A histochemical and immunohistochemical study on the gastrointestinal tract of sparrowhawk (Accipiter nisus) / Estudio histoquímico e inmunohistoquímico del tracto gastrointestinal del gavilán (Accipiter nisus)

SUMMARY: In the present study, we aimed to determine the localization and distribution of entero-endocrine cells in the gastrointestinal tract by immunohistochemical methods and understand the structure of the glycoproteins elaborated by the epithelium the digestive tract regions by histochemical methods. The nine sparrowhawks were euthanized, and gastrointestinal tract tissues were removed and fixed in formalin. The gastrointestinal tract sections were stained with immunohistochemical and histochemical techniques to evaluate the enteroendocrine cells and histomorphometric analysis. The results showed that the numbers of somatostatin in the ventriculus, gastrin in the proventriculus, serotonin in the duodenum and jejunum immunopositivity are higher, remaining segments of the gastrointestinal tract are detected slight positivity in the glucagon, gastrin, serotonin, and somatostatin. In conclusion, some endocrine cells localization and distribution and histomorphometry, and goblet cell counts were revealed in the gastrointestinal tract of the sparrowhawks.

RESUMEN: El objetivo del presente estudio fue determinar la localización y distribución de células enteroendocrinas en el tracto gastrointestinal de gavilán, a través de métodos inmunohistoquímicos y comprender la estructura de las glicoproteínas elaboradas por el epitelio de las regiones del tracto digestivo. Se sacrificaron nueve gavilanes y los tejidos del tracto gastrointestinal se extrajeron y se fijaron en formalina. Las secciones del tracto gastrointestinal se tiñeron con técnicas inmunohistoquímicas e histoquímicas para evaluar las células enteroendocrinas y se realizó análisis histo-morfométrico. Los re- sultados indicaron que los números de inmunopositividad de somatostatina en el ventrículo, gastrina en el proventrículo, serotonina en el duodeno y yeyuno son más altos, en los segmentos restantes del tracto gastrointestinal, se detecta además una ligera positividad de glucagón, gastrina, serotonina y somatostatina. En conclusión en el tracto gastrointestinal de gavilán se observó cierta localización y distribución de células endocrinas e histomorfometría, y recuentos de células caliciformes.

An Expression Levels Analysis of the Bitter Taste Receptors in the Murine Exocrine Glands

Recent findings indicate that Type 2 taste receptors (T2Rs) are expressed outside the gustatory system, including in the gastrointestinal tracts and the exocrine glands, such as the submandibular (SM), parotid (P), lacrimal (L) glands and pancreas (PC). Specifically, T2Rs are found in some of the gastrointestinal endocrine cells, and these cells secreted peptide hormones in response to stimulation by bitter-tasting compounds. The results show that T2Rs may have significant physiological roles besides bitter taste reception. The functions of the T2Rs in the exocrine glands remain poorly understood. An expression levels analysis of T2Rs will help to determine those functions in the exocrine glands. The expression levels of the T2Rs in the exocrine glands were discovered via the qPCR. C57BL/6J mice of 42~60-day-old were used. Messenger RNAs were extracted from S, P, L and PC. Cloned DNAs were synthesized by reverse transcription. Quantitative PCRs were performed using the SYBR Green method. The expression levels of the T2Rs were calculated as relative expression levels to that of the GAPDH. The statistical significance among the observed exocrine glands was tested using the variance analysis (ANOVA test). Tas2r108, out of murine 35 T2Rs, was the most highly expressed in every observed exocrine gland. This finding was similar to previous results from tongue papillae, but the expression levels were lower than those of the tongue papillae. Tas2r137 of SM, P, L and PC were expressed a little lower than that of tongue papillae. The T2Rs in the exocrine glands may play slightly different roles from those in the tongue. We suggest that physiological studies such as a patch clamp and functional Ca²⁺ imaging of acinar cells are necessary for understanding the Tas2r108 functions.

