Regulation Of Acid Secretion Research Articles

Cross-species single-cell transcriptomic analysis of animal gastric antrum reveals intense porcine mucosal immunity

As an important part of the stomach, gastric antrum secretes gastrin which can regulate acid secretion and gastric emptying. Although most cell types in the gastric antrum are identified, the comparison of cell composition and gene expression in the gastric antrum among different species are not explored. In this study, we collected antrum epithelial tissues from human, pig, rat and mouse for scRNA-seq and compared cell types and gene expression among species. In pig antral epithelium, we identified a novel cell cluster, which is marked by high expression of AQP5, F3, CLCA1 and RRAD. We also discovered that the porcine antral epithelium has stronger immune function than the other species. Further analysis revealed that this may be due to the insufficient function of porcine immune cells. Together, our results replenish the information of multiple species of gastric antral epithelium at the single cell level and provide resources for understanding the homeostasis maintenance and regeneration of gastric antrum epithelium.

Histamine Signaling Is Essential for Tissue Macrophage Differentiation and Suppression of Bacterial Overgrowth in the Stomach.

Histamine in the stomach traditionally is considered to regulate acid secretion but also has been reported to participate in macrophage differentiation, which plays an important role in tissue homeostasis. Therefore, this study aimed to uncover the precise role of histamine in mediating macrophage differentiation and in maintaining stomach homeostasis. Here, we expand on this role using histidine decarboxylase knockout (Hdc-/-) mice with hypertrophic gastropathy. In-depth invivo studies were performed in Hdc-/- mice, germ-free Hdc-/- mice, and bone-marrow-transplanted Hdc-/- mice. The stomach macrophage populations and function were characterized by flow cytometry. To identify stomach macrophages and find the new macrophage population, we performed single-cell RNA sequencing analysis on Hdc+/+ and Hdc-/- stomach tissues. Single-cell RNA sequencing and flow cytometry of the stomach cells of Hdc-/- mice showed alterations in the ratios of 3 distinct tissue macrophage populations (F4/80+Il1bhigh, F4/80+CD93+, and F4/80-MHC class IIhighCD74high). Tissue macrophages of the stomachs of Hdc-/- mice showed impaired phagocytic activity, increasing the bacterial burden of the stomach and attenuating hypertrophic gastropathy in germ-free Hdc-/- mice. The transplantation of bone marrow cells of Hdc+/+ mice to Hdc-/- mice recovered the normal differentiation of stomach macrophages and relieved the hypertrophic gastropathy of Hdc-/- mice. This study showed the importance of histamine signaling in tissue macrophage differentiation and maintenance of gastric homeostasis through the suppression of bacterial overgrowth in the stomach.

Cortisol and glucocorticoid receptor 2 regulate acid secretion in medaka (Oryzias latipes) larvae.

Freshwater fish live in environments where pH levels fluctuate more than those in seawater. During acidic stress, the acid-base balance in these fish is regulated by ionocytes in the gills, which directly contact water and function as an external kidney. In ionocytes, apical acid secretion is largely mediated by H+-ATPase and the sodium/hydrogen exchanger (NHE). Control of this system was previously proposed to depend on the hormone, cortisol, mostly based on studies of zebrafish, a stenohaline fish, which utilize H+-ATPase as the main route for apical acid secretion. However, the role of cortisol is poorly understood in euryhaline fish species that preferentially use NHE as the main transporter. In the present study, we explored the role of cortisol in NHE-mediated acid secretion in medaka larvae. mRNA expression levels of transporters related to acid secretion and cortisol-synthesis enzyme were enhanced by acidic FW treatment (pH 4.5, 2 days) in medaka larvae. Moreover, exogenous cortisol treatment (25mg/L, 2 days) resulted in upregulation of nhe3 and rhcg1 expression, as well as acid secretion in 7 dpf medaka larvae. In loss-of-function experiments, microinjection of glucocorticoid receptor (GR)2 morpholino (MO) caused reductions in nhe3 and rhcg1 expression and diminished acid secretion, but microinjection of mineralocorticoid receptor (MR) and GR1 MOs did not. Together, these results suggest a conserved action of cortisol and GR2 on fish body fluid acid-base regulation.

