ライフサイエンスコーパス: GLUT2

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

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

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

4 ness can be augmented by the coexpression of GLUT2.

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

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

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

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

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

10 , and SGLT1 was required for upregulation of GLUT2.

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

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

13 Inhibition of apical GLUT2 absorption coincided with inhibition of unidirecti

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

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

16 Glucose uptake via GLUT2 also raises oocyte tonicity.

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

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

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

20 30 mmol/l glucose, in line with decreases in Glut2 and glucokinase gene expression, and attenuated gl

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

22 Conversely, GLUT2 and glucokinase mRNA levels were appropriately reg

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

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

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

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

27 GLUT2 and GLUT4 mRNA are not detected in chondrocytes.

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

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

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

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

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

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

34 ilability via inhibition of small intestinal GLUT2 and GLUT8.

35 iated by the facilitative sugar transporters GLUT2 and GLUT8.

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

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

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

39 Islet GLUT2 and insulin mRNA were measured with quantitative r

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

69 (6%), Cdx2 by 31% (10%), DPP-4 by 15% (6%), GLUT2 by 40% (11%), SLFN12 by 61% (14%), and sucrase-iso

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 There was no GLUT2 expression in the VMH.

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

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

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

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

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

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

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

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

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

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

103 GLUT2/GK coexpression further increased glycolytic flux

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 GLUT2 immunoreactivity was seen in the ependymal cells o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

149 8 express the glucose transporters GLUT1 and GLUT2, isoforms expressed in both normal and neoplastic

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

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

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

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

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

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

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

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

158 GLUT2 may be recruited from the basolateral to the apica

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

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

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

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

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

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

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

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

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

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

169 Given that GLUT2 modified gut peptide secretion stimulated by gluco

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

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

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

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

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

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

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

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

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

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

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

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

182 This apical GLUT2 pathway of intestinal sugar absorption is present

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

206 Loss of Glut2 suppressed hepatic glucose uptake but not glucose

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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