Crosstalk between FXR and TGR5 controls glucagon-like peptide 1 secretion to maintain glycemic homeostasis / 한국실험동물학회지

Though bile acids have been well known as digestive juice, recent studies have demonstrated that bile acids bind to their endogenous receptors, including Farnesoid X receptor (FXR) and G protein-coupled bile acid receptor 1 (GPBAR1; TGR5) and serve as hormone to control various biological processes, including cholesterol/bile acid metabolism, glucose/lipid metabolism, immune responses, and energy metabolism. Deficiency of those bile acid receptors has been reported to induce diverse metabolic syndromes such as obesity, hyperlipidemia, hyperglycemia, and insulin resistance. As consistent, numerous studies have reported alteration of bile acid signaling pathways in type II diabetes patients. Interestingly, bile acids have shown to activate TGR5 in intestinal L cells and enhance secretion of glucagon-like peptide 1 (GLP-1) to potentiate insulin secretion in response to glucose. Moreover, FXR has been shown to crosstalk with TGR5 to control GLP-1 secretion. Altogether, bile acid receptors, FXR and TGR5 are potent therapeutic targets for the treatment of metabolic diseases, including type II diabetes.

YH18968, a Novel 1,2,4-Triazolone G-Protein Coupled Receptor 119 Agonist for the Treatment of Type 2 Diabetes Mellitus

G protein-coupled receptor 119 (GPR119) is expressed in the pancreas and gastrointestinal tract, and its activation promotes insulin secretion in the beta cells of the pancreatic islets as well as the secretion of glucagon-like peptide-1 (GLP-1) in intestinal L cells, consequently improving glucose-stimulated insulin secretion. Due to this dual mechanism of action, the development of small-molecule GPR119 agonists has received significant interest for the treatment of type 2 diabetes. We newly synthesized 1,2,4-triazolone derivatives of GPR119 agonists, which demonstrated excellent outcomes in a cyclic adenosine monophosphate (cAMP) assay. Among the synthesized derivatives, YH18968 showed cAMP=2.8 nM; in GLUTag cell, GLP-1secretion=2.3 fold; in the HIT-T15 cell, and insulin secretion=1.9 fold. Single oral administration of YH18968 improved glucose tolerance and combined treatment with a dipeptidyl peptidase 4 (DPP-4) inhibitor augmented the glucose lowering effect as well as the plasma level of active GLP-1 in normal mice. Single oral administration of YH18968 improved glucose tolerance in a diet induced obese mice model. This effect was maintained after repeated dosing for 4 weeks. The results indicate that YH18968 combined with a DPP-4 inhibitor may be an effective therapeutic candidate for the treatment of type 2 diabetes.

In Vivo Models for Incretin Research: From the Intestine to the Whole Body

Incretin hormones are produced by enteroendocrine cells (EECs) in the intestine in response to ingested nutrient stimuli. The incretin effect is defined as the difference in the insulin secretory response between the oral glucose tolerance test and an isoglycemic intravenous glucose infusion study. The pathophysiology of the decreased incretin effect has been studied as decreased incretin sensitivity and/or β-cell dysfunction per se. Interestingly, robust increases in endogenous incretin secretion have been observed in many types of metabolic/bariatric surgery. Therefore, metabolic/bariatric surgery has been extensively studied for incretin physiology, not only the hormones themselves but also alterations in EECs distribution and genetic expression levels of gut hormones. These efforts have given us an enormous understanding of incretin biology from synthesis to in vivo behavior. Further innovative studies are needed to determine the mechanisms and targets of incretin hormones.