Breaking Out From Tradition: Redesign of Large Physiology Lecture Increases Engagement, Inclusion, and Student Outcomes

Mounting evidence suggests that traditional lecturing is less effective, less engaging, and less inclusive than active learning. However, transitioning to active learning, particularly in a large science course, presents unique administrative and pedagogical challenges. In this study, we present the results of our recent effort to redesign and restructure our large human anatomy and physiology course at the University of Connecticut.In place of a traditional lecture, we developed an active instructional model that subdivided hundreds of students into “break out” groups of no more than five students. Breakout groups met concurrently in multiple classrooms during the scheduled lecture time to work through modules in the renal and digestive systems with an undergraduate peer facilitator. Modules were designed with input from undergraduate facilitators, with attention to scientific teaching techniques (active learning, inclusive teaching, assessment). Students concept mapped the molecular basis of urine formation in nephrons and the regulation of acid secretion in the gastric pit; worked through an interrupted case study on ulcer formation and modified think‐pair‐share question sets on renal and gastric pharmacology; and practiced critical reflection on the clinical and socioeconomic factors influencing the incidence and treatment of disease.At the end of the semester, students registered in the redesigned course were compared to peers registered in another section, taught by the same instructors, that followed a traditional large lecture format. This assessment involved an analysis of student performance on paired exam questions of varied difficulty, a modified SALG (Student Assessment of Learning Gains), and solicited and unsolicited student feedback. Our results indicate that, on average, students in the redesigned course performed better on exam questions related to the renal and digestive systems. Furthermore, many of these questions were found to be less “discriminating”, indicating less disparity between higher performing and lower performing students. The vast majority (95%) of students gave positive feedback on the redesigned classes, and nearly 90% reported learning gains related to the major concepts from the digestive and renal system. Summarily, our study describes and evaluates a new instructional model for large, undergraduate anatomy and physiology courses that has been developed and implemented using undergraduate students. Most importantly, we offer preliminary evidence supporting the conclusion that this model is more inclusive, more effective, and better liked than traditional lecturing.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The Duodenum

The duodenum is the first part of the small intestine that arises from the embryologic foregut and midgut. With maturation, it lies mostly retroperitoneal and is intimately associated with nearby structures such as the pancreas, hepatoduodenal ligament, and transverse colon mesentery. It is well vascularized with a rich lymphatic network and supports digestive, absorptive, immune, and endocrine functions. The duodenum receives food bolus from the stomach and releases various hormones important for regulating motility and gastric acid secretion. In the duodenum, food content mixes with bile and pancreatic enzymes to continue digestion of and initiate absorption for fats, carbohydrates, proteins, and vitamins and minerals. The duodenum experiences substantial exposure to the external environment and therefore contains an extensive immune barrier, including mucosa-associated lymphoid tissue. Additionally, there is a significant neuroendocrine network within the duodenum and small intestine that possesses a variety of endocrine functions, including regulation of acid secretion, motility, pancreatic function, bile flow, and mucosal cell growth. These enterochromaffin cells are the source duodenal neuroendocrine tumors (carcinoid) and can be classified according to subtype or grade. The duodenum is a diverse component of the small intestine that is uniquely suited to its numerous functions. Key words: absorption, acid secretion, anatomy, digestion, duodenum, intestinal immune system, microstructure, motility, mucosa-associated lymphoid tissue, neuroendocrine

The Duodenum

The duodenum is the first part of the small intestine that arises from the embryologic foregut and midgut. With maturation, it lies mostly retroperitoneal and is intimately associated with nearby structures such as the pancreas, hepatoduodenal ligament, and transverse colon mesentery. It is well vascularized with a rich lymphatic network and supports digestive, absorptive, immune, and endocrine functions. The duodenum receives food bolus from the stomach and releases various hormones important for regulating motility and gastric acid secretion. In the duodenum, food content mixes with bile and pancreatic enzymes to continue digestion of and initiate absorption for fats, carbohydrates, proteins, and vitamins and minerals. The duodenum experiences substantial exposure to the external environment and therefore contains an extensive immune barrier, including mucosa-associated lymphoid tissue. Additionally, there is a significant neuroendocrine network within the duodenum and small intestine that possesses a variety of endocrine functions, including regulation of acid secretion, motility, pancreatic function, bile flow, and mucosal cell growth. These enterochromaffin cells are the source duodenal neuroendocrine tumors (carcinoid) and can be classified according to subtype or grade. The duodenum is a diverse component of the small intestine that is uniquely suited to its numerous functions. Key words: absorption, acid secretion, anatomy, digestion, duodenum, intestinal immune system, microstructure, motility, mucosa-associated lymphoid tissue, neuroendocrine

Gastrin attenuates ischemia-reperfusion-induced intestinal injury in rats.

