ライフサイエンスコーパス: SGLT1

1 SGLT1 activity is paradoxically higher for mice consumin

2 SGLT1 and SGLT2 mRNA and protein expression decreased un

3 SGLT1 enables the small intestine to absorb glucose and

4 SGLT1 expression was determined using transport studies,

5 SGLT1 incorporates 14 membrane spans.

6 SGLT1 is a sodium/glucose cotransporter that moves two N

7 SGLT1 mRNA expression was determined by quantitative rev

8 SGLT1 mRNA levels varied significantly, with the maximum

9 SGLT1 was located in luminal membranes of cells immunopo

10 SGLT1-dependent glucose uptake occurs at the attachment

11 SGLT1-mediated glucose transport was assessed using ever

12 SGLT1-mediated Na-glucose co-transport stimulates NHE3 a

13 /insertion of Na(+)/glucose cotransporter 1 (SGLT1) and of aquaporin 1 (Aqp1), a water channel, at th

14 ion of the sodium-D-glucose cotransporter 1 (SGLT1) and of the concentrative nucleoside transporter 1

15 Na(+)-d-glucose cotransporter 1 (SGLT1) is rate-limiting for glucose absorption in the sm

16 The sodium-glucose cotransporter 1 (SGLT1) substrate alpha-MG induced secretion, and the res

17 NHE3 and the sodium/glucose cotransporter 1 (SGLT1) were studied by fluorometry, before and after siR

18 he sodium-dependent glucose cotransporter 1 (SGLT1) with phloridzin partially inhibited GIP, GLP-1 an

19 e high affinity Na+/glucose cotransporter 1 (SGLT1), which absorbs dietary glucose and galactose, exh

20 Na(+)-glucose cotransporter 1 (SGLT1)-mediated glucose uptake leads to activation of Na

21 signaled by sodium-glucose cotransporter-1 (SGLT1), sweet taste receptors, or both.

22 ium-dependent glucose transporter isoform 1 (SGLT1).

23 ium-dependent glucose transporter protein 1 (SGLT1), was not regulated by luminal fructose.

24 in, mucin 2, Na(+)/glucose co-transporter 1 (SGLT1) and transcription factors, Hes1, HATH1, NeuroD1,

25 nmetabolizable sodium-glucose transporter 1 (SGLT1) substrate, methyl-alpha-D-glucopyranoside (alpha-

26 Accordingly, SGLT1 deficiency did not prevent HG-induced NOX2 activat

27 rt the discovery of LX2761, a locally acting SGLT1 inhibitor that is highly potent in vitro and delay

28 The high affinity SGLT1, found in the S3 segment, has a coupling ratio of

29 PK to Akt2, ezrin, and NHE3 activation after SGLT1-mediated transport.

30 mammalian proteins, 457, is conserved in all SGLT1 proteins as glutamine.

31 n bronchoalveolar lavage (BAL); and alveolar SGLT1 was analyzed by immunohistochemistry.

32 y, the results indicate a relationship among SGLT1 activity, ASL glucose concentration and pulmonary

33 the abundance of ovine intestinal HNF-1 and SGLT1 transcripts during transition from preruminant to

34 A significant increase in mucin 2 and SGLT1 expression was detected in the obese duodenum.

35 via glucose transporter isoforms GLUT1-5 and SGLT1.

36 ium glucose up-regulated SGLT1 abundance and SGLT1 promoter activity, and increased intracellular cAM

37 functional inhibition of host-cell AQP1 and SGLT1 hampers C. parvum invasion of cholangiocytes.

38 -mediated dUTP nick-end labeling assay), and SGLT1 in situ hybridization.

39 e amounts of SGLT1 and GLUT2 in the BBM, and SGLT1 was required for upregulation of GLUT2.

40 In the absence of substrate, GAT1 and SGLT1 exhibited charge movements that manifested as pre-

41 decreased the apparent affinity of GAT1 and SGLT1 for Na(+) and the organic substrate.

42 Thus, in both GAT1 and SGLT1, Cl(-) modulates the kinetics of cotransport by al

43 ) and Na(+)/glucose cotransporters (GAT1 and SGLT1, respectively) expressed in Xenopus laevis oocytes

44 ion showed a significant decrease in GGT and SGLT1, consistent with membrane internalization.

45 ibit intestinal sugar transporters GLUT5 and SGLT1 that were injected and expressed in Xenopus oocyte

46 jor intestinal sugar transporters, GLUT5 and SGLT1, were unaffected by flavonoids.

