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[PMID]:28938466
[Au] Autor:Chimerel C; Riccio C; Murison K; Gribble FM; Reimann F
[Ad] Endereço:Metabolic Research Laboratories and Medical Research Council (MRC) Metabolic Diseases Unit, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Hospital, University of Cambridge, Cambridge CB2 0QQ, United Kingdom.
[Ti] Título:Optogenetic Analysis of Depolarization-Dependent Glucagonlike Peptide-1 Release.
[So] Source:Endocrinology;158(10):3426-3434, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Incretin hormones play an important role in the regulation of food intake and glucose homeostasis. Glucagonlike peptide-1 (GLP-1)-secreting cells have been demonstrated to be electrically excitable and to fire action potentials (APs) with increased frequency in response to nutrient exposure. However, nutrients can also be metabolized or activate G-protein-coupled receptors, thus potentially stimulating GLP-1 secretion independent of their effects on the plasma membrane potential. Here we used channelrhodopsins to manipulate the membrane potential of GLUTag cells, a well-established model of GLP-1-secreting enteroendocrine L cells. Using channelrhodopsins with fast or slow on/off kinetics (CheTA and SSFO, respectively), we found that trains of light pulses could trigger APs and calcium elevation in GLUTag cells stably expressing either CheTA or SSFO. Tetrodotoxin reduced light-triggered AP frequency but did not impair calcium responses, whereas further addition of the calcium-channel blockers nifedipine and ω-conotoxin GVIA abolished both APs and calcium transients. Light pulse trains did not trigger GLP-1 secretion from CheTA-expressing cells under basal conditions but were an effective stimulus when cyclic adenosine monophosphate (cAMP) concentrations were elevated by forskolin plus 3-isobutyl 1-methylxanthine. In SSFO-expressing cells, light-stimulated GLP-1 release was observed at resting and elevated cAMP concentrations and was blocked by nifedipine plus ω-conotoxin GVIA but not tetrodotoxin. We conclude that cAMP elevation or cumulative membrane depolarization triggered by SSFO enhances the efficiency of light-triggered action potential firing, voltage-gated calcium entry, and GLP-1 secretion.
[Mh] Termos MeSH primário: Potenciais de Ação/efeitos dos fármacos
Bloqueadores dos Canais de Cálcio/farmacologia
Células Enteroendócrinas/efeitos dos fármacos
Peptídeo 1 Semelhante ao Glucagon/efeitos dos fármacos
Potenciais da Membrana/efeitos dos fármacos
[Mh] Termos MeSH secundário: 1-Metil-3-Isobutilxantina/farmacologia
Animais
Cálcio/metabolismo
Colforsina/farmacologia
Células Enteroendócrinas/metabolismo
Células Enteroendócrinas/secreção
Peptídeo 1 Semelhante ao Glucagon/secreção
Camundongos
Nifedipino/farmacologia
Optogenética
Técnicas de Patch-Clamp
Inibidores de Fosfodiesterase/farmacologia
Rodopsina
Bloqueadores dos Canais de Sódio/farmacologia
Tetrodotoxina/farmacologia
Vasodilatadores/farmacologia
ômega-Conotoxina GVIA/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 0 (Phosphodiesterase Inhibitors); 0 (Sodium Channel Blockers); 0 (Vasodilator Agents); 1F7A44V6OU (Colforsin); 4368-28-9 (Tetrodotoxin); 89750-14-1 (Glucagon-Like Peptide 1); 9009-81-8 (Rhodopsin); 92078-76-7 (omega-Conotoxin GVIA); I9ZF7L6G2L (Nifedipine); SY7Q814VUP (Calcium); TBT296U68M (1-Methyl-3-isobutylxanthine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00434


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[PMID]:28781254
[Au] Autor:Gnatenko DA; Kopantzev EP; Sverdlov ED
[Ad] Endereço:Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences.
[Ti] Título:[Fibroblast growth factors and their effects in pancreas organogenesis].
[Ti] Título:Vliianie faktorov rosta fibroblastov na organogenez podzheludochnoi zhelezy..
[So] Source:Biomed Khim;63(3):211-218, 2017 May.