Intestinal ischemia-reperfusion (I/R) injury is a devastating complication when the blood supply is reflowed in ischemic organs. Gastrin has critical function in regulating acid secretion, proliferation, and differentiation in the gastric mucosa. We aimed to determine whether gastrin has an effect on intestinal I/R damage. Intestinal I/R injury was induced by 60-min occlusion of the superior mesenteric artery followed by 60-min reperfusion, and the rats were induced to be hypergastrinemic by pretreated with omeprazole or directly injected with gastrin. Some hypergastrinemic rats were injected with cholecystokinin-2 (CCK-2) receptor antagonist prior to I/R operation. After the animal surgery, the intestine was collected for histological analysis. Isolated intestinal epithelial cells or crypts were harvested for RNA and protein analysis. CCK-2 receptor expression, intestinal mucosal damage, cell apoptosis, and apoptotic protein caspase-3 activity were measured. We found that high gastrin in serum significantly reduced intestinal hemorrhage, alleviated extensive epithelial disruption, decreased disintegration of lamina propria, downregulated myeloperoxidase activity, tumor necrosis factor-α, and caspase-3 activity, and lead to low mortality in response to I/R injury. On the contrary, CCK-2 receptor antagonist L365260 could markedly impair intestinal protection by gastrin on intestinal I/R. Severe edema of mucosal villi with severe intestinal crypt injury and numerous intestinal villi disintegrated were observed again in the hypergastrinemic rats with L365260. The survival in the hypergastrinemic rats after intestinal I/R injury was shortened by L365260. Finally, gastrin could remarkably upregulated intestinal CCK-2 receptor expression. Our data suggest that gastrin by omeprazole remarkably attenuated I/R induced intestinal injury by enhancing CCK-2 receptor expression and gastrin could be a potential mitigator for intestinal I/R damage in the clinical setting.

Hepcidin is localised in gastric parietal cells, regulates acid secretion and is induced by Helicobacter pylori infection

Backgrounds and aimsHepcidin is an antimicrobial peptide and the central regulator of iron metabolism. Given that hepcidin was shown to be expressed in a variety of extrahepatic tissues and that...

Parietal cell activation by arborization of ECL cell cytoplasmic projections is likely the mechanism for histamine induced secretion of hydrochloric acid

Background and aims. Enterochromaffin-like (ECL) cells are central in the regulation of acid secretion. G cells release gastrin and activate ECL cell histamine secretion which stimulates parietal cell H2 receptors initiating acid secretion. It is unclear whether histamine-mediated parietal cell activation is via a vascular or paracrine pathway. To assess this, we utilized immunohistochemistry (IHC) and electron microscopy to examine gastric tissue and used visualization of formalin fixed dispersed gastric cells and glands to investigate and define the anatomical relationship between ECL and parietal cells. Material and methods. Sprague–Dawley rat stomachs were instilled with formalin. Thereafter fixed mucosal cells and whole gastric glands were dispersed by mechanical and chemical dissolution and enzymatic digestion. Smears with fixed isolated cells and whole glands were stained by IHC with histidine decarboxylase (HDC) and H+/K+-ATPase antibodies. Whole tissue samples of Sprague–Dawley and cotton rat oxyntic mucosa were investigated with IHC using HDC, VMAT2 and H+/K+-ATPase antibodies, and electron microscopy was performed to further delineate the precise anatomic relationship between ECL cells and parietal cells. Results. Each ECL cell generated a network of HDC- and VMAT2-positive dendritic-like elongations that were in direct contact with several parietal cells. Thus, ECL cells at the base of the gland were in communication with parietal cells in the middle of the gland. Electron microscopy confirmed that the cytoplasmic ECL cell elongations containing secretory vesicles were in direct juxtaposition to parietal cells. Conclusions. These findings indicate that ECL cells directly regulate parietal cell function in a neurocrine manner via slender neuron-like elongations.

