ライフサイエンスコーパス: enteroendocrine

1 l types in the gut wall such as enterocytes, enteroendocrine and immune cells and are therefore emerg

2 e in crypt cell proliferation and numbers of enteroendocrine and Paneth cells, an increase in numbers

3 lumnar cell pool and a decrease in secretory enteroendocrine and Paneth cells.

4 ng pathways in cell lines of cholangiocytic, enteroendocrine, and enterocytic origin.

5 colonies that differentiate into enterocyte, enteroendocrine, and goblet cell lineages.

6 loss of Math1 leads to depletion of goblet, enteroendocrine, and Paneth cells without affecting ente

7 testinal epithelium (enterocytes and goblet, enteroendocrine, and Paneth cells) and are physiological

8 cells suggests that secretory cells (goblet, enteroendocrine, and Paneth cells) arise from a common p

9 multipotent stem cell: enterocytes, goblet, enteroendocrine, and Paneth cells.

10 Here, we show that specification of enteroendocrine but not Paneth cells occurs independentl

11 me transcription factors as their intestinal enteroendocrine cell counterparts.

12 , is both necessary and sufficient for human enteroendocrine cell development in vitro.

13 To understand the molecular basis of enteroendocrine cell development, we have used gene targ

14 g that Arx is required in the progenitor for enteroendocrine cell development.

15 eurogenin 3 stimulated a program of terminal enteroendocrine cell development.

16 Neurogenin 3 is essential for enteroendocrine cell development; however, it is unknown

17 RB has relatively subtle effects on enteroendocrine cell differentiation and is not required

18 f the beta-catenin gene at an early stage of enteroendocrine cell differentiation induced small-intes

19 nin-3 overexpression induced goblet cell and enteroendocrine cell differentiation, respectively, cons

20 cellular and molecular mechanisms governing enteroendocrine cell diversity.

21 ngenital malabsorptive diarrhea secondary to enteroendocrine cell dysgenesis.

22 hat peptide profiles are a stable feature of enteroendocrine cell identity during homeostasis and fol

23 We describe a type of enteroendocrine cell in mouse duodenum that is defined b

24 kinin (CCK) secretion in humans and from the enteroendocrine cell line STC-1 depends critically on ac

25 Using the enteroendocrine cell line STC-1, the aim of this study w

26 Recently, we proposed that the murine enteroendocrine cell line, STC-1, responds to insoluble

27 ne, glucagon-like peptide (GLP-1), using the enteroendocrine cell line, STC-1.

28 eta and kappa casein) and hydrolysates on an enteroendocrine cell line.

29 receptors also was found in STC-1 cells, an enteroendocrine cell line.

30 cose homeostasis through a modulation of the enteroendocrine cell lineage.

31 s role in the development and maintenance of enteroendocrine cell lineages in the mouse duodenum and

32 cellular Ca2+ concentration ([Ca2+]i) in two enteroendocrine cell lines (STC-1 and GLUTag).

33 CK) secretion both in humans and from murine enteroendocrine cell lines.

34 The K cell is a specific sub-type of enteroendocrine cell located in the proximal small intes

35 s in a profound deficit in expression of the enteroendocrine cell markers CCK, secretin and glucagon

36 egatively regulating chromogranin A-positive enteroendocrine cell number.

37 controlling incretin secretion, we analyzed enteroendocrine cell pathways important for hormone bios

38 Nkx2.2 null mice, several hormone-producing enteroendocrine cell populations are absent or reduced a

39 s the differentiation of progressively fewer enteroendocrine cell populations when deleted from Ngn3(

40 examined whether the densities of stem- and enteroendocrine cell progenitors are abnormal in the ile

41 related with abnormalities in stem cells and enteroendocrine cell progenitors.

42 Beta casein significantly stimulated enteroendocrine cell proliferation and all caseins were

43 Although Nkx2.2 regulates enteroendocrine cell specification in the duodenum at al

44 e body, but remarkably little is known about enteroendocrine cell type specification in the embryo an

45 antral stomach and intestine, whereas other enteroendocrine cell types exhibited much lower cell cyc

46 developing endoderm results in a decrease of enteroendocrine cell types including gastrin-, glucagon/

47 continued in a significant fraction of most enteroendocrine cell types throughout fetal and postnata

48 Other enteroendocrine cell types were not ablated.

49 g embryonic development Nkx2.2 regulates all enteroendocrine cell types, except gastrin and preproglu

50 ssociated with reduced expression of PYY, an enteroendocrine cell-derived hormone that normally inhib

51 ed for intestinal secretory (goblet, Paneth, enteroendocrine) cell differentiation.