Extrapancreatic Effect of Glucagon like Peptide-1 / 대한내과학회지

Glucagon like peptide-1 (GLP-1) is an intestinal L cell derived incretin hormone which stimulates insulin secretion of beta cell and inhibits glucagon secretion of alpha cell of pancreatic islets. GLP-1 receptors are located in pancreas as well as in a wide variety of tissue such as gastrointestinal tract, heart, blood vessel, lung, brain, kidney, and bone. Therefore GLP-1 and GLP-1 based treatment have multiple extrapancreatic effects which are inhibition of gastrointestinal motility, reduction of appetite, weight loss, increase of cardiac output, cardiovascular protection, neuroprotection, renoprotection, and increase of bone mineral density. Recently, besides GLP-1 receptor dependent pathway, GLP-1 receptor independent pathway has been identified in the extrapancreatic effect of GLP-1 in liver, adipose tissue, muscle, cardiovascular system. This review provides an overview of the pleiotropic effect of GLP-1 in the extrapancreatic organ through review of animal and clinical research.

Naringenin stimulates cholecystokinin secretion in STC-1 cells

BACKGROUND/OBJECTIVES: Cholecystokinin (CCK), a hormone or neuropeptide, is secreted in response to intraluminal nutrients by enteroendocrine I-cells of the intestine and has important physiological actions related to appetite regulation and satiety. The stimulation on CCK secretion from the intestine is of potential relevance for body weight management. Naringenin (4',5,7-trihydroxyflavanone) and its glycoside naringin (naringenin 7-rhamnoglucoside) have been reported to have many biological functions. In the current study, we investigated the question of whether naringenin and naringin could stimulate CCK secretion and then examined the mechanisms involved in CCK release. MATERIALS/METHODS: STC-1 cells were used as a model of enteroendocrine cells. CCK release and changes in intracellular Ca2+ ([Ca2+]i) were measured after incubation of cells with naringenin and naringin for 1 h. RESULTS: Naringenin caused significant (P < 0.05) stimulation of CCK secretion, but naringin did not. In addition, regarding the secretory mechanisms, naringenin-induced CCK secretion involved increases in [Ca2+]i, influx of extracellular Ca2+, at least in part, and activation of TRP channels, including TRPA1. CONCLUSION: Findings of this study suggest that naringenin could have a role in appetite regulation and satiety.

Descrubrimientos sobre reprogramación nuclear merecen el premio Nobel en 2012 / Discoveries on nuclear reprogramming deserves the Nobel prize in 2012

Este artículo fue escrito para honrar a J.B Gurdon y S. Yamanaka, laureados con el Premio Nobel en Fisiología p Medicina 2012 "por el descubrimiento de que las células maduras pueden ser reprogramadas para volverse pluripotentes". Se presentan en forma concisa sus aportes científicos y reseñas biográficas. J.B. Gardon, en Inglaterra, demostró hace 50 años en anfibios que al trasplantar el núcleo de una célula intestinal a un huevo u ovocito enuncleado se obtiene una célula totipotente que se convierte en un embrión y se desarrolla hasta convertirse en una rana adulta, lo cual implica la conservación de genoma en el proceso de diferenciación y la resersibilidad de dicho proceso. Estos descubrimientos llevaron a que otros autores realizaran la clonación de mamiferos utilizando el núcleo de células somáticas y la obtención de células madre pluripotentes a partir de los embrines que se producen in vitro por el desarrollo de las células totipotentes. Se mencionan varias aplicaciones y las contribuciones de Gurdon para comprender el proceso de reprogramación. S. Yamanaka, en Japón, hace seis años, reprogramó al estado embrionario fibroblastos cutáneos de ratones y humanos adultos insertando mediante vectores retrovirales una combinación de los genes de cuatro factores de transcripción: Oct3/4, Sox2, Klf4 y c-Myc. Las células reprogramadas fueron denominadas células madre pluripotentes inducidas. Utilizando la técnica desarrollada por Yamanaka y otras surgidas a raiz de sus descrubrimientos, miles de personas obtienen ahora células madre pluripotentes inducidas a partir de muchas especies y tejidos, incluyendo seres humanos sanos y enfermos. Las células madre pluripotentes o sus derivadas tienen un amplio potencial de aplicación, entre ellas, estudios de embriología y fisiopatología, modelos de enfermedades, descubrimiento de drogas y terapias celulares