Gastric secretion

This review summarizes the past year's literature regarding the regulation of gastric exocrine and endocrine secretion at the central, peripheral, and cellular levels. Gastric acid secretion is an intricate and dynamic process that is regulated by neural (efferent and afferent), hormonal (e.g., gastrin), and paracrine (e.g., histamine, ghrelin, somatostatin) pathways as well as mechanical (e.g., distension) and chemical (e.g., protein, glutamate, coffee, and ethanol) stimuli. Secretion of hydrochloric acid by the parietal cell involves recruitment and fusion of HK-adenosine triphosphatase (HK-ATPase)-containing cytoplasmic tubulovesicles with the apical membrane with subsequent electroneutral transport of hydronium ions in exchange for potassium; the source of the latter is the potassium channel, KCNQ1. Concomitantly, chloride exits via the cystic fibrosis transmembrane regulator. Inhibition of the HK-ATPase by proton pump inhibitors leads to a compensatory hypergastrinemia which, if prolonged, results in parietal and enterochromaffin-like cell hyperplasia. The clinical consequence is rebound acid secretion which may induce dyspeptic symptoms in healthy individuals and exacerbate reflux symptoms in patients with gastroesophageal reflux disease. We continue to make progress in our understanding of the regulation of gastric acid secretion in health and disease. A better understanding of the pathways and mechanisms regulating acid secretion should lead to improved management of patients with acid-induced disorders as well as those who secrete too little acid.

Rab27b Localizes to the Tubulovesicle Membranes of Gastric Parietal Cells and Regulates Acid Secretion

Rabs are monomeric guanosine triphosphatases that regulate membrane trafficking and acid secretion in gastric parietal cells. Using a proteomics approach, we identified a new Rab, Rab27b, in tubulovesicle membranes and determined its role in parietal cell activation. We used mass spectrometry (MS) to identify Rab27b in purified tubulovesicular membrane fractions and used immunoblot and immunofluorescence analyses to study its expression. Wild-type, constitutively active (Rab27bQ78L), and dominant negative (Rab27bN133I) forms of Rab27b were tagged with yellow fluorescent protein (YFP) and expressed in parietal cells using adenoviral constructs to study localization and function. Localization was visualized by fluorescence microscopy in resting and stimulated cells. Acid secretion in primary cell cultures was measured by aminopyrine accumulation. A tandem MS peptide mass fingerprint was matched to 7 peptides of Rab27b. Rab27b localized to tubulovesicle membranes, based on immunoblot and immunocytochemical analyses. Endogenous Rab27b, YFP/wild-type Rab27b, Rab27bQ78L, and Rab27bN133I all distributed throughout the cytoplasm of resting parietal cells. After stimulation, wild-type Rab27b and YFP-Rab27bQ78L translocated to the apical membrane, but YFPR-ab27bN133I did not. Expression of wild-type YFP-Rab27b or YFP-Rab27bQ78L did not affect acid secretion, whereas expression of Rab27bN133I almost completely inhibited acid secretion. Rab27b is associated with tubulovesicle membranes in the parietal cell and Rab27b may play a role in stimulation-associated membrane recruitment and gastric acid secretion.

Identification of endocrine cells of the stomach that express acid-sensitive background potassium (K2P9.1/TASK3) channels

The family of two-pore domain potassium (K(₂P)) channels is important in setting and controlling the background potassium current of excitable cells. This study examines the localisation of the acid-sensitive channel, K(₂P)9.1 (TASK3), in cells of the gastric mucosa. We observed K(₂P)9.1 immunoreactivity in endocrine cells of the mucosal glands of the guinea-pig, rat and mouse but the channels were not detected in parietal, chief, or mucous cells. K(₂P)9.1 channel immunoreactivity was consistently co-localised with histidine decarboxylase immunopositive enterochromaffin-like (ECL) cells, and with the majority of ghrelin immunoreactive X/A cells. Localisation in somatostatin immunoreactive D cells was rare in the guinea-pig, and did not occur in the stomach of rat, but, in the mouse, K(₂P)9.1 channels were observed in the majority of somatostatin-immunoreactive D cells. Conversely, sections taken from the guinea-pig and mouse stomachs, but not rat stomach, revealed K(₂P)9.1 in gastrin-containing G cells. These results demonstrate the presence of K(₂P)9.1 channels in the entero-endocrine ECL, G and D cell populations of the stomach that regulate acid secretion through the release of histamine, gastrin and somatostatin. K(₂P)9.1 channels were located in the ghrelin X/A cells that regulate food intake.