[Is] ISSN:2310-6972
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Fibroblast growth factors (FGF) - growth factors that regulate many important biological processes, including proliferation and differentiation of embryonic cells during organogenesis. In this review, we will summarize current information about the involvement of FGFs in the pancreas organogenesis. Pancreas organogenesis is a complex process, which involves constant signaling from mesenchymal tissue. This orchestrates the activation of various regulator genes at specific stages, determining the specification of progenitor cells. Alterations in FGF/FGFR signaling pathway during this process lead to incorrect activation of the master genes, which leads to different pathologies during pancreas development. Understanding the full picture about role of FGF factors in pancreas development will make it possible to more accurately understand their role in other pathologies of this organ, including carcinogenesis.
[Mh] Termos MeSH primário: Células Enteroendócrinas/metabolismo
Fatores de Crescimento de Fibroblastos/genética
Regulação da Expressão Gênica no Desenvolvimento
Organogênese/genética
Pâncreas/metabolismo
Receptor Tipo 1 de Fator de Crescimento de Fibroblastos/genética
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Linhagem da Célula/genética
Células Enteroendócrinas/citologia
Fatores de Crescimento de Fibroblastos/classificação
Fatores de Crescimento de Fibroblastos/metabolismo
Proteínas de Homeodomínio/genética
Proteínas de Homeodomínio/metabolismo
Seres Humanos
Pâncreas/citologia
Pâncreas/crescimento & desenvolvimento
Receptor Tipo 1 de Fator de Crescimento de Fibroblastos/metabolismo
Fatores de Transcrição SOX9/genética
Fatores de Transcrição SOX9/metabolismo
Transdução de Sinais
Transativadores/genética
Transativadores/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Homeodomain Proteins); 0 (SOX9 Transcription Factor); 0 (SOX9 protein, human); 0 (Trans-Activators); 0 (Transcription Factors); 0 (pancreatic and duodenal homeobox 1 protein); 0 (transcription factor PTF1); 62031-54-3 (Fibroblast Growth Factors); EC 2.7.10.1 (FGFR1 protein, human); EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE
[do] DOI:10.18097/PBMC20176303211


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[PMID]:28751238
[Au] Autor:Hartenstein V; Takashima S; Hartenstein P; Asanad S; Asanad K
[Ad] Endereço:Department of Molecular Cell and Developmental Biology, University of California Los Angeles, Los Angeles, CA 90095-1606, USA. Electronic address: volkerh@mcdb.ucla.edu.
[Ti] Título:bHLH proneural genes as cell fate determinants of entero-endocrine cells, an evolutionarily conserved lineage sharing a common root with sensory neurons.
[So] Source:Dev Biol;431(1):36-47, 2017 11 01.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Entero-endocrine cells involved in the regulation of digestive function form a large and diverse cell population within the intestinal epithelium of all animals. Together with absorptive enterocytes and secretory gland cells, entero-endocrine cells are generated by the embryonic endoderm and, in the mature animal, from a pool of endoderm derived, self-renewing stem cells. Entero-endocrine cells share many structural/functional and developmental properties with sensory neurons, which hints at the possibility of an ancient evolutionary relationship between these two cell types. We will survey in this article recent findings that emphasize the similarities between entero-endocrine cells and sensory neurons in vertebrates and insects, for which a substantial volume of data pertaining to the entero-endocrine system has been compiled. We will then report new findings that shed light on the specification and morphogenesis of entero-endocrine cells in Drosophila. In this system, presumptive intestinal stem cells (pISCs), generated during early metamorphosis, undergo several rounds of mitosis that produce the endocrine cells and stem cells (ISCs) with which the fly is born. Clonal analysis demonstrated that individual pISCs can give rise to endocrine cells expressing different types of peptides. Immature endocrine cells start out as unpolarized cells located basally of the gut epithelium; they each extend an apical process into the epithelium which establishes a junctional complex and apical membrane specializations contacting the lumen of the gut. Finally, we show that the Drosophila homolog of ngn3, a bHLH gene that defines the entero-endocrine lineage in mammals, is expressed and required for the differentiation of this cell type in the fly gut.
