ライフサイエンスコーパス: GLUT2

1 pression of intestinal genes (MGA, DPP4, and GLUT2).

2 the glucose-facilitated transporter type 2 (GLUT2).

3 synthase) and a gene for glucose absorption (Glut2).

4 on of the mature beta-cell factors, MafA and Glut2.

5 ng the component now known to be mediated by GLUT2.

6 ness can be augmented by the coexpression of GLUT2.

7 romosome 3q, which harbors the gene encoding GLUT2.

8 beta-cell-specific factors like insulin and Glut2.

9 horylation and modifying the ratio of SGLT-1:GLUT2.

10 d GLP-1, and 3) triggers the upregulation of GLUT2.

11 by decreased levels of PPARgamma, PDX-1, and GLUT2.

12 , and SGLT1 was required for upregulation of GLUT2.

13 pancreatic duodenal homeobox-1 (PDX-1), and GLUT2.

14 sion of glucose transporters SGLT1 (38-92%), GLUT2 (45-96%), GLUT5 (28-89%) and the enzyme sucrase-is

15 te carrier family 2, member 2 (also known as GLUT2), a glucose transporter expressed in the liver, is

16 Inhibition of apical GLUT2 absorption coincided with inhibition of unidirecti

17 rse range of stimulators and discovered that GLUT2 affected membrane depolarisation through the closu

18 Although expression of GLUT2 alone had negligible effects on glucose usage and

19 Glucose uptake via GLUT2 also raises oocyte tonicity.

20 GLUT2 and CasR regulate K- and L-cell activity in respon

21 Among genes that are atRA responsive, Glut2 and Gck mRNA levels were decreased in isolated isl

22 s well as expression of the nutrient sensors Glut2 and Glp1r.

23 30 mmol/l glucose, in line with decreases in Glut2 and glucokinase gene expression, and attenuated gl

24 s that are further engineered to express the GLUT2 and glucokinase genes demonstrate stable expressio

25 Conversely, GLUT2 and glucokinase mRNA levels were appropriately reg

26 ts, P < 0.01), have two- to threefold higher GLUT2 and glucokinase steady-state mRNA levels, take up

27 (PsiS)-L-Ala (1 mM), while increasing apical GLUT2 and glucose absorption within minutes.

28 gest a secondary, but participating, role of GLUT2 and glucose metabolism for GLP-1 secretion via an

29 ng of an inward-facing conformation model of GLUT2 and glucose uptake assays in a hexose transporter-

30 mmunohistochemistry was performed for GLUT1, GLUT2 and GLUT4 in frozen sections of hypothalami from n

31 GLUT2 and GLUT4 mRNA are not detected in chondrocytes.

32 (the red cell glucose transporter) and then GLUT2 and GLUT4, the red cell anion exchange protein (Ba

33 ed whether facilitative glucose transporters GLUT2 and GLUT5-12 transported DHA.

34 Maximal rates for DHA transport mediated by GLUT2 and GLUT8 in oocytes were lower than maximal rates

35 Only GLUT2 and GLUT8, known to be expressed in intestines, tr

36 cose (Vmax of 224 and 32 pmol/min/oocyte for GLUT2 and GLUT8, respectively) and fructose (Vmax of 406

37 ose (Vmax of 406 and 116 pmol/min/oocyte for GLUT2 and GLUT8, respectively).

38 ilability via inhibition of small intestinal GLUT2 and GLUT8.

39 iated by the facilitative sugar transporters GLUT2 and GLUT8.

40 Menten constant (6.1+/-1.5 mM) is in between GLUT2 and GLUT9.

41 xpress low levels of the glucose transporter Glut2 and homeodomain factor Nkx 6-1.

42 dietary arginine level significantly lowered GLUT2 and increased PK mRNA levels.

43 Islet GLUT2 and insulin mRNA were measured with quantitative r

44 s was associated with reduced mRNA levels of Glut2 and islet beta-cell transcription factors such as

45 luences and required delivery of glucose via GLUT2 and mitochondrial metabolism.

46 higher expression of insulin, somatostatin, GLUT2 and Nkx6.1 genes.