217 The Role of Umami and Glutamate Receptors in the Gastrin-EC Cell Axis and the Implications of a Serotonin-Gastrin Interface in the Regulation of Acid Secretion

217 The Role of Umami and Glutamate Receptors in the Gastrin-EC Cell Axis and the Implications of a Serotonin-Gastrin Interface in the Regulation of Acid Secretion

Genetically engineered mice: a new paradigm to study gastric physiology

To summarize key aspects from recent research as well as review articles on the topic of genetic mouse models, particularly in knockout mice, that have considerably contributed to understanding the pathways and mechanisms underlying gastric physiology. A series of knockout mouse models has proven to be invaluable in elucidating the mechanism and validating the current model of acid secretion. The interaction between the gastrin-histamine and cholecystokinin-somatostatin pathways was identified using the genetic approach as being critical in regulating acid secretion. Curiously, neither ghrelin nor ghrelin receptor knockout mice displayed the expected lean phenotype. Importantly, the study of obestatin in GPR39 knockout mice could be misleading, as zinc rather than obestatin is the endogenous ligand for GPR39. The physiological roles of ghrelin and obestatin have yet to be confirmed using knockout mouse models. The knockout mouse continues to serve as an excellent model to dissect the complexity of the mechanism of gastric acid secretion and to study the physiological importance of gastric ghrelin.

Control of Gastric Acid Secretion in Somatostatin Receptor 2 Deficient Mice: Shift from Endocrine/Paracrine to Neurocrine Pathways

The gastrin-enterochromaffin-like (ECL) cell-parietal cell axis is known to play an important role in the regulation of gastric acid secretion. Somatostatin, acting on somatostatin receptor type 2 (SSTR(2)), interferes with this axis by suppressing the activity of the gastrin cells, ECL cells, and parietal cells. Surprisingly, however, freely fed SSTR(2) knockout mice seem to display normal circulating gastrin concentration and unchanged acid output. In the present study, we compared the control of acid secretion in these mutant mice with that in wild-type mice. In SSTR(2) knockout mice, the number of gastrin cells was unchanged; whereas the numbers of somatostatin cells were reduced in the antrum (-55%) and increased in the oxyntic mucosa (35%). The ECL cells displayed a reduced expression of histidine decarboxylase and vesicle monoamine transport type 2 (determined by immunohistochemistry), and an impaired transformation of the granules to secretory vesicles (determined by electron microscopic analysis), suggesting low activity of the ECL cells. These changes were accompanied by an increased expression of galanin receptor type 1 in the oxyntic mucosa. The parietal cells were found to respond to pentagastrin or to vagal stimulation (evoked by pylorus ligation) with increased acid production. In conclusion, the inhibitory galanin-galanin receptor type 1 pathway is up-regulated in the ECL cells, and the direct stimulatory action of gastrin and vagal excitation is enhanced on the parietal cells in SSTR(2) knockout mice. We suggest that there is a remodeling of the neuroendocrine mechanisms that regulate acid secretion in these mutant mice.

Physiological and clinical significance of enterochromaffin-like cell activation in the regulation of gastric acid secretion

Gastric acid plays an important role in digesting food (especially protein), iron absorption, and destroying swallowed micro-organisms. H+ is secreted by the oxyntic parietal cells and its secretion is regulated by endocrine, neurocrine and paracrine mechanisms. Gastrin released from the antral G cell is the principal physiological stimulus of gastric acid secretion. Activation of the enterochromaffin-like (ECL) cell is accepted as the main source of histamine participating in the regulation of acid secretion and is functionally and trophically controlled by gastrin, which is mediated by gastrin/CCK-2 receptors expressed on the ECL cell. However, long-term hypergastrinemia will induce ECL cell hyperplasia and probably carcinoids. Clinically, potent inhibitors of acid secretion have been prescribed widely to patients with acid-related disorders. Long-term potent acid inhibition evokes a marked increase in plasma gastrin levels, leading to enlargement of oxyntic mucosa with ECL cell hyperplasia. Accordingly, the induction of ECL cell hyperplasia and carcinoids remains a topic of considerable concern, especially in long-term use. In addition, the activation of ECL cells also induces another clinical concern, i.e., rebound acid hypersecretion after acid inhibition. Recent experimental and clinical findings indicate that the activation of ECL cells plays a critical role both physiologically and clinically in the regulation of gastric acid secretion.