This paper was written to honor J.B Gurdon y S. Yamanaka, 2012 Nobel Prize laureates in Physiology or Medicine for "the discovery that mature cells can be reprogrammed to become pluripotent". Their main scientific contributions and biography are presented in a concise manner. JB Gurdon, in England, showed fifty years ago in amphibians that the transplantation of the nucleus of an intestinal cell to an enucleated egg or oocyte produces a totipotent cell that develops into an embryo and adult frog. This implies that cellular differentiation is reversible and the genome is conserved in that process. The discoveries led to the cloning of mammals by other authors using the nucleus of somatic cells and to obtain pluripotent stem cells in vitro from the embryos produced by development of the totipotent cells. Some applications are considered. Gurdon's contribution to the understanding of the reprogramming process is mentioned. S. Yamanaka six years ago in Japan reprogrammed skin fibroblastis from adult mice and humans to the embryonic state by introducing via retroviral vectors a combination of the genes of 4 transcription factors, Oct3/4. Sox2, Klf4 and c-Myc. The reprogammed cells were named induced pluripontent stem cells. Throusands of people are now producing induced pluripotent stem cells from many tissues and species, including healthy and ill humans, using Yamanaka's methods and other techniques stimulated by his work. Pluripotent stem cells or their derivatives have great potential for a wide range of applications including research in embryology and pathophysiology, disease modeling, drug discovery and cell transplantation therapies

Argyrophil cell density in the oxyntic mucosa is higher in female than in male morbidly obese patients

Obesity is a multifactorial disorder often associated with many important diseases such as diabetes, hypertension and other metabolic syndrome conditions. Argyrophil cells represent almost the total population of endocrine cells of the human gastric mucosa and some reports have described changes of specific types of these cells in patients with obesity and metabolic syndrome. The present study was designed to evaluate the global population of argyrophil cells of the gastric mucosa of morbidly obese and dyspeptic non-obese patients. Gastric biopsies of antropyloric and oxyntic mucosa were obtained from 50 morbidly obese patients (BMI >40) and 50 non-obese patients (17 dyspeptic overweight and 33 lean individuals) and processed for histology and Grimelius staining for argyrophil cell demonstration. Argyrophil cell density in the oxyntic mucosa of morbidly obese patients was higher in female (238.68 ± 83.71 cells/mm2) than in male patients (179.31 ± 85.96 cells/mm2) and also higher in female (214.20 ± 50.38 cells/mm2) than in male (141.90 ± 61.22 cells/mm2) morbidly obese patients with metabolic syndrome (P = 0.01 and P = 0.02, respectively). In antropyloric mucosa, the main difference in argyrophil cell density was observed between female morbidly obese patients with (167.00 ± 69.30 cells/mm2) and without (234.00 ± 69.54 cells/mm2) metabolic syndrome (P = 0.001). In conclusion, the present results show that the number of gastric argyrophil cells could be under gender influence in patients with morbid obesity. In addition, gastric argyrophil cells seem to behave differently among female morbidly obese patients with and without metabolic syndrome.

Hesperetin Stimulates Cholecystokinin Secretion in Enteroendocrine STC-1 Cells

Hesperetin (3',5,7-trihydroxy 4'-methoxyflavanone) and its glycoside hesperidin (hesperetin 7-rhamnoglucoside) in oranges have been reported to possess pharmacological effects related to anti-obesity. However, hesperetin and hesperidin have not been studied on suppressive effects on appetite. This study examined that hesperetin and hesperidin can stimulate the release of cholecystokinin (CCK), one of appetite-regulating hormones, from the enteroendocrine STC-1 cells, and then examined the mechanisms involved in the CCK release. Hesperetin significantly and dose-dependently stimulated CCK secretion with an EC50 of 0.050 mM and increased the intracellular Ca2+ concentrations ([Ca2+]i) compared to the untreated control. The stimulatory effect by hesperetin was mediated via the entry of extracellular Ca2+ and the activation of TRP channels including TRPA1. These results suggest that hesperetin can be a candidate biomolecule for the suppression of appetite and eventually for the therapeutics of obesity.