47 Immunostaining for both GLUT2 and Nkx6.1 was mainly cytoplasmic.

48 sequence of an intracellular accumulation of Glut2 and overall decreased levels of Glut2 protein.

49 PancMet KO mouse islets failed to upregulate GLUT2 and pancreatic duodenal homeobox-1 mRNA, insulin c

50 of insulin-positive cells that co-expressed Glut2 and Pdx1 compared to controls.

51 oretin or cytochalasin B was used to inhibit GLUT2 and phloridzin to inhibit SGLT1.

52 the terminal web and in the levels of apical GLUT2 and PKC betaII, but not SGLT1.

53 We determined levels of GLUT2 and SGLT-1 proteins and phosphorylation of AMPKalp

54 inant adenoviruses to express high levels of GLUT2 and the beta-cell isoform of glucokinase (GK).

55 We conclude that GLUT2 and/or glucokinase expression imposes tight regula

56 maintaining glucose homeostasis (insulin and Glut2) and beta-cell formation and function (Pax4 and Pa

57 reduced expression of Slc2a2 (also known as Glut2) and Gck (encoding glucokinase) in beta-cells, whi

58 min by reducing glucose transporter type 2 (Glut2) and glucokinase (GK) activities.

59 ound up-regulation of glucose transporter 2 (GLUT2) and glycogen synthase 2 (GYS2); while expression

60 2a1 (GLUT1), decreased expression of Slc2a2 (GLUT2) and Slc5a1 (SGLT1) whilst increasing GLUT-depende

61 , sucrase-isomaltase, glucose transporter 2 (GLUT2), and dipeptidyl peptidase 4 (DPP-4), as well as t

62 ted genes, including Ins1 (insulin), Slc2a2 (GLUT2), and Gck (glucokinase).

63 lets express insulin, glucose transporter 2 (GLUT2), and transcription factors typically found in pan

64 tidase 4 (Dpp4); glucose transporter type 2 (Glut2); and villin were measured by quantitative reverse

65 ule function, including NaPi2A, NHE3, SGLT2, GLUT2, and AQP1, are downregulated as part of the diseas

66 The mucosal mRNA levels of Slfn3, SI, Glut2, and Dpp4 were all substantially higher in the rat

67 treatment also increased pancreatic insulin, GLUT2, and glucokinase mRNA in the old rats.

68 f several beta-cell specific genes (insulin, GLUT2, and glucokinase).

69 ombinations of genes encoding human insulin, GLUT2, and glucokinase.

70 of the glucose transporter proteins (Glut)1, Glut2, and Glut4, and, therefore, glucose uptake.

71 mulated insulin secretion, including Ins1/2, Glut2, and MafA.

72 IGRP gene expression, as it is for glucagon, GLUT2, and Pdx-1 gene expression.

73 els of the differentiation markers SI, Dpp4, Glut2, and villin.

74 DHA transport activity in GLUT2- and GLUT8-expressing oocytes was inhibited by glu

75 Alterations in the function or expression of GLUT2 are involved in the Fanconi-Bickel syndrome, diabe

76 absence of glucose, suggesting that mutated GLUT2, as a sugar receptor, triggers a signaling pathway

77 he glucose transporter SLC2A2 gene, encoding GLUT2, as an example, we find that LDB1 regulates gene e

78 e, diminished the phloretin-sensitive apical GLUT2 but not the phloretin-insensitive SGLT1 component

79 ly diminished the phloretin-sensitive apical GLUT2, but not the phloretin-insensitive SGLT1 component

80 (6%), Cdx2 by 31% (10%), DPP-4 by 15% (6%), GLUT2 by 40% (11%), SLFN12 by 61% (14%), and sucrase-iso

81 GLUT2 can transport the amino sugar glucosamine (GlcN),

82 In hepatocytes, P-Rex2 suppresses Glut2 cell surface levels, mitochondrial membrane potent

83 ining IASGFR but not by Glut1/Glut4 or Glut1/Glut2 chimeras lacking these residues.