Gastric secretion

To summarize the literature over the past year on the regulation of gastric exocrine and endocrine secretion. Gastric acid secretion by parietal cells is precisely regulated by overlapping neural, hormonal, and paracrine pathways, both centrally and peripherally. Too much acid can induce gastroduodenal injury. Too little acid can interfere with the absorption of iron, calcium, vitamin B12, and certain drugs as well as predispose the patient to enteric infection. A number of peptides implicated in the central control of food intake such as ghrelin, orexin, and leptin are present in the stomach and are capable of modulating acid secretion. The precise mechanisms whereby Helicobacter pylori produces perturbations in acid secretion are not precisely known but appear to involve changes in somatostatin and perhaps ghrelin secretion. Both gastrin and gastrin-receptor knockout mice as well as gastrin-overexpressing and cAMP-overexpressing mice develop gastric atrophy; gastric atrophy is associated with antiparietal cell antibodies and may be a model for autoimmune gastritis. A better understanding of the pathways and mechanisms regulating acid secretion as well as the development of genetically engineered mouse models should lead to new strategies to prevent and treat a variety of gastric disorders, including peptic ulcer disease, neoplasia, and autoimmune gastritis.

Tissue‐specific Expression of Kir2.1, Clca3 and Aquaporin 4 in Adult and Embryonic Mouse Tissues

Gastric acid secretion occurs when activated parietal cells undergo a dynamic transformation in which tubulovesicles fuse with the apical membrane, resulting in proton secretion into the stomach via the H+/K+-ATPase. Recent studies have shown that various channels and exchangers also may play a role in the regulation of acid secretion from parietal cells. However, it is unknown precisely when the expression of these genes is initiated in embryonic development, which may give clues as to the timing of early gastric acid secretion. The overall goal of this research was to analyze expression of potassium inward rectifying channel 2.1 (Kir2.1), calcium-activated chloride channel–3 (Clca3), and the water channel aquaporin-4 (Aqp4) in mouse adult and embryonic tissues. RT-PCR was used to analyze expression of these genes in mouse embryos at various stages as well as in adult stomach, heart, small intestine, large intestine, spleen, brain, lung, testes, placenta, liver, skeletal muscle, kidney, skin, thymus, tongue, and eye. Preliminary results showed that Kir2.1 was expressed in the adult brain, heart, fundus, antrum, and spleen, but was not expressed at any of the embryonic stages tested (E11–E16). Clca3 was expressed in all adult tissues tested except for spleen, kidney, and liver, and was expressed in embryos at E11 and E16. Aqp4 was expressed in the brain, fundus, and placenta, and was expressed in embryos at E11 and E16. Further analysis will determine precisely when expression of these genes is initiated in embryonic development, allowing a more thorough understanding of the timing of acid secretion in mammalian development.

Transcriptomes of purified gastric ECL and parietal cells: identification of a novel pathway regulating acid secretion

The gastric entero-chromaffin-like (ECL) cell plays a key regulatory role in peripheral regulation of acid secretion due to the release of histamine that stimulates acid secretion by the parietal cell. Studies in intact animals, gastric glands, and isolated cells after short-term culture have shown expression of stimulatory CCK2 and PAC1 and inhibitory SST2 and Gal1 receptors as well as histidine decarboxylase. However, the pattern of its gene expression as a neuroendocrine cell has not been explored. Comparison of gene expression by 95% pure ECL cells obtained by density gradient, elutriation, and fluorescence-assisted cell sorting with isolates of the intact fundic gastric epithelium (i.e., "subtractive hybridization") identified a variety of additional expressed gene families characteristic of this neuroendocrine cell. These include genes 1) involved in neuropeptide synthesis and secretory vesicle exocytosis, 2) involved in control of inflammation, 3) implicated in healing of the epithelium, 4) encoding inhibitory Gi protein-coupled receptors, 5) playing a role in neuroendocrine regulation of food intake, and 6) encoding proteins likely involved in maintenance of circadian rhythm, in addition to the ECL cell-specific genes histidine decarboxylase and monoamine transporter. Particularly, the inhibitory apelin receptor gene, APJ, was highly expressed in the ECL cell preparation. Because parietal cells express apelin, immunohistochemical and functional studies showed that there is an inhibitory feed back loop between the parietal and ECL cell during gastrin stimulation, providing evidence for a novel pathway of downregulation of acid secretion due to interaction between these two cell types.

Gastrin (G) cells and somatostatin (D) cells in patients with dyspeptic symptoms: Helicobacter pylori associated and non-associated gastritis

Background: Gastrin G cells and somatostatin D cells are important regulators of gastric acid secretion and alterations in their relative numbers may play a key role in gastroduodenal disease. Aim:...