52 In obese patients, the total number of enteroendocrine cells (EEC) and EECs containing gut horm

53 nin (CCK) and secretin, peptides released by enteroendocrine cells (EECs) in the duodenum/jejunum, wh

54 av1.8-expressing vagal afferents with select enteroendocrine cells (i.e., ghrelin, glucagon, GLP-1).

55 Intestinal enteroendocrine cells (IECs) secrete gut peptides in res

56 However, we recently uncovered in intestinal enteroendocrine cells a cytoplasmic process that we name

57 Here we report a novel function of enteroendocrine cells acting as local regulators of inte

58 are incretins secreted by respective K and L enteroendocrine cells after eating and amplify glucose-s

59 focal immunohistochemistry with serotonin in enteroendocrine cells and also with endothelial nitric o

60 nd unexpected diversity in hormone-secreting enteroendocrine cells and constructed the taxonomy of ne

61 late GLP-1 and GIP secretion from intestinal enteroendocrine cells and increase GSIS from pancreatic

62 t T2R gene expression in both cultured mouse enteroendocrine cells and mouse intestine is regulated b

63 by biologic agents produced and released by enteroendocrine cells and neurons as well as by exogenou

64 europods provide a direct connection between enteroendocrine cells and neurons innervating the small

65 a small number of cell types, including gut enteroendocrine cells and sympathetic ganglia, where it

66 s on endogenous enteric hormones produced by enteroendocrine cells and the enteric nervous system.

67 Peptide YY(+) cells gave rise to all L-type enteroendocrine cells and to islet partial differential

68 FFA3 was immunolocalized to enteroendocrine cells and to the enteric neural plexuses

69 +) cells from Bmi1(GFP) mice are preterminal enteroendocrine cells and we identify CD69(+)CD274(+) ce

70 The abnormalities in the ileal enteroendocrine cells appear to be caused by two mechani

71 IBS), and whether any abnormalities in ileal enteroendocrine cells are correlated with abnormalities

72 Intestinal enteroendocrine cells are critical to central regulation

73 Despite being electrically excitable, enteroendocrine cells are generally thought to communica

74 5HT-containing enteroendocrine cells are most numerous in the duodenum

75 Enteroendocrine cells are one of the four major cell typ

76 although goblet cells resist E11 infection, enteroendocrine cells are permissive, suggesting that en

77 r results indicate that all small intestinal enteroendocrine cells arise from ngn3-expressing cells a

78 ondin domain-containing protein expressed in enteroendocrine cells as well as in epithelial cells in

79 In the intestine, Pak3 is expressed in enteroendocrine cells but is not necessary for their dif

80 Transformation of secretin-producing enteroendocrine cells by SV40 requires functional cooper

81 We find that class I and class II enteroendocrine cells can be distinguished locally by co

82 urogenin3 (Neurog3)-expressing cells, unlike enteroendocrine cells elsewhere in the digestive tract.

83 Enteroendocrine cells engineered to secrete recombinant

84 a cells, and for terminal differentiation of enteroendocrine cells expressing the hormone secretin.

85 ion, secretin- and cholecystokinin-producing enteroendocrine cells failed to develop in the absence o

86 NA from three unrelated patients with sparse enteroendocrine cells for mutations of NEUROG3.

87 mice to study neural circuits, we found that enteroendocrine cells have the necessary elements for ne

88 xhibit greater than 90% decrease in tuft and enteroendocrine cells in both crypts and villi of the sm

89 We studied a subset of these enteroendocrine cells in duodenum that produce several p

90 We observed loss of Paneth, goblet, and enteroendocrine cells in Math1-null crypts.

91 stem cells that generate new enterocytes and enteroendocrine cells in response to tissue requirements

92 Enteroendocrine cells in the gastrointestinal tract play

93 redominantly in pancreatic beta-cells and in enteroendocrine cells in the gastrointestinal tract.

94 y participate in GABA-modulated functions of enteroendocrine cells in the GI lumen.

95 in-coupled receptor expressed by a subset of enteroendocrine cells in the gut epithelium.

96 e of regulating peptide hormone release from enteroendocrine cells in the gut.