47 GLUT2, GLUT5, and SGLT1 did not transport DHA and none of the isoforms tra

48 Unbinding forces between ligands and SGLT1 were recorded at different loading rates by changi

49 Maltase and SGLT1 capacities increased only sublinearly with load du

50 ition resulted in an increase in maltase and SGLT1 capacities mediated non-specifically by an increas

51 ed expression and protein levels of NHE3 and SGLT1 in the brush border membrane.

52 f glucose in the kidney along with SGLT2 and SGLT1.

53 one precursors was synthesized and tested as SGLT1/SGLT2 inhibitors using a cell-based fluorescence a

54 Because SGLT1 mRNA levels also varied in rhesus monkeys (offset

55 The differences between SGLT1 and SGLT2 were that (i) the apparent affinity cons

56 former indicates that in the membrane-bound SGLT1 the pathway to sugar translocation involves severa

57 f the GLUT2-mediated component controlled by SGLT1 through the glucose-induced activation and recruit

58 Na(+)/glucose cotransport by SGLT1 is a tightly coupled process that is driven by the

59 testinal D-glucose absorption is mediated by SGLT1 localized in the brush border membrane of small in

60 intestinal BBM was predominantly mediated by SGLT1, independent the glucose load.

61 Mannitol was transported by C5 but not by SGLT1 or control oocytes.

62 MDG uptake by E225A was identical to that by SGLT1, whereas transport was reduced by over 90% for D27

63 ys a critical role in sugar translocation by SGLT1.

64 nal glucose absorption in which transport by SGLT1 induces rapid insertion and activation of GLUT2 in

65 In contrast, Cl(-) was not transported by SGLT1.

66 thout affecting intestinal glucose uptake by SGLT1.

67 high affinity Na(+)-coupled glucose carrier SGLT1.

68 fection of cholangiocytes recruits host-cell SGLT1, a Na+/glucose cotransporter, and aquaporin 1 (AQP

69 S1-Reg blocks release of vesicles containing SGLT1 or concentrative nucleoside transporter 1.

70 the intestinal sodium/glucose cotransporter SGLT1 by its substrate glucose and sweet taste analogs.

71 ology of the human Na+/glucose cotransporter SGLT1 has been probed using N-glycosylation scanning mut

72 ications of the sodium glucose cotransporter SGLT1 in either pumping water or passively channeling wa

73 ogical role of Na(+)-D-glucose cotransporter SGLT1 in small intestine and kidney, Sglt1(-/-) mice wer

74 n of the Na(+)-coupled glucose cotransporter SGLT1 is regulated post-transcriptionally at the level o

75 In contrast, the Na(+)-glucose cotransporter SGLT1 mediated efficient plasma membrane glucose transpo

76 The sodium-dependent glucose cotransporter SGLT1 undergoes a series of voltage- and ligand-induced

77 he electrogenic sodium-glucose cotransporter SGLT1, or by closure of ATP-sensitive potassium channels

78 nt mediated by the Na+-glucose cotransporter SGLT1.

79 the intestinal sodium/glucose cotransporter SGLT1.

80 minal half of the Na+/glucose cotransporter (SGLT1) contains the sugar permeation pathway, a cDNA con

81 for example, the Na+/glucose cotransporter (SGLT1) couples sugar transport to Na+ gradients across t

82 The Na(+)/glucose cotransporter (SGLT1) is highly selective for its natural substrates, d

83 ne domains of the Na+/glucose cotransporter (SGLT1) that form salt bridges, to obtain information abo

84 it isoform of the Na+/glucose cotransporter (SGLT1) was examined using the twoelectrode voltage clamp

85 eptidase (GGT), Na(+)-glucose cotransporter (SGLT1), and apically biotinylated proteins, were not she

86 and GLUT9), a sodium-glucose cotransporter (SGLT1), and two components of the ATP-gated K(+) (K(ATP)

87 ion domain of the Na+/glucose cotransporter (SGLT1).

88 of the intestinal Na+/glucose cotransporter, SGLT1, in many species.

89 t by the apical Na(+)-glucose cotransporter, SGLT1, triggers translocation of NHE3, Na(+)-H(+) antipo

90 r membrane by the Na+/glucose cotransporter, SGLT1.

91 he kidney by two Na+/glucose cotransporters (SGLT1 and SGLT2).

92 es in regulating Na+/glucose cotransporters, SGLT1, expressed in Xenopus laevis oocytes.

93 se SGLT1 activity) or phlorizin (to decrease SGLT1 activity); 2 hours later, glucose concentration an

94 nt bacterial proliferation whereas decreased SGLT1 activity can exacerbate it.

95 RS1-Reg-derived peptides that downregulate SGLT1 at high intracellular glucose concentrations may b

96 btained a RS1-Reg variant that downregulates SGLT1 in the brush-border membrane at high luminal gluco

97 ols injected with H(2)O or with RNA encoding SGLT1, NKCC2, or PepT1.