Gastric stem cells and gastric cancer stem cells / 대한해부학회지

The gastric epithelium is continuously regenerated by gastric stem cells, which give rise to various kinds of daughter cells, including parietal cells, chief cells, surface mucous cells, mucous neck cells, and enteroendocrine cells. The self-renewal and differentiation of gastric stem cells need delicate regulation to maintain the normal physiology of the stomach. Recently, it was hypothesized that cancer stem cells drive the cancer growth and metastasis. In contrast to conventional clonal evolution hypothesis, only cancer stem cells can initiate tumor formation, self-renew, and differentiate into various kinds of daughter cells. Because gastric cancer can originate from gastric stem cells and their self-renewal mechanism can be used by gastric cancer stem cells, we review here how critical signaling pathways, including hedgehog, Wnt, Notch, epidermal growth factor, and bone morphogenetic protein signaling, may regulate the self-renewal and differentiation of gastric stem cells and gastric cancer stem cells. In addition, the precancerous change of the gastric epithelium and the status of isolating gastric cancer stem cells from patients are reviewed.

Pleiotropic Effects of an Incretin Hormone / 임상당뇨병

The incretin hormones glucagon like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) have recently received much attention for their roles in type 2 diabetes therapy. GLP-1 stimulated insulin secretion in a glucose-dependent manner and is secreted by intestinal L cells. It also regulates blood glucose concentration, stomach motility, appetite, and body weight. These actions are mediated through G-protein-coupled receptors highly expressed on pancreatic beta cells and also exert indirect metabolic actions. Activation of GLP-1 receptors also produces nonglycemic effects in various tissues. The pleiotropic effects of GLP-1 have been recently reported. The mechanisms identified in preclinical studies have potential translational relevance for the treatment of disease. Here, the nonglycemic effects of GLP-1, especially those on the liver, central nervous system, and bone, were reviewed.

Yin and Yang: the Gastric X/A-like Cell as Possible Dual Regulator of Food Intake

Ingestion of food affects secretion of hormones from enteroendocrine cells located in the gastrointestinal mucosa. These hormones are involved in the regulation of various gastrointestinal functions including the control of food intake. One cell in the stomach, the X/A-like has received much attention over the past years due to the production of ghrelin. Until now, ghrelin is the only known orexigenic hormone that is peripherally produced and centrally acting to stimulate food intake. Subsequently, additional peptide products of this cell have been described including desacyl ghrelin, obestatin and nesfatin-1. Desacyl ghrelin seems to be involved in the regulation of food intake as well and could play a counter-balancing role of ghrelin's orexigenic effect. In contrast, the initially proposed anorexigenic action of obestatin did not hold true and therefore the involvement of this peptide in the regulation of feeding is questionable. Lastly, the identification of nesfatin-1 in the same cell in different vesicles than ghrelin extended the function of this cell type to the inhibition of feeding. Therefore, this X/A-like cell could play a unique role by encompassing yin and yang properties to mediate not only hunger but also satiety.

The Role of the Sweet Taste Receptor in Enteroendocrine Cells and Pancreatic beta-Cells

The sweet taste receptor is expressed in taste cells located in taste buds of the tongue. This receptor senses sweet substances in the oral cavity, activates taste cells, and transmits the taste signals to adjacent neurons. The sweet taste receptor is a heterodimer of two G protein-coupled receptors, T1R2 and T1R3. Recent studies have shown that this receptor is also expressed in the extragustatory system, including the gastrointestinal tract, pancreatic beta-cells, and glucose-responsive neurons in the brain. In the intestine, the sweet taste receptor regulates secretion of incretin hormones and glucose uptake from the lumen. In beta-cells, activation of the sweet taste receptor leads to stimulation of insulin secretion. Collectively, the sweet taste receptor plays an important role in recognition and metabolism of energy sources in the body.