84 retin demonstrated that stress inhibited the GLUT2 component by 42.8 +/- 3.8%, which correlated with

85 he effects of building-induced stress on the GLUT2 component of absorption.

86 Selective inhibition of the GLUT2 component with phloretin demonstrated that stress

87 Astrocyte GLUT2 controls glucose counterregulatory hormone secreti

88 s that the facilitative glucose transporter, GLUT2, could act as a glucose sensor and the calcium-sen

89 Genetic inactivation of mice GLUT2 decreases hyperglycemia-induced SCO-spondin secret

90 Collectively, our data show that GLUT2-dependent control of parasympathetic activity defi

91 GlcN stimulated ESC proliferation in a GLUT2-dependent fashion but did not regulate pluripotenc

92 nd VMNvl GABA neurons may exhibit divergent, GLUT2-dependent GABA neurotransmission patterns in the h

93 lucose-induced activation and recruitment of GLUT2 does not occur in high stress perfusions.

94 via the facilitative glucose transporter 2 (GLUT2) during diabetes may lead to renal proximal tubule

95 hus, targeting peripheral CB1R or inhibiting GLUT2 dynamics in RPTCs has the potential to treat and a

96 The higher number of high K(m) GLUT2 ensures that glucose reabsorption is increased by

97 ibition of glucose and fructose transport by GLUT2 expressed in Xenopus laevis oocytes was produced b

98 in was a potent non-competitive inhibitor of GLUT2 expressed in Xenopus oocytes; K(i) 22.8 microm.

99 ation by embryos, as exogenous GlcN does for GLUT2-expressing ESC, and may explain the need for GLUT2

100 taG I/17 cells engineered for high levels of GLUT2 expression and a twofold increase in glucokinase a

101 on and Arx, and the addition of Pdx1 induces Glut2 expression and glucose-responsive insulin secretio

102 otting and immunohistochemistry demonstrated GLUT2 expression at the BBM during diabetes, but the pro

103 expressing ESC, and may explain the need for GLUT2 expression by embryos.

104 h decreased pancreas duodenum homeobox-1 and GLUT2 expression in cultured islets.

105 the dominating transcriptional regulator of GLUT2 expression in hepatocytes in vivo.

106 xample, glucagon expression in the pancreas, GLUT2 expression in the liver, and tyrosine hydroxylase

107 There was no GLUT2 expression in the VMH.

108 Inhibition of CB1R also downregulated GLUT2 expression, affected the dynamic translocation of

109 Endogenous GLUT2 expression, in contrast, is rapidly extinguished d

110 rglycemia with reduced beta-cell insulin and Glut2 expression.

111 a low glucose concentration, suggesting that GLUT2 facilitates the homeostasis of key cellular pathwa

112 st is challenging due to the low affinity of GLUT2 for glucose and fructose and the scarcity of GLUT-

113 GLUT2, found predominantly in liver, intestine, kidney,

114 -glucagonemia by GLUT2 siRNA infers that VMN GLUT2 function imposes an inhibitory tone on these hormo

115 In contrast, GLUT2 gene and protein expression levels were reduced af

116 VMN GLUT2 gene knockdown suppressed or stimulated hypoglycem

117 is mutation was originally discovered in the Glut2 gene of a patient with type 2 diabetes.

118 partially explained by reduced levels of the GLUT2 gene transcripts; 2) the reduction of beta-cell in

119 ding to the chromatin in the promoter of the Glut2 gene, thereby regulating GLUT2 protein levels in p

120 otic cells, and IB1, a transactivator of the GLUT2 gene.

121 ssessed the impact of glucose transporter 2 (Glut2) gene inactivation in adult mouse liver (LG2KO mic

122 The restoration of the Ins1/2 and Glut2 genes corresponded to a two- to threefold increase

123 recruitment, particularly at the Ins1/2 and Glut2 genes.

