutathione (GSH) levels, and reduction in lipid peroxide (LPO) and tumor necrosis factor (TNF)-α levels in the gastric mucosa. The antisecretory properties of 2-PQ were confirmed by the decreased volume and total acidity of the gastric juice, and it reduced histamine- or pentagastrin-stimulated gastric acid secretion. However, 2-PQ did not change the in vitro H⁺/K⁺-ATPase activity or the content of gastric-adhered mucous in mice. In addition, pretreatment with N-ethylmaleimide, NG-nitro-l-arginine methyl esters, yohimbine, or indomethacin reversed the gastroprotective effect of 2-PQ, suggesting nitric oxide, nonprotein sulfhydryl compounds, α-2-receptors, and prostaglandin were involved.Conclusion: 2-PQ provides gastroprotection by reducing oxidative damage and inhibiting acid secretion mediated by histaminergic and gastrinergic regulatory pathways. [ABSTRACT FROM AUTHOR]

Nesfatin-1, a recently discovered neuropeptide involved in satiety. Recent studies have revealed that central nesfatin-1 inhibits gastric emptying and gastric acid secretion, though the mechanisms involved in these processes are not known. We aim to explore the effects of nesfatin-1 on a population of gastric distension (GD)-sensitive neurons in the lateral hypothalamus (LHA), gastric motility, and gastric secretion and the role for an arcuate nucleus (Arc)-LHA neural pathway in these processes. Single unit extracellular discharge recordings were made in of LHA. Further, gastric motility and gastric secretion in rats were monitored. Retrograde tracing and fluorescent immunohistochemical staining were used to explore nesfatin-1 neuron projection. The results revealed that administration of nesfatin-1 to the LHA or electric stimulation of the Arc could alter the neuronal activity of melanin-concentrating hormone (MCH)-responsive, GD-responsive neurons in LHA, which could be blocked by pretreatment with MCH receptor-1 antagonist PMC-3881-PI or weakened by pretreatment of a nesfatin-1 antibody in LHA. Administration of nesfatin-1 into LHA could inhibit gastric motility and gastric secretion, and these effects could be enhanced by administration of PMC-3881-PI. Electrical stimulation of Arc promoted the gastric motility and gastric secretion. Nesfatin-1 antibody or PMC-3881-PI pretreatment to LHA had no effect on Arc stimulation-induced gastric motility, but these pretreatments did alter Arc stimulation-induced effects on gastric secretion. Our findings suggest that nesfatin-1 signaling in LHA participates in the regulation of efferent information from the gastrointestinal tract and gastric secretion which also involve MCH signaling. Further, they show that a nesfatin-1-positive Arc to LHA pathway is critical for these effects. [ABSTRACT FROM AUTHOR]