97 otropic polypeptide (GIP)) are secreted from enteroendocrine cells in the intestinal epithelium, and

98 nsmembrane receptor that is expressed in the enteroendocrine cells in the intestine and in the islets

99 ause GABArho receptors are normally found in enteroendocrine cells in the lumen of the digestive trac

100 Secretin-producing enteroendocrine cells in the murine small intestine show

101 peptide-1 (GLP-1) and peptide YY (PYY), from enteroendocrine cells in the small intestine.

102 ngn3 is required for the differentiation of enteroendocrine cells in the stomach and the maintenance

103 l of the abnormal epithelium, the numbers of enteroendocrine cells in the villi are greatly reduced.

104 ymphocytes and goblet cells reduced, and the enteroendocrine cells increased.

105 erizing the roles and functions of different enteroendocrine cells is an essential step in understand

106 absorptive diarrhea and a lack of intestinal enteroendocrine cells is caused by loss-of-function muta

107 tificial pancreas based on insulin-secreting enteroendocrine cells is insufficient as a standalone th

108 Expression of the hormone secretin in enteroendocrine cells is restricted to the nondividing v

109 These include the release from enteroendocrine cells of mediators including 5HT, CCK, G

110 Enteroendocrine cells of the gastrointestinal (GI) tract

111 ptide predominantly localized in specialized enteroendocrine cells of the small intestine and release

112 pancreatic beta-cells and incretin-producing enteroendocrine cells of the small intestine.

113 reting copper cells, interstitial cells, and enteroendocrine cells of the stomach.

114 The transgene was not expressed in goblet or enteroendocrine cells or in crypts.

115 canonical Notch signaling, was restricted to enteroendocrine cells or undetectable in the mucosa of t

116 Stimulus-coupled incretin secretion from enteroendocrine cells plays a fundamental role in glucos

117 Enteroendocrine cells populate gastrointestinal tissues

118 The patients had few intestinal enteroendocrine cells positive for chromogranin A, but t

119 Secretin-producing enteroendocrine cells represent a nondividing subpopulat

120 xis of the gastrointestinal system, discrete enteroendocrine cells respond to both mechanical and che

121 epithelium, enterochromaffin (EC) cells are enteroendocrine cells responsible for producing >90% of

122 mice, expression of NT in Drosophila midgut enteroendocrine cells results in increased lipid accumul

123 Loss of enteroendocrine cells reveals the critical need for ente

124 K) is a satiety hormone produced by discrete enteroendocrine cells scattered among absorptive cells o

125 Mechanistically, midgut enteroendocrine cells secrete the neuroendocrine hormone

126 ntains a diffuse endocrine system comprising enteroendocrine cells that secrete peptides or biogenic

127 Enteroendocrine cells throughout the gut and pancreas se

128 cy caused by disruption of PCSK1, failure of enteroendocrine cells to produce functional hormones res

129 How fatty acids stimulate enteroendocrine cells to release cholecystokinin (CCK) i

130 that fatty acids can interact directly with enteroendocrine cells to stimulate CCK secretion via inc

131 cids directly influence peptide release from enteroendocrine cells using STC-1, a mouse intestinal en

132 tic of enterocytes, and a loss of goblet and enteroendocrine cells was observed.

133 In keeping with this, no enteroendocrine cells were detected in intestinal biopsy

134 ght junctions and desmosomes, and goblet and enteroendocrine cells were present.

135 ction and transduction are also expressed in enteroendocrine cells where they underlie the chemosenso

136 reconstituted in vitro by coculturing single enteroendocrine cells with sensory neurons.

137 ation, and altered proportions of goblet and enteroendocrine cells) was inhibited by AG1024.

138 , goblet cells, Paneth cells, tuft cells and enteroendocrine cells), presence of functional brush-bor

139 s requires sensing of meal components by gut enteroendocrine cells, activation of neural and humoral

140 ocrine-cell progenitors differentiating into enteroendocrine cells, and (2) switching on the expressi

141 usion casein proteins are not detrimental to enteroendocrine cells, and alpha and beta casein are par

142 (NPS), is expressed by gastrointestinal (GI) enteroendocrine cells, and is involved in inflammation,

143 HRVs infect differentiated enterocytes and enteroendocrine cells, and viroplasms and lipid droplets

144 three secretory lineages, goblet, paneth, or enteroendocrine cells, are not fully understood.