98 the epitope tag is dominant over endogenous SGLT1 apical targeting information and can direct polyto

99 G-protein (Gi)-specific inhibitor, enhanced SGLT1 protein abundance to levels observed in response t

100 investigated the role of alveolar epithelial SGLT1 activity on ASL glucose concentration and bacteria

101 apitulate a monolayer phenotype only express SGLT1 at low levels.

102 by control oocytes and by oocytes expressing SGLT1 and C5 was studied by uptake measurements of the 1

103 lockers, the Lp values of oocytes expressing SGLT1 and GAT1 were indistinguishable from the Lp of con

104 ments into Xenopus laevis oocytes expressing SGLT1 or CNT1 and measuring the expressed uptake of alph

105 Shortly after intake of glucose-rich food, SGLT1 abundance in the luminal membrane of the small int

106 oefficient for Na+ was 1 for SGLT2 but 2 for SGLT1.

107 to 2.4 for maltase, and from 1.1 to 0.5 for SGLT1.

108 binding is increased from 10 x 5 x 5 (A) for SGLT1 to 11 x 18 x 5 (A) for the chimera.

109 The apparently low safety factor for SGLT1 is made possible by the contribution of hindgut fe

110 ours, before harvest of proximal jejunum for SGLT1 analysis with Western blotting and quantitative po

111 ants (K(0.5)) for Cl(-) of 21 and 115 mm for SGLT1 and GAT1, respectively.

112 10-13 form the sugar permeation pathway for SGLT1.

113 -state kinetic model previously proposed for SGLT1 indicated that many of the kinetic properties obse

114 f sugar into the enterocytes is required for SGLT1 induction, and delineate the signal-transduction p

115 in the model, suggesting a crucial role for SGLT1 in triggering GLP-1 release in agreement with expe

116 opyranoside (0.2 mM) was similar to that for SGLT1, and like SGLT1 the chimera transported D-galactos

117 is sensed by a glucose sensor, distinct from SGLT1, residing on the external face of the lumenal memb

118 e glycol) 600 led to induction of functional SGLT1, but the compound did not inhibit Na+/glucose tran

119 The resultant chimeric globin/SGLT1 mRNA expressed after transfection into LLC-PK1 cel

120 The rabbit Na+-glucose (SGLT1) and the human Na+-Cl--GABA (GAT1) cotransporters

121 onsistent with a role in sweet taste, GLUT4, SGLT1, and SUR1 were expressed preferentially in T1r3-po

122 o acid level) to its high affinity homologue SGLT1.

123 rat SGLT1, but increased transport by human SGLT1.

124 hC5 (the human equivalent of C5), hC4 (human SGLT1 amino acids 407-648, helices 10-13), and hN13 (ami

125 in with 70% amino acid identity to the human SGLT1.

126 lectively inhibited human SGLT2 versus human SGLT1, the major cotransporter of glucose in the gut, an

127 In healthy humans, SGLT1 substrates stimulate GLP-1 and GIP and slow gastri

128 orrelation spectroscopy served to assess (i) SGLT1 abundance in both vesicles and plasma membranes an

129 In SGLT1, substitution of H+ or Li+ for Na+ caused a kineti

130 T3b mutants that recapitulate residue 457 in SGLT1 and hSGLT3, glutamine and glutamate, respectively.

131 ease in apical GLUT2 level, but no change in SGLT1 level.

132 partners contributes to circadian changes in SGLT1 transcription.

133 Malabsorption (GGM) is caused by a defect in SGLT1.

134 ated secretion of gut hormones implicated in SGLT1 up-regulation.

135 SGLT known to be of functional importance in SGLT1 were replaced individually with cysteine in the cy

136 trium in wild type (Slc5a1 (+/+)) but not in SGLT1 deficient (Slc5a1 (-/-)) mice.

137 f D-glucose led to 2.9-fold up-regulation in SGLT1 compared with water or iso-osmotic D-mannitol; thi

138 ces, suggests that residue 460 (threonine in SGLT1, and serine in SGLT2 and SGLT3) are involved in hy

139 Because the daily variation in SGLT1 activity is established by the feeding schedule (w

140 ated with saline, isoproterenol (to increase SGLT1 activity) or phlorizin (to decrease SGLT1 activity

141 isk, such as in diabetic subjects, increased SGLT1 activity may prevent bacterial proliferation where

142 ry sugar and artificial sweeteners increased SGLT1 mRNA and protein expression, and glucose absorptiv

143 d to inhibit GLUT2 and phloridzin to inhibit SGLT1.

144 ical GLUT2 but not the phloretin-insensitive SGLT1 component of glucose absorption in rat jejunum per

145 cal GLUT2, but not the phloretin-insensitive SGLT1 component of glucose absorption.