[Mh] Termos MeSH primário: Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Evolução Biológica
Células Enteroendócrinas/citologia
Células Enteroendócrinas/metabolismo
Células Receptoras Sensoriais/citologia
Células Receptoras Sensoriais/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem da Célula/genética
Proteínas de Drosophila/genética
Drosophila melanogaster/citologia
Drosophila melanogaster/genética
Drosophila melanogaster/crescimento & desenvolvimento
Evolução Molecular
Regulação da Expressão Gênica no Desenvolvimento
Genes de Insetos
Modelos Biológicos
Morfogênese/genética
Neuropeptídeos/genética
Fatores de Transcrição/genética
Vertebrados/anatomia & histologia
Vertebrados/genética
Vertebrados/crescimento & desenvolvimento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Drosophila Proteins); 0 (Neuropeptides); 0 (Transcription Factors); 0 (target of Poxn protein, Drosophila)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE


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[PMID]:28737477
[Au] Autor:Mazzawi T; El-Salhy M
[Ad] Endereço:1 Division of Gastroenterology, Department of Clinical Medicine, University of Bergen, Bergen 5021, Norway.
[Ti] Título:Changes in duodenal enteroendocrine cells in patients with irritable bowel syndrome following dietary guidance.
[So] Source:Exp Biol Med (Maywood);242(13):1355-1362, 2017 Jul.
[Is] ISSN:1535-3699
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The densities of enteroendocrine cells are abnormal in patients with irritable bowel syndrome (IBS); however, they tend to change toward normal levels in stomach, ileum, and colon following dietary guidance. The aim was to identify the types of duodenal enteroendocrine cells affected after receiving dietary guidance in the same group of patients with IBS. Fourteen patients with IBS and 14 control subjects were included. The patients received three sessions of dietary guidance. Both groups underwent gastroscopies at baseline, and again for the patients after 3-9 months (median, four months) from receiving dietary guidance. Tissue biopsies were collected from the descending part of the duodenum and were immunostained for all the types of enteroendocrine cells and were then quantified by using computerized image analysis. Using the Kruskal-Wallis non-parametric test with Dunn's test as a post-test, the results showed a significant difference in the secretin cell densities between control subjects and patients with IBS prior to and following dietary guidance ( P = 0.0001 and 0.011, respectively). The corresponding P values for cholecystokinin (CCK) cell densities were 0.03 and 0.42, respectively; gastric inhibitory peptide (GIP) cell densities were 0.06 and 0.43, respectively; serotonin cell densities were <0.0001 and 0.002, respectively; and for somatostatin cell densities were <0.0001 and 0.052, respectively. The Paired t-test showed a significant difference only in the serotonin ( P = 0.03) and somatostatin ( P < 0.0001) cell densities between IBS patients prior to and following dietary guidance. The changes in the cell densities of secretin, CCK, and GIP were not significant between IBS patients prior to and following dietary guidance. In conclusion, the densities of several duodenal enteroendocrine cells in IBS patients changed toward the values measured in control subjects following dietary guidance. The changes in serotonin and somatostatin cell densities may have contributed to the improvements in IBS symptoms, particularly pain and diarrhea. Impact statement Several contributing factors to the symptomology of irritable bowel syndrome (IBS) have been identified, such as abnormal densities of enteroendocrine cells and diet; however, the interactions between these factors have not been studied yet. The current study aims at exploring the dynamic changes between these two factors by studying the effect of using low fermentable oligo-, di-, monosaccharides and polyol (FODMAP) diet (known to improve IBS symptoms) through dietary guidance on the enteroendocrine cell densities in the duodenum. The findings showed that the densities of different enteroendocrine cells in the duodenum were abnormal before the patients received dietary guidance and tend to change/normalize after receiving guidance, which may have contributed in improving the symptoms of IBS. These findings highlight the importance of enteroendocrine cells in IBS pathophysiology and the mechanism behind the positive effect of low FODMAP dietary guidance in improving IBS symptoms and its usage as first step in the line of IBS management.