124 GLUT2/GK coexpression further increased glycolytic flux

125 Despite enhanced glycolytic fluxes, GLUT2/GK-coexpressing cells showed glucose dose-dependen

126 eta-cell identity, such as downregulation of GLUT2, GLP1R, and MafA, and in vitro knockdown of GLUT2

127 of glucose-6-phosphatase and suppression of GLUT2, glucokinase, and glycerol-3-phosphate dehydrogena

128 ted insulin secretion, including that of the Glut2 glucose transporter.

129 transcription factors MafA and Nkx6.1 or the GLUT2 glucose transporter.

130 n, specific phenolic inhibitors of SGLT1 and GLUT2 glucose transporters, reduced the glucose transpor

131 development and function (insulin I and II, Glut2, glucose kinase, islet amyloid polypeptide, nestin

132 sed plasma glucose by 50% and reduced PEPCK, GLUT2, glucose-6-phosphatase, tyrosine aminotransferase,

133 re amplified by expression of Glut4/Glut1 or Glut2/Glut1 chimeras containing IASGFR but not by Glut1/

134 ncoding the sugar transporters SGLT1, GLUT1, GLUT2, GLUT3, GLUT4, and GLUT5.

135 fied by overexpression of the Glut1, but not Glut2, Glut3, or Glut4, glucose transporter.

136 chemistry, we determined that several GLUTs (GLUT2, GLUT4, GLUT8, and GLUT9), a sodium-glucose cotran

137 GLUT2, GLUT5, and SGLT1 did not transport DHA and none o

138 demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do not mediate this effe

139 block glucose entry in cancer cells, and the GLUT2/GLUT5 inhibitor can reduce the intestinal absorpti

140 GLUT2 has been found widely expressed in the brain and G

141 Glucose transporter 2 (GLUT2) has been proposed as a glucose sensor in pancreat

142 ive for GLUT3, inhibiting less strongly only GLUT2 (IC(50) ~ 29 uM).

143 GLUT2 immunofluorescence in the beta-cell of Px rats was

144 GLUT2 immunoreactivity was seen in the ependymal cells o

145 of the debate, to show how our proposals on GLUT2 impact on different aspects of the debate and to l

146 In vitro suppression of GLUT2 impaired lysosomal autophagy as shown by transcrip

147 , GLP1R, and MafA, and in vitro knockdown of GLUT2 in beta-cells-mimicking its phenotype-decreased st

148 role of the fructose transporters GLUT5 and GLUT2 in causing, contributing to or exacerbating these

149 in Glut2(-/-) mice confirm the importance of GLUT2 in glucose absorption across the proximal tubule.

150 ate the functional requirements of GLUT1 and GLUT2 in glucose uptake and insulin secretion through ch

151 In this study, we overexpressed GLUT2 in GT1-7 neuroblastoma cells and investigated the

152 Simultaneous inhibition of SGLT1 and GLUT2 in high stress perfusions with phloridzin and cyto

153 To examine the mechanisms for this loss of GLUT2 in normal islets exposed to hyperglycemia, we perf

154 depletion results in impaired trafficking of Glut2 in pancreatic beta-cells as a consequence of an in

155 r samples, suggesting a key role for hepatic GLUT2 in regulation of metformin action.

156 ets and SC-islets and genetically disrupting GLUT2 in SC-islets.

157 T1 induces rapid insertion and activation of GLUT2 in the apical membrane by a PKC betaII-dependent m

158 ion via SGLT1 and facilitated absorption via GLUT2 in the apical membrane.

159 ntrations increased the amounts of SGLT1 and GLUT2 in the BBM, and SGLT1 was required for upregulatio

160 olate) indicating a fundamental position for GLUT2 in the gut peptide secretory mechanism.

161 been found widely expressed in the brain and GLUT2 in the hypothalamus and hindbrain has been suggest

162 of the islet genes Irs1, SERCA, Ins1/2, and Glut2 in treated animals.

163 with inactivation of glucose transporter 2 (Glut2) in the nervous system (NG2KO mice).

164 Glucose tolerance was initially normal after Glut2 inactivation, but LG2KO mice exhibited progressive

165 LP-1 secretion was also sensitive to luminal GLUT2 inhibition (phloretin), but in contrast to SGLT1 i

166 essed individually, we identified eleven new GLUT2 inhibitors (IC(50) ranging from 0.61 to 19.3 uM).