Insulin is secreted upon glucose stimulation by both gastrointestinal enteroendocrine K-cells and L-cells engineered with the preproinsulin gene

Transgenic mice carrying the human insulin gene driven by the K-cell glucose-dependent insulinotropic peptide (GIP) promoter secrete insulin and display normal glucose tolerance tests after their pancreatic p-cells have been destroyed. Establishing the existence of other types of cells that can process and secrete transgenic insulin would help the development of new gene therapy strategies to treat patients with diabetes mellitus. It is noted that in addition to GIP secreting K-cells, the glucagon-like peptide 1 (GLP-1) generating L-cells share/ many similarities to pancreatic p-cells, including the peptidases required for proinsulin processing, hormone storage and a glucose-stimulated hormone secretion mechanism. In the present study, we demonstrate that not only K-cells, but also L-cells engineered with the human preproinsulin gene are able to synthesize, store and, upon glucose stimulation, release mature insulin. When the mouse enteroendocrine STC-1 cell line was transfected with the human preproinsulin gene, driven either by the K-cell specific GIP promoter or by the constitutive cytomegalovirus (CMV) promoter, human insulin co-localizes in vesicles that contain GIP (GIP or CMV promoter) or GLP-1 (CMV promoter). Exposure to glucose of engineered STC-1 cells led to a marked insulin secretion, which was 7-fold greater when the insulin gene was driven by the CMV promoter (expressed both in K-cells and L-cells) than when it was driven by the GIP promoter (expressed only in K-cells). Thus, besides pancreatic p-cells, both gastrointestinal enteroendocrine K-cells and L-cells can be selected as the target cell in a gene therapy strategy to treat patients with type 1 diabetes mellitus.

Irritable Bowel Syndrome in Inflammatory Bowel Disease

Clinicians are frequently challenged to interpret gastrointestinal symptoms in patients with inflammatory disease (IBD). Irritable bowel syndrome (IBS)-like symptoms are common in patients with IBD and the underlying mechanism is likely to be active or occult inflammation of the bowel rather than co-existing IBS. Biopsychosocial construct and mucosal inflammation, stress, alteration of the hypothalamic-pituitary-adrenal axis, and autonomic dysregulation are contributing factors to IBD-IBS. In particular, low-grade inflammation and immune activation are recent topics regarding the underlying mechanism. Some authors have claimed that inflammation could be a common pathophysiologic factor, in which IBS and IBD might represent the two ends of a wide spectrum of chronic inflammatory conditions. Mast cells, enteroendocrine cells, T cells, and B cells are main effector cells in immune responses. Differentiating IBS symptoms from exacerbation of IBD is important, thus preventing the use of excessive IBD medications, with the potential side effects, or narcotics. Medical treatments with anti-diarrheals, anti-spasmodics, anti-depressants, and anxiolytics can be helpful. However, abuse can lead to medication-dependency and bring about side effects. A healthy, balanced lifestyle, including diet and exercise, should be endorsed.

Stimulation of Glucagon Like Peptide-1 Secretion in Enteroendocrine L cells / 당뇨병

GLP-1 (glucagon like peptide-1) is new anti-diabetic drug with a number of beneficial effects. It stimulates glucose dependant insulin secretion and restoration of beta cell mass through enhancement of islet mass. However, it is easily inactivated after being secreted from enteroendocrine L cells. Recent trial to increased GLP-1 is to directly stimulate L cells through its receptor located in the surface of L cell. Taste receptor in the apical surface of L cell is activated by various tastants contained in the food. Tongue perceives taste sense through the heterotrimeric G-protein (alpha-gustducin) and its downstream signaling cascades. Same taste receptors are also expressed in enteroendocrine cells. In duodenal L cell, alpha-gustducin was detected by immunofluorescence stainig at the luminal projections of enteroendocrine cells. And several other taste signaling elements were also found in L cells. Ingestion of sweet or bitter compounds revealed stimulation of GLP-1 secretion and the regulation of plasma insulin and glucose. In this review, I will briefly introduce the possibilities to stimulate GLP-1 secretion though the membrane receptor in enteroendocrine cell. And it will be the good candidate to develop the treatment modality for obesity, diabetes and abnormal gut motility.

