ライフサイエンスコーパス: enteroendocrine

1 this metabolic control system, IELs modulate enteroendocrine activity by acting as gatekeepers that l

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

3 vation of Jonah66Ci increases the numbers of enteroendocrine and mitotic cells in the gut of uninfect

4 Activation of GPR119 receptors, expressed on enteroendocrine and pancreatic islet cells, augments glu

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

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

7 hat the ablated Paneth cells are replaced by enteroendocrine and tuft cells.

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

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

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

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

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

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

14 d increased markers of stem, goblet, Paneth, enteroendocrine, and tuft cells, compared with control e

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

16 me transcription factors as their intestinal enteroendocrine cell counterparts.

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

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

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

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

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

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

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

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

25 cellular and molecular mechanisms governing enteroendocrine cell diversity.

26 ngenital malabsorptive diarrhea secondary to enteroendocrine cell dysgenesis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 egatively regulating chromogranin A-positive enteroendocrine cell number.

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

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

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

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

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

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

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

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

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

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

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

53 Other enteroendocrine cell types were not ablated.

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

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

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

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

58 d microbial stimuli using epithelial sensory enteroendocrine cells (EEC).

59 A population of enteroendocrine cells (EECs) are specialized mechanosens

60 Enteroendocrine cells (EECs) are specialized sensory cel

61 As enteroendocrine cells (EECs) comprise only ~1% of the in

62 ithelial cells, with chromogranin A-positive enteroendocrine cells (EECs) identified as a permissive

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

64 s of experiments collectively indicated that enteroendocrine cells (EECs) in the posterior midgut pro

65 Enteroendocrine cells (EECs) produce hormones such as gl

66 Enteroendocrine cells (EECs) sense intestinal content an

67 emistry showed major up-regulation of CCK in enteroendocrine cells (EECs) that were glucagon-like pep

68 atients are macroscopically normal, but lack enteroendocrine cells (EECs), suggesting an essential ro

69 senting intestinal stem cells, enteroblasts, enteroendocrine cells (EEs), and enterocytes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 Intestinal enteroendocrine cells are critical to central regulation

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

90 5HT-containing enteroendocrine cells are most numerous in the duodenum

91 Enteroendocrine cells are one of the four major cell typ

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

93 Enteroendocrine cells are specialised sensory cells loca

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

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

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

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

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

99 an jejunal enteroids engineered to make more enteroendocrine cells demonstrated that Hld alone is suf

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

101 Enteroendocrine cells engineered to secrete recombinant

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

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

104 n intestinotrophic growth factor released by enteroendocrine cells following food intake.

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

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

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

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

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

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

111 d relative densities of enterochromaffin and enteroendocrine cells in small intestinal tissue.

112 to conditionally delete Paneth, goblet, and enteroendocrine cells in the epithelium to investigate t

113 Enteroendocrine cells in the gastrointestinal tract play

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

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

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

117 ino acids from food acutely activate Dh31(+) enteroendocrine cells in the gut, increasing Dh31 levels

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 strictly agonist-dependent fashion whilst in enteroendocrine cells of the colon both Ser(296)/Ser(297

133 imals, nutrient sensors are found within the enteroendocrine cells of the digestive system; however,

134 Enteroendocrine cells of the gastrointestinal (GI) tract

135 eurotensin (NT), a gut hormone released from enteroendocrine cells of the small bowel, contribute to

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

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

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

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

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

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

142 Enteroendocrine cells populate gastrointestinal tissues

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

144 Secretin-producing enteroendocrine cells represent a nondividing subpopulat

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

146 Enteroendocrine cells respond to digestion products of d

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

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

149 Loss of enteroendocrine cells reveals the critical need for ente

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

151 Mechanistically, midgut enteroendocrine cells secrete the neuroendocrine hormone

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

153 Enteroendocrine cells throughout the gut and pancreas se

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 cell types, including enteric neurons, glia, enteroendocrine cells, immune cells and bacteria, integr

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

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

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

178 blood flow, but the ENS also interacts with enteroendocrine cells, influences epithelial proliferati

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

180 stricted expression, including expression in enteroendocrine cells, pineal gland, and dental enamel.