167 s or the development of novel renal-specific GLUT2 inhibitors against DN.

168 The GLUT2 inhibitors described here have various application

169 completely abolished in the presence of the GLUT2 inhibitors phloretin or cytochalasin B.

170 (20) phosphorylation is necessary for apical GLUT2 insertion.

171 se concentrations promote rapid insertion of GLUT2 into the apical membrane, so that absorptive capac

172 a(2+)- and PKC betaII-dependent insertion of GLUT2 into the apical membrane.

173 cin-induced diabetes causes the insertion of GLUT2 into the BBM and this may provide a low affinity/h

174 ent insertion of glucose transporter type 2 (GLUT2) into the apical membrane.

175 Reduction of GLUT2 is associated with loss of glucose-induced insulin

176 In comparison, GLUT2 is detected in a small yet significant subpopulati

177 We conclude that GLUT2 is important in glucose liver transport and reabso

178 Indeed, the glucose transporter GLUT2 is located at the basolateral, vascular side, whil

179 The loss of GLUT2 is overcome in engineered cell ines in which trans

180 Trafficking of apical GLUT2 is rapidly up-regulated by glucose and artificial

181 Apical GLUT2 is therefore a target for multiple short-term and

182 8 express the glucose transporters GLUT1 and GLUT2, isoforms expressed in both normal and neoplastic

183 VMNdm GABA neurons exhibited GLUT2 knockdown-sensitive up-regulated 5'-AMP-activated

184 Using renal Slc2a2 (also known as Glut2) knockout mice, we demonstrate that elevated glyco

185 tocytes, where we found normal expression of Glut2, L-Pk, and Hnf-4alpha in the liver of Hnf-1alpha(-

186 e there was a significant decrease in apical GLUT2 level, but no change in SGLT1 level.

187 vivo and ex vivo, restoring PPARgamma/PDX-1/GLUT2 levels.

188 ed with a corresponding diminution in apical GLUT2 levels: the SGLT1 component and its level were una

189 nr, Apelin and Apela was quantified in Ins(+)Glut2(LO) cells isolated from mouse pancreata and found

190 plnr was predominantly associated with Ins(+)Glut2(LO) cells.

191 expressing, glucose transporter 2-low (Ins(+)Glut2(LO)) progenitor cells.

192 rget genes, including glucose transporter 2 (Glut2), MAF BZIP transcription factor A (MafA), and unco

193 sion of the beta-cell-specific markers pdx1, glut2, mafA, and nkx6.1 and increased expression of the

194 intracellular accumulation of proinsulin and Glut2, massive endoplasmic reticulum (ER) expansion, and

195 Glucose transported by GLUT2 may act after metabolization, closing KATP channel

196 eoxy-d-glucose (2DG), implicating that brain GLUT2 may be important in the regulation of food intake.

197 GLUT2 may be recruited from the basolateral to the apica

198 llatory uptake, and that impaired uptake via GLUT2 may be the cause of the oscillation loss in type 2

199 Likewise, GLUT2 may contribute to the development of non-alcoholic

200 s essential for insulin secretion, decreased GLUT2 may contribute to the etiology of diabetes in pdx1

201 ther ventromedial hypothalamic nucleus (VMN) GLUT2 may regulate dorsomedial (VMNdm) and/or ventrolate

202 y SGLT1 but also indirectly that part of the GLUT2-mediated component controlled by SGLT1 through the

203 GLUT5- and GLUT2-mediated fructose effects on intestinal electrolyt

204 at luminal supply of Ca(2+) is necessary for GLUT2-mediated glucose absorption.