145 rminal differentiation of the pancreatic and enteroendocrine cells, as well as for the survival of ph

146 ating glucagon-like peptide-1 secretion from enteroendocrine cells, enhancing glucose uptake in 3T3-L

147 pecialized elements of the mucosa (including enteroendocrine cells, enterocytes and immune cells) and

148 and molecular bridge between enteric nerves, enteroendocrine cells, immune cells, and epithelial cell

149 ween Nav1.8-expressing mucosal afferents and enteroendocrine cells, including apparent neuroendocrine

150 ng nutrient sensing and peptide secretion by enteroendocrine cells, including novel taste-like pathwa

151 Our results suggest that RB is required for enteroendocrine cells, particularly serotonin cells, to

152 enterocytes, goblet cells, Paneth cells, and enteroendocrine cells, suggesting that the fusion partne

153 Enteroendocrine cells, the largest and most diverse popu

154 the taste G protein gustducin, expressed in enteroendocrine cells, underlie intestinal sugar sensing

155 chromogranin A (CgA), a protein secreted by enteroendocrine cells, was exclusively associated with 6

156 T2Rs are also expressed in gut-derived enteroendocrine cells, where they have also been hypothe

157 or the normal development of mouse and human enteroendocrine cells.

158 TRPA1 to excite primary sensory neurons and enteroendocrine cells.

159 g progeny that replace dying enterocytes and enteroendocrine cells.

160 he development of both pancreatic islets and enteroendocrine cells.

161 l enterocytes, as well as goblet, Paneth and enteroendocrine cells.

162 level of constitutive expression of NT/N in enteroendocrine cells.

163 and of preproglucagon, which is expressed in enteroendocrine cells.

164 signaling, specify their daughters to become enteroendocrine cells.

165 , including Paneth and goblet cells, but not enteroendocrine cells.

166 ge analysis to generate both enterocytes and enteroendocrine cells.

167 inal cell populations, including a subset of enteroendocrine cells.

168 y generalized malabsorption and a paucity of enteroendocrine cells.

169 lycan expression and a paucity of goblet and enteroendocrine cells.

170 , have fewer goblet cells, and supernumerary enteroendocrine cells.

171 quired to produce an appropriate fraction of enteroendocrine cells.

172 but are interspersed with hormone-producing enteroendocrine cells.

173 egulatory elements are not active in gastric enteroendocrine cells.

174 cosal T lymphocytes and serotonin-containing enteroendocrine cells.

175 or activator binding in islet beta-cells and enteroendocrine cells.

176 rminal differentiation of secretin-producing enteroendocrine cells.

177 receptors are expressed, at least partly, in enteroendocrine cells.

178 proteins are bioactive, nor their effects on enteroendocrine cells.

179 certain other hormones in other types of the enteroendocrine cells.

180 reprogram extant class I cells into class II enteroendocrine cells.

181 A2 and FFA3 were immunolocalised to duodenal enteroendocrine cells.

182 tty acids (LCFAs) and SCFAs are expressed in enteroendocrine cells.

183 d in the infection of mucosal nerves through enteroendocrine cells.

184 teria stimulate epithelial biosensors called enteroendocrine cells.

185 innervated sensory epithelial cells, such as enteroendocrine cells.

186 eages: intermediate-like (Paneth/goblet) and enteroendocrine cells.

187 iously unrecognized tissue-intrinsic role of enteroendocrine cells.

188 related p107 protein appears dispensable for enteroendocrine differentiation and does not functionall

189 efines a novel pathway required for tuft and enteroendocrine differentiation and provides an importan

190 f exon 3 of beta-catenin at a later stage of enteroendocrine differentiation did not produce tumors.

191 an innovative strategy for the treatment of enteroendocrine disorders.

192 ns and beta-lactoglobulin hydrolysates on an enteroendocrine (EE) cell model were examined.

193 estinal stem cell (ISC) expansion as well as enteroendocrine (EE) cell reduction.

194 ntiated cells that are lost and replenished: enteroendocrine (EE) cells and enterocytes (ECs).

195 erminally differentiated enterocyte (EC) and enteroendocrine (EE) cells are generated from an intesti

196 ghters, but not in terminally differentiated enteroendocrine (ee) cells or enterocyte (EC) cells.

197 cells (ISCs) generate enterocytes (ECs) and enteroendocrine (ee) cells.

198 asts (EB), and an increase in differentiated enteroendocrine (EE) cells.

199 -GFP(+) cells were distinct and enriched for enteroendocrine (EE) markers, including Prox1.

200 intained into the adult stage in a subset of enteroendocrine/enterochromaffin cells.