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

182 Enteroendocrine cells, the largest and most diverse popu

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

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

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

186 labsorptive diarrhea due to complete loss of enteroendocrine cells, whereas endocrine pancreas develo

187 Enteroendocrine cells, which are relatively rare in the

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

189 teria stimulate epithelial biosensors called enteroendocrine cells.

190 innervated sensory epithelial cells, such as enteroendocrine cells.

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

192 iously unrecognized tissue-intrinsic role of enteroendocrine cells.

193 hormones until the discovery of synapses in enteroendocrine cells.

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

195 TRPA1 to excite primary sensory neurons and enteroendocrine cells.

196 g progeny that replace dying enterocytes and enteroendocrine cells.

197 he development of both pancreatic islets and enteroendocrine cells.

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

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

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

201 signaling, specify their daughters to become enteroendocrine cells.

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

203 ge analysis to generate both enterocytes and enteroendocrine cells.

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

205 y generalized malabsorption and a paucity of enteroendocrine cells.

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

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

208 quired to produce an appropriate fraction of enteroendocrine cells.

209 but are interspersed with hormone-producing enteroendocrine cells.

210 egulatory elements are not active in gastric enteroendocrine cells.

211 cosal T lymphocytes and serotonin-containing enteroendocrine cells.

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

213 rminal differentiation of secretin-producing enteroendocrine cells.

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

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

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

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

218 A2 and FFA3 were immunolocalised to duodenal enteroendocrine cells.

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

220 n the absence of natural IELs depends on the enteroendocrine-derived incretin GLP-1(2), which is norm

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

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

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

224 The authors' close examination of intestinal enteroendocrine differentiation reveals new lineage feat

225 an innovative strategy for the treatment of enteroendocrine disorders.

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

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

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

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

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

231 Enteroendocrine (EE) cells within the intestinal epithel

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

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

234 and DamID profiling show that Klu suppresses enteroendocrine (EE) fate by repressing the action of th

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

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

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

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

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

240 The enteroendocrine hormone, gastrin, exerts trophic effects

241 Steroid and enteroendocrine hormones functionally remodel these neur

242 Fasting enteroendocrine hormones were quantified at each time po

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

244 l, mechanical, and metabolic branches of the enteroendocrine innate immune system and argue that this

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

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

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

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

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

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

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

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

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

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

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

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

257 We investigate whether enteroendocrine L-cells, well known for their production

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

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

260 erentiated secretory cells of the Paneth and enteroendocrine lineage.

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

262 onditions that direct differentiation to the enteroendocrine lineage.

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

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

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

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

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

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

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

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

271 , immune dysregulation, barrier dysfunction, enteroendocrine pathways, and genetics), and animal mode

272 focusing on large-molecule formats (notably enteroendocrine peptides and proteins) and discuss the a

273 the expansion of tuft cells, which adopt an enteroendocrine phenotype and contribute to increased mu

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

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

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

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

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

279 Loss of enteroendocrine products results in loss of anterograde

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

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

282 Transcription factor Neurod1 is required for enteroendocrine progenitor differentiation and maturatio

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

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

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

286 (GLP-1/PYY/NT), but not proximal (CCK/GIP), enteroendocrine responses were generally greater in RYGB

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

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

289 ffective than 2-OG plus MCFAs in stimulating enteroendocrine secretion in RYGB-operated and matched c

290 20 mL) and its derivates, LCFAs and 2-OG, on enteroendocrine secretions [glucagon-like peptide-1 (GLP

291 The enteroendocrine signalling compound, serotonin (5-HT), i

292 r ability to induce CCK and GLP-1 release in enteroendocrine STC-1 cells.

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

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

295 The enteroendocrine system is the primary sensor of ingested

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

297 The enteroendocrine system orchestrates how the body respond

298 Glucagon-like-peptide-2 (GLP-2) is an enteroendocrine tissue hormone produced by intestinal L

299 Thus, enteroendocrine tuft cells appear essential to maintain

300 specific signaling networks in stem, Paneth, enteroendocrine, tuft and goblet cells, as well as enter