205 into wild-type, Sglt1(-/-) , Sglt2(-/-) and Glut2(-/-) mice and their dynamic whole-body distributio

206 the absence of reabsorption in the kidney in Glut2(-/-) mice confirm the importance of GLUT2 in gluco

207 ittle change in the distribution of 2-FDG in Glut2(-/-) mice, apart from a reduction in the rate of u

208 Me-4FDG was not reabsorbed in the kidney in Glut2(-/-) mice.

209 Given that GLUT2 modified gut peptide secretion stimulated by gluco

210 Glucose transporter-2 (GLUT2) monitors cellular glucose uptake.

211 ydrogenase-A and -B were ubiquitous, whereas GLUT2, monocarboxylate transporters-1 and -2, and leptin

212 pressing an siRNA specific for GLUT2 reduced GLUT2 mRNA and protein levels by 80% in the INS-1-derive

213 The level of GLUT2 mRNA from Px islets was 24 +/- 4% of that of islet

214 expression in ileal enterocytes and induced GLUT2 mRNA in mice, supporting its role in enhancing int

215 GLUT2 mRNA was decreased, but other beta-cell-associated

216 espite a reduction in glucose transporter 2 (GLUT2) mRNA.

217 els of genes encoding glucose transporter 2 (Glut2), neutral and basic amino acid transporter, liver

218 t neither the content of glucose transporter GLUT2 nor the phosphorylation state of the insulin recep

219 However, some genes (i.e., Hb9 and Glut2) only appeared to be impacted by Ldb1 during devel

220 eucine mutation at amino acid residue 197 of Glut2 or the equivalent residue 165 of Glut1 has been sh

221 d not affect the fructose transport of human GLUT2 or the glucose transport of human GLUT1-4 or bacte

222 Sugar transport by GLUT2 overexpressed in pituitary cells and naturally pre

223 lastoma cells and investigated the effect of GLUT2 overexpression on cellular energy status in these

224 Compared with control cells, GLUT2 overexpression resulted in significantly increased

225 This apical GLUT2 pathway of intestinal sugar absorption is present

226 transport, the other is the diffusive apical GLUT2 pathway.

227 GLUT2(Pax8Cre+) mice developed time-dependent glycogen a

228 and expressed higher mRNA levels of insulin, Glut2, Pdx1, MafA and Nkx6.1, but lower CCND1 and CDK4 l

229 tate dehydrogenase LDH5, glucose transporter GLUT2, phosphorylated pyruvate dehydrogenase pPDH and PD

230 he rat CSF stimulates glucose transporter 2 (GLUT2)-positive subcommissural organ (SCO) cells to rele

231 nd Brunner's glands, which are replaced by a GLUT2-positive cuboidal epithelium resembling the bile d

232 nificant difference in HNF6 occupancy at the Glut2 promoter between Foxa2-deficient and control liver

233 These data suggest that 1) the loss of GLUT2 protein associated with hyperglycemia is at least

234 he INS-1-derived beta-cell line, 832/13, and GLUT2 protein levels by >90% in primary rat islets.

235 omoter of the Glut2 gene, thereby regulating GLUT2 protein levels in pancreatic islets and in beta ce

236 In Zucker diabetic rats, GLUT2 protein levels of renal proximal tubules were high

237 target molecules including Cd36, Ppargamma, Glut2 protein, Akt phosphorylation, and lipocalin2, Vamp

238 ion of Glut2 and overall decreased levels of Glut2 protein.

239 solated Px islets also showed a reduction in GLUT2 protein; densitometry measurements were 36 +/- 3%

240 al pore of Na(+)-dependent cotransporters or GLUT2 provides the necessary precondition for an osmotic

241 se inflow via the narrow external orifice of GLUT2 raises vestibular tonicity relative to the externa

242 to known precursor proteins, three of which--GLUT2 receptor, phosphatidylinositol-glycan-specific pho

243 to coordinate regulation of PepT1 and apical GLUT2 reciprocally through a common enterocytic pool of

244 ith a virus expressing an siRNA specific for GLUT2 reduced GLUT2 mRNA and protein levels by 80% in th

245 +)/oligopeptide transporter PepT1 and apical GLUT2, reflecting the fact that trafficking of PepT1 and

246 ional consequences of apical and basolateral GLUT2 regulation are discussed in the context of Western

247 Data also document differential GLUT2 regulation of VMNdm versus VMNvl GABA nerve cell S

248 ls to examine the pathophysiological role of GLUT2 relative to other GLUTs, the pan-Class I GLUT inhi

249 However, the link between CB1R and GLUT2 remains to be determined.

250 Permanent apical GLUT2, resulting in increased sugar absorption, is a cha

251 BIGU resulted from an increase in GLUT1 and GLUT2, secondary to ATF4 and AMPK.

252 Among them, nine were GLUT2-selective, one inhibited GLUT1-4 (pan-Class I GLUT

253 on of AMPKalpha2 and a rapid increase of the GLUT2/SGLT-1 protein ratio in the brush border membrane.