[Mh] Termos MeSH primário: Dietoterapia/métodos
Duodeno/patologia
Células Enteroendócrinas/citologia
Síndrome do Intestino Irritável/terapia
[Mh] Termos MeSH secundário: Biópsia
Gastroscopia
Seres Humanos
Processamento de Imagem Assistida por Computador
Imuno-Histoquímica
Microscopia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170725
[St] Status:MEDLINE
[do] DOI:10.1177/1535370217699537


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[PMID]:28666112
[Au] Autor:Beumer J; Clevers H
[Ad] Endereço:Hubrecht Institute, Royal Netherlands Academy of Arts and Sciences (KNAW), Uppsalalaan 8, 3584 CT, Utrecht, the Netherlands; Cancer Genomics Netherlands, UMC Utrecht, 3584 GC, Utrecht, the Netherlands.
[Ti] Título:How the Gut Feels, Smells, and Talks.
[So] Source:Cell;170(1):10-11, 2017 06 29.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gut-brain signaling plays a central role in a range of homeostatic processes, yet details of this cross-talk remain enigmatic. In this issue of Cell, Bellono and colleagues identify a variety of luminal stimuli acting on serotonin-secreting enteroendocrine cells and, for the first time, demonstrate a functional synaptic interaction with neurons.
[Mh] Termos MeSH primário: Células Enteroendócrinas
Serotonina
[Mh] Termos MeSH secundário: Transdução de Sinais
Olfato
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
333DO1RDJY (Serotonin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE


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[PMID]:28665193
[Au] Autor:Romanski KW
[Ad] Endereço:1 Department of Animal Physiology, Faculty of Veterinary Medicine, Wroclaw University of Environmental and Life Sciences , Wroclaw, Poland.
[Ti] Título:Importance of the enteric nervous system in the control of the migrating motility complex.
[So] Source:Physiol Int;104(2):97-129, 2017 Jun 01.
[Is] ISSN:2498-602X
[Cp] País de publicação:Hungary
[La] Idioma:eng
[Ab] Resumo:The migrating motility complex (MMC), a cyclical phenomenon, represents rudimentary motility pattern in the gastrointestinal tract. The MMC is observed mostly in the stomach and gut of man and numerous animal species. It contains three or four phases, while its phase III is the most characteristic. The mechanisms controlling the pattern are unclear in part, although the neural control of the MMC seems crucial. The main goal of this article was to discuss the importance of intrinsic innervation of the gastrointestinal tract in MMC initiation, migration, and cessation to emphasize that various MMC-controlling mechanisms act through the enteric nervous system. Two main neural regions, central and peripheral, are able to initiate the MMC. However, central regulation of the MMC may require cooperation with the enteric nervous system. When central mechanisms are not active, the MMC can be initiated peripherally in any region of the small bowel. The enteric nervous system affects the MMC in response to the luminal stimuli which can contribute to the initiation and cessation of the cycle, and it may evoke irregular phasic contractions within the pattern. The hormonal regulators released from the endocrine cells may exert a modulatory effect upon the MMC mostly through the enteric nervous system. Their central action could also be considered. It can be concluded that the enteric nervous system is involved in the great majority of the MMC-controlling mechanisms.
[Mh] Termos MeSH primário: Sistema Nervoso Entérico/fisiologia
Células Enteroendócrinas/fisiologia
Trânsito Gastrointestinal/fisiologia
Modelos Neurológicos
Músculo Liso/fisiologia
Complexo Mioelétrico Migratório/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Endócrinas
Seres Humanos
Músculo Liso/inervação
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE
[do] DOI:10.1556/2060.104.2017.2.4


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[PMID]:28636167
[Au] Autor:Yue M; Xia Y; Shi C; Guan C; Li Y; Liu R; Wei Z; Dai Y
[Ad] Endereço:Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing, China.
[Ti] Título:Berberine ameliorates collagen-induced arthritis in rats by suppressing Th17 cell responses via inducing cortistatin in the gut.
[So] Source:FEBS J;284(17):2786-2801, 2017 Sep.