201 lated kinase 1/2 (ERK1/2) phosphorylation in enteroendocrine GLUTag cells via mechanisms sensitive to

202 acting on sweet taste receptors expressed on enteroendocrine GLUTag cells, stimulated secretion of gu

203 al cell lineages, including the enterocytes, enteroendocrine, Goblet and Paneth cells, from the stem

204 The enteroendocrine hormone, gastrin, exerts trophic effects

205 Fasting enteroendocrine hormones were quantified at each time po

206 aken together, these findings define a local enteroendocrine-IEL axis linking energy availability, ho

207 LP-1) is a polypeptide hormone secreted from enteroendocrine L cells and potentiates glucose-dependen

208 Nutrient stimulation of enteroendocrine L cells induces the release of the incre

209 ent receptor potential (TRP) ion channels in enteroendocrine L cells producing GLP-1.

210 fatty acid receptor 2 (FFA2) is expressed on enteroendocrine L cells that release glucagon-like pepti

211 resent TRPA1 as a novel sensory mechanism in enteroendocrine L cells, coupled to the facilitation of

212 id proglucagon-derived peptide secreted from enteroendocrine L cells.

213 vasopressin (AVP) stimulates the release of enteroendocrine L-cell derived hormones glucagon-like pe

214 ike peptide (GLP)-1 and GLP-2, the two major enteroendocrine L-cell peptides.

215 We hypothesized that enteroendocrine L-cells producing glucagon-like peptide

216 which we identified as a product of colonic enteroendocrine L-cells, better known for their secretio

217 The receptor is found on gut enteroendocrine L-cells, pancreatic beta-cells, and symp

218 ng glucagon-like peptide-1 (GLP-1) secreting enteroendocrine L-cells, we have designed TGR5 agonists

219 Moreover, the enteroendocrine L-type cell lineage is modified, as asse

220 omaffin cells were the most severely reduced enteroendocrine lineage in the duodenum and colon.

221 erentiated secretory cells of the Paneth and enteroendocrine lineage.

222 act on a transcription factor network in the enteroendocrine lineage.

223 onditions that direct differentiation to the enteroendocrine lineage.

224 stine and increased production of goblet and enteroendocrine lineages in Mtgr1(-/-) mice.

225 and Foxa2 are essential regulators of these enteroendocrine lineages in vivo.

226 This suggested that multiple enteroendocrine lineages were related to peptide YY-prod

227 cells undergoing commitment to the Paneth or enteroendocrine lineages, while retaining some stem cell

228 mostly limited to the brain and specialized enteroendocrine N cells in the distal small intestine.

229 opsis of the molecular mechanisms underlying enteroendocrine nutrient sensing and highlights our curr

230 of the lingual epithelium is operational in enteroendocrine open GI cells that sense the chemical co

231 ells giving rise to secretory cells (CGPCPs, enteroendocrine or Tuft cells) and proliferative absorpt

232 ification in the pancreatic islet and in the enteroendocrine population of the intestine.

233 ates cell fate choices within the intestinal enteroendocrine population; in the Nkx2.2 null mice, sev

234 specification and homeostatic maintenance of enteroendocrine populations, and identify Lmx1a as a nov

235 lity, suggesting that the loss of additional enteroendocrine products in ascl1a-/- embryos also contr

236 ndocrine cells reveals the critical need for enteroendocrine products in maintenance of normal intest

237 Loss of enteroendocrine products results in loss of anterograde

238 dly, somatic ablation of Foxo1 in Neurog3(+) enteroendocrine progenitor cells gives rise to gut insul

239 In developing Ngn3(+) enteroendocrine progenitor cells, Nkx2.2 is not required

240 The data indicate that Neurog3(+) enteroendocrine progenitors require active Foxo1 to prev

241 fi1 functions to select goblet/Paneth versus enteroendocrine progenitors.

242 ber of goblet cells remained stable, whereas enteroendocrine relative cell number declined.

243 ng the hormone secretin is expressed only in enteroendocrine S cells and insulin-producing pancreatic

244 Important attributes of GLP-1 action and enteroendocrine science are reviewed, with emphasis on m

245 cell population and a redistribution of the enteroendocrine subpopulations, all toward an ileal phen

246 etion, including the interaction between the enteroendocrine system and the enteric nervous system.

247 The enteroendocrine system is the primary sensor of ingested

248 e cell fate in various tissues including the enteroendocrine system of the gastrointestinal tract.

249 The enteroendocrine system orchestrates how the body respond