254 GLUT2 siRNA blunted (VMNdm) or exacerbated (VMNvl) hypog

255 hypercorticosteronemia and -glucagonemia by GLUT2 siRNA infers that VMN GLUT2 function imposes an in

256 GLUT2 siRNA pretreatment also modified co-expressed tran

257 Nvl GABA neuron AMPKalpha2 was refractory to GLUT2 siRNA.

258 express the mature beta-cell markers MafA or Glut2 (Slc2a2), suggesting that additional activator fun

259 The hexose transporter, GLUT2 (SLC2A2), which is expressed by mouse embryos, is

260 rs described here have various applications; GLUT2-specific inhibitors can serve as tools to examine

261 lation of the insulin receptor and increased GLUT2, SREBP-1c and FASN expression.

262 Loss of Glut2 suppressed hepatic glucose uptake but not glucose

263 ates the major glucose transporter of liver, GLUT2, through G(q) -MAPK-FoxA3 and inhibits insulin-Akt

264 pathway is regulated by rapid trafficking of GLUT2 to the apical membrane induced by glucose during a

265 cting the fact that trafficking of PepT1 and GLUT2 to the apical membrane is inhibited and activated

266 ssion, affected the dynamic translocation of GLUT2 to the brush border membrane of RPTCs, and reduced

267 lucose-induced activation and recruitment of GLUT2 to the brush-border membrane.

268 ment of the facilitative glucose transporter GLUT2 to the brush-border membrane; regulation involves

269 elivers glucagon-like peptide 1 receptor and GLUT2 to the plasma membrane.

270 The ensuing inhibition of GLUT2 trafficking and absorption seems necessary to prev

271 mutant animals, as it activates insulin and Glut2 transcription.

272 Distinguishing GLUT2 transport in tissues where other GLUTs coexist is

273 ted that in long-term uncontrolled diabetes, GLUT2 transporters are overexpressed in renal tubules.

274 at, like mouse embryos, expresses functional GLUT2 transporters.

275 GLUT2 transports both glucose and fructose with low affi

276 porter 1 (SGLT-1) and glucose transporter 2 (GLUT2); various peptides and hormones control this proce

277 We investigated how GLUT2 was able to influence gut peptide secretion mediat

278 f transgenic islets, the glucose transporter GLUT2 was absent or severely reduced.

279 for the plasma membrane glucose transporter GLUT2 was decreased by 64% in the fasted and 93% in the

280 GLUT2 was detected on the apical side of Caco-2E cells,

281 pical side of Caco-2E cells, indicating that GLUT2 was in the correct orientation to be inhibited by

282 er the dominant intestinal sugar transporter GLUT2 was inhibited by intestinal luminal compounds that

283 peculiar double phenotype glucagon-positive/GLUT2(+) was observed.

284 encodes the facilitated glucose transporter GLUT2, was associated with a 0.17% (P = 6.6 x 10(-14)) g

285 ouse livers, and HNF6 binding to its target, Glut2, was determined by quantitative PCR.

286 he brush-border membrane (BBM) via SGLT1 and GLUT2 were analyzed.

287 of beta-cell-associated genes, insulin, and GLUT2 were decreased.

288 However, Pdx1, Nkx6.1, and GLUT2 were selectively lost in these insulin-deficient c

289 f the Na(+)/glucose cotransporter SGLT-1 and GLUT2 were unaffected in LEPR-B-KO jejunum, while GLUT5-

290 curs within minutes by an increase in apical GLUT2, which correlates with reciprocal regulation of T1