[Is] ISSN:1742-4658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Berberine, an isoquinoline alkaloid, has been reported to ameliorate various autoimmune diseases including rheumatoid arthritis by oral administration. However, its mechanism remains mysterious due to an extremely low bioavailability. The fact that berberine readily accumulates in the gut, the largest endocrine organ in the body, attracted us to explore its anti-arthritic mechanism in view of the induction of intestinal immunosuppressive neuropeptides. In this study, berberine (200 mg·kg , i.g.) was shown to ameliorate collagen-induced arthritis in rats, which was manifested by the reduction of clinical signs and joint destruction, as well as marked down-regulation of Th17 cell frequency and interleukin-17 level in blood. In contrast, an intravenous injection of berberine failed to affect arthritis in rats, implying that its anti-arthritic effect was gut-dependent. Further studies revealed that oral berberine selectively elevated the levels of cortistatin, of five gut-derived neuropeptides tested, in the intestines and sera of arthrititic rats. Antagonists of ghrelin/growth hormone secretagogue receptor 1 (a subtype of cortistatin receptor) almost completely abolished the ameliorative effect of berberine on arthritis and Th17 cell responses in rats. In vitro, berberine showed a moderate ability to promote the expression of cortistatin in nerve cells, which was strengthened when the nerve cells were cocultured with enteroendocrine cells to induce an autocrine/paracrine environment. In summary, oral berberine exerted anti-arthritic effect through inhibiting the Th17 cell response, which was closely associated with the induction of cortistatin generation from gut through augmenting autocrine/paracrine action between enteric nerve cells and endocrine cells.
[Mh] Termos MeSH primário: Antirreumáticos/farmacologia
Artrite Experimental/tratamento farmacológico
Berberina/farmacologia
Imunossupressores/farmacologia
Neuropeptídeos/genética
Células Th17/efeitos dos fármacos
[Mh] Termos MeSH secundário: Administração Oral
Animais
Antirreumáticos/uso terapêutico
Artrite Experimental/imunologia
Artrite Experimental/metabolismo
Comunicação Autócrina
Berberina/uso terapêutico
Avaliação Pré-Clínica de Medicamentos
Sistema Nervoso Entérico/efeitos dos fármacos
Sistema Nervoso Entérico/metabolismo
Células Enteroendócrinas/efeitos dos fármacos
Células Enteroendócrinas/metabolismo
Feminino
Imunossupressores/uso terapêutico
Intestino Delgado/efeitos dos fármacos
Neuropeptídeos/metabolismo
Células PC12
Ratos
Ratos Wistar
Células Th17/metabolismo
Ativação Transcricional/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antirheumatic Agents); 0 (Immunosuppressive Agents); 0 (Neuropeptides); 0 (cortistatin); 0I8Y3P32UF (Berberine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE
[do] DOI:10.1111/febs.14147


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[PMID]:28628110
[Au] Autor:Crespo M; Vilar E; Tsai SY; Chang K; Amin S; Srinivasan T; Zhang T; Pipalia NH; Chen HJ; Witherspoon M; Gordillo M; Xiang JZ; Maxfield FR; Lipkin S; Evans T; Chen S
[Ad] Endereço:Department of Surgery, Weill Cornell Medical College, New York, New York, USA.
[Ti] Título:Colonic organoids derived from human induced pluripotent stem cells for modeling colorectal cancer and drug testing.
[So] Source:Nat Med;23(7):878-884, 2017 Jul.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:With the goal of modeling human disease of the large intestine, we sought to develop an effective protocol for deriving colonic organoids (COs) from differentiated human embryonic stem cells (hESCs) or induced pluripotent stem cells (iPSCs). Extensive gene and immunohistochemical profiling confirmed that the derived COs represent colon rather than small intestine, containing stem cells, transit-amplifying cells, and the expected spectrum of differentiated cells, including goblet and endocrine cells. We applied this strategy to iPSCs derived from patients with familial adenomatous polyposis (FAP-iPSCs) harboring germline mutations in the WNT-signaling-pathway-regulator gene encoding APC, and we generated COs that exhibit enhanced WNT activity and increased epithelial cell proliferation, which we used as a platform for drug testing. Two potential compounds, XAV939 and rapamycin, decreased proliferation in FAP-COs, but also affected cell proliferation in wild-type COs, which thus limits their therapeutic application. By contrast, we found that geneticin, a ribosome-binding antibiotic with translational 'read-through' activity, efficiently targeted abnormal WNT activity and restored normal proliferation specifically in APC-mutant FAP-COs. These studies provide an efficient strategy for deriving human COs, which can be used in disease modeling and drug discovery for colorectal disease.