146 ssive urea or water transport through intact SGLT1.

147 Intestinal SGLT1 is a putative target for antidiabetic therapy; how

148 the activity, and expression, of intestinal SGLT1 is regulated by dietary sugars.

149 this paper that regulation of the intestinal SGLT1 gene by lumenal sugar is due, in part, to an incre

150 glucose-induced activation of the intestinal SGLT1 promoter and identification of a glucose-responsiv

151 Seven SGLT isoforms (SGLT1 to 6 and sodium-myoinositol cotransporter-1, SMIT1

152 tivity characteristics of the SGLT isoforms (SGLT1 transports both glucose and galactose, but SGLT2 a

153 In the kidney, SGLT1 reabsorbed approximately 3% of the filtered glucos

154 Like SGLT1 in choline buffer, the C5-mediated uptake was inse

155 mM) was similar to that for SGLT1, and like SGLT1 the chimera transported D-galactose and 3-O-methyl

156 in the 3'-UTR as critical for cAMP-mediated SGLT1 message stabilization.

157 We monitored SGLT1 kinetics, the number of SGLT1 cotransporters in th

158 -tagged SGLT1 was similar to that for native SGLT1.

159 When compared with native SGLT1 transfectants, the apparent Km for sugar transport

160 No SGLT1 charge movements were observed with the mutant pro

161 The nonmetabolized SGLT1 substrate alpha-methyl-D-Glu (alpha-MD-G) activate

162 wed that NHE3 colocalizes with SGLT2 but not SGLT1 in the rat renal proximal tubule.

163 vels of apical GLUT2 and PKC betaII, but not SGLT1.

164 hich contains transmembrane helices 10-14 of SGLT1 and functions as a low affinity glucose uniporter,

165 In the absence of SGLT1 activity (or presence of phloridzin), the secretio

166 (P < 0.02) C. parvum-induced accumulation of SGLT1 at infection sites (by approximately 80%).

167 activity and (ii) the apparent affinities of SGLT1 for Na+, and indirectly sugar in the cotransport m

168 cose concentrations increased the amounts of SGLT1 and GLUT2 in the BBM, and SGLT1 was required for u

169 hus, to facilitate studies of the biology of SGLT1 function in epithelial monolayers, we engineered a

170 In the case of SGLT1, we suggest that both the water channel and water

171 or this post-translational downregulation of SGLT1 and CNT1.

172 We suggest that the downregulation of SGLT1 contributes to the body-weight independent improve

173 in the small intestine by downregulation of SGLT1-mediated glucose uptake.

174 testine resulted in > 50-fold enhancement of SGLT1 expression.

175 cAMP-PKA pathway resulting in enhancement of SGLT1 expression.

176 tory increases in activity and expression of SGLT1 and other GLUTs.

177 Although expression of SGLT1 is regulated by luminal monosaccharides, the lumin

178 terocytes, it is unclear whether function of SGLT1 is altered by DJB and whether this contributes to

179 ects of the epitope on critical functions of SGLT1.

180 ve carboxy-terminal transmembrane helices of SGLT1 form a channel for the permeation of small molecul

181 The impact of SGLT1 on renal glucose handling was investigated by micr

182 Simultaneous inhibition of SGLT1 and GLUT2 in high stress perfusions with phloridzi

183 all interfering RNA (siRNA) or inhibition of SGLT1 by a specific pharmacologic inhibitor, phlorizin.

184 nital infection, and excessive inhibition of SGLT1 can cause gastro-intestinal symptoms.

185 Inhibition of SGLT1 does not affect actin accumulation but decreases t

186 Inhibition of SGLT1 may offer a potential therapeutic target to dimini

187 nsitive (a specific competitive inhibitor of SGLT1).

188 3 nM) were considerably weaker inhibitors of SGLT1 (IC50 = 10-19 muM).

189 d phloretin, specific phenolic inhibitors of SGLT1 and GLUT2 glucose transporters, reduced the glucos

190 induces membrane translocation/insertion of SGLT1/Aqp1 are obscure.

191 e life time increased for the interaction of SGLT1 with thioglucose (coupled via acrylamide to a long

192 is sugar selectivity on the human isoform of SGLT1, single site mutants of hSGLT1, and the pig SGLT3

193 he effect of H+, Li+, and Na+ on kinetics of SGLT1 was compared to the effects of these cations on th

194 ere used: (i) immunohistochemical mapping of SGLT1 and SGLT2 distribution in tumors; (ii) measurement

195 The model of SGLT1 secondary structure and the predicted helix ends s

196 On a structural model of SGLT1, based on the homology structure of vSGLT, we iden