Transdifferentiation of Enteroendocrine K-cells into Insulin-expressing Cells / 당뇨병

BACKGROUND: Despite a recent breakthough in human islet transplantation for treating type 1 diabetes mellitus, the limited availability of donor pancreases remains a major obstacle. Endocrine cells within the gut epithelium (enteroendocrine cells) and pancreatic beta cells share similar pathways of differentiation during embryonic development. In particular, K-cells that secrete glucose-dependent insulinotropic polypeptide (GIP) have been shown to express many of the key proteins found in beta cells. Therefore, we hypothesize that K-cells can be transdifferentiated into beta cells because both cells have remarkable similarities in their embryonic development and cellular phenotypes. METHODS: K-cells were purified from heterogeneous STC-1 cells originating from an endocrine tumor of a mouse intestine. In addition, a K-cell subclone expressing stable Nkx6.1, called "Kn4-cells," was successfully obtained. In vitro differentiation of K-cells or Kn4-cells into beta cells was completed after exendin-4 treatment and serum deprivation. The expressions of insulin mRNA and protein were examined by RT-PCR and immunocytochemistry. The interacellular insulin content was also measured. RESULTS: K-cells were found to express glucokinase and GIP as assessed by RT-PCR and Western blot analysis. RT-PCR showed that K-cells also expressed Pdx-1, NeuroD1/Beta2, and MafA, but not Nkx6.1. After exendin-4 treatment and serum deprivation, insulin mRNA and insulin or C-peptide were clearly detected in Kn4-cells. The intracellular insulin content was also increased significantly in these cells. CONCLUSION: K-cells are an attractive potential source of insulin-producing cells for treatment of type 1 diabetes mellitus. However, more experiments are necessary to optimize a strategy for converting K-cells into beta cells.

Immunocytochemical study of gastrintestinal endocrine cells in insectivorous bats (Mammalia: Chiroptera) / Estudo imunocitoquímico das células endócrinas gastrintestinais de morcegos insetívoros (Mammalia: Chiroptera)

The regional distribution and relative frequency of endocrine cells in the stomach and intestine of Phyllostomidae: Lonchorhina aurita and Molossidae: Molossus molossus bats were studied immunohistochemically. Three types of immunoreactive (IR) endocrine cells - to serotonin (5-HT), gastrin (GAS) and enteroglucagon (GLUC) - were found in the gastric mucosa and four types of IR cells were identified in the intestinal mucosa. This study showed an interespecfic difference in the regional distribution and relative frequency of endocrine cells in the Chiropteran alimentary tract.

A distribuição regional e a freqüência relativa das células endócrinas no estômago e intestino dos morcegos insetívoros Phyllostomidae: Lonchorhina aurita e Mormoopidae: Molossus molossus foram estudadas pelo método de imunohistoquímica. Três tipos de células endócrinas imunorreativas (IR) à serotonina (5-HT), gastrina (GAS) e enteroglucagon (GLUC) foram localizadas na mucosa gástrica e quatro tipos de células endócrinas IR à 5-HT, GAS, colecistoquinina (CCK) e GLUC foram identificadas na mucosa intestinal. Este estudo mostrou uma diferença interespecífica na distribuição regional e na freqüência relativa das células endócrinas no trato alimentar de Chiropteros.

Decrease in intestinal endocrine cells in Balb/c mice with CT-26 carcinoma cells

The density of intestinal endocrine cells, in Balb/c mice with colon 26 (CT-26) carcinoma cells, were examined immunohistochemically at 28 days after implantation. After CT-26 cell administration there was a significant decrease in most of the intestinal endocrine cells (p < 0.01) compared with the control group. The significant quantitative changes in the intestinal endocrine cell density might contribute to the development of the gastrointestinal symptoms commonly encountered in cancer patients.