[Mh] Termos MeSH primário: Adenoma/genética
Polipose Adenomatosa do Colo/genética
Antibióticos Antineoplásicos/farmacologia
Proliferação Celular/efeitos dos fármacos
Colo/efeitos dos fármacos
Neoplasias Colorretais/genética
Células-Tronco Embrionárias Humanas
Organoides/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenoma/patologia
Proteína da Polipose Adenomatosa do Colo/genética
Western Blotting
Diferenciação Celular
Colo/citologia
Colo/metabolismo
Neoplasias Colorretais/patologia
Ensaios de Seleção de Medicamentos Antitumorais
Células Enteroendócrinas/citologia
Citometria de Fluxo
Imunofluorescência
Perfilação da Expressão Gênica
Gentamicinas/farmacologia
Mutação em Linhagem Germinativa
Células Caliciformes/citologia
Compostos Heterocíclicos com 3 Anéis/farmacologia
Seres Humanos
Imuno-Histoquímica
Células-Tronco Pluripotentes Induzidas
Microscopia Confocal
Mutação
Organoides/citologia
Organoides/metabolismo
Organoides/patologia
Reação em Cadeia da Polimerase em Tempo Real
Sirolimo/farmacologia
Via de Sinalização Wnt
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (APC protein, human); 0 (Adenomatous Polyposis Coli Protein); 0 (Antibiotics, Antineoplastic); 0 (Gentamicins); 0 (Heterocyclic Compounds, 3-Ring); 0 (XAV939); A08F5XTI6G (antibiotic G 418); W36ZG6FT64 (Sirolimus)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4355


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[PMID]:28596237
[Au] Autor:Wheeler SE; Stacey HM; Nahaei Y; Hale SJ; Hardy AB; Reimann F; Gribble FM; Larraufie P; Gaisano HY; Brubaker PL
[Ad] Endereço:Department of Physiology, University of Toronto, Toronto, Ontario, Canada.
[Ti] Título:The SNARE Protein Syntaxin-1a Plays an Essential Role in Biphasic Exocytosis of the Incretin Hormone Glucagon-Like Peptide 1.
[So] Source:Diabetes;66(9):2327-2338, 2017 Sep.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Exocytosis of the hormone glucagon-like peptide 1 (GLP-1) by the intestinal L cell is essential for the incretin effect after nutrient ingestion and is critical for the actions of dipeptidyl peptidase 4 inhibitors that enhance GLP-1 levels in patients with type 2 diabetes. Two-photon microscopy revealed that exocytosis of GLP-1 is biphasic, with a first peak at 1-6 min and a second peak at 7-12 min after stimulation with forskolin. Approximately 75% of the exocytotic events were represented by compound granule fusion, and the remainder were accounted for by full fusion of single granules under basal and stimulated conditions. The core SNARE protein syntaxin-1a (syn1a) was expressed by murine ileal L cells. At the single L-cell level, first-phase forskolin-induced exocytosis was reduced to basal ( < 0.05) and second-phase exocytosis abolished ( < 0.05) by syn1a knockout. L cells from intestinal-epithelial syn1a-deficient mice demonstrated a 63% reduction in forskolin-induced GLP-1 release in vitro ( < 0.001) and a 23% reduction in oral glucose-stimulated GLP-1 secretion ( < 0.05) in association with impairments in glucose-stimulated insulin release (by 60%; < 0.01) and glucose tolerance (by 20%; < 0.01). The findings identify an exquisite mechanism of metered secretory output that precisely regulates release of the incretin hormone GLP-1 and hence insulin secretion after a meal.
[Mh] Termos MeSH primário: Exocitose/fisiologia
Regulação da Expressão Gênica/fisiologia
Peptídeo 1 Semelhante ao Glucagon/metabolismo
Sintaxina 1/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Diabetes Mellitus Tipo 2/metabolismo
Células Enteroendócrinas/fisiologia
Feminino
Peptídeo 1 Semelhante ao Glucagon/genética
Peptídeo 1 Semelhante ao Glucagon/secreção
Glucose/metabolismo
Íleo/citologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Obesidade/metabolismo
Sintaxina 1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Syntaxin 1); 89750-14-1 (Glucagon-Like Peptide 1); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1403


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[PMID]:28533434
[Au] Autor:Harada K; Kitaguchi T; Kamiya T; Aung KH; Nakamura K; Ohta K; Tsuboi T
[Ad] Endereço:From the Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Tokyo 153-8902, Japan.
[Ti] Título:Lysophosphatidylinositol-induced activation of the cation channel TRPV2 triggers glucagon-like peptide-1 secretion in enteroendocrine L cells.
[So] Source:J Biol Chem;292(26):10855-10864, 2017 Jun 30.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The lysophosphatidylinositol (LPI) has crucial roles in multiple physiological processes, including insulin exocytosis from pancreatic islets. However, the role of LPI in secretion of glucagon-like peptide-1 (GLP-1), a hormone that enhances glucose-induced insulin secretion, is unclear. Here, we used the murine enteroendocrine L cell line GLUTag and primary murine small intestinal cells to elucidate the mechanism of LPI-induced GLP-1 secretion. Exogenous LPI addition increased intracellular Ca concentrations ([Ca ] ) in GLUTag cells and induced GLP-1 secretion from both GLUTag and acutely prepared primary intestinal cells. The [Ca ] increase was suppressed by an antagonist for G protein-coupled receptor 55 (GPR55) and by silencing of GPR55 expression, indicating involvement of G and G signaling pathways in the LPI-induced increased [Ca ] levels and GLP-1 secretion. However, GPR55 agonists did not mimic many of the effects of LPI. We also found that phospholipase C inhibitor and Rho-associated kinase inhibitor suppressed the [Ca ] increase and that LPI increased the number of focal adhesions, indicating actin reorganization. Of note, blockage or silencing of transient receptor potential cation channel subfamily V member 2 (TRPV2) channels suppressed both the LPI-induced [Ca ] increase and GLP-1 secretion. Furthermore, LPI accelerated TRPV2 translocation to the plasma membrane, which was significantly suppressed by a GPR55 antagonist. These findings suggest that TRPV2 activation via actin reorganization induced by G and G signaling is involved in LPI-stimulated GLP-1 secretion in enteroendocrine L cells. Because GPR55 agonists largely failed to mimic the effects of LPI, its actions on L cells are at least partially independent of GPR55 activation.
[Mh] Termos MeSH primário: Canais de Cálcio/metabolismo
Sinalização do Cálcio/fisiologia
Células Enteroendócrinas/metabolismo
Peptídeo 1 Semelhante ao Glucagon/secreção
Lisofosfolipídeos/metabolismo
Canais de Cátion TRPV/metabolismo
[Mh] Termos MeSH secundário: Animais
Canais de Cálcio/genética
Células Cultivadas
Adesões Focais/genética
Adesões Focais/metabolismo
Subunidades alfa de Proteínas de Ligação ao GTP/genética
Subunidades alfa de Proteínas de Ligação ao GTP/metabolismo
Peptídeo 1 Semelhante ao Glucagon/genética
Camundongos
Transporte Proteico/fisiologia
Receptores de Canabinoides/genética
Receptores de Canabinoides/metabolismo
Canais de Cátion TRPV/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels); 0 (GPR55 protein, mouse); 0 (GTP-Binding Protein alpha Subunits); 0 (Lysophospholipids); 0 (Receptors, Cannabinoid); 0 (TRPV Cation Channels); 0 (Trpv2 protein, mouse); 0 (lysophosphatidylinositol); 89750-14-1 (Glucagon-Like Peptide 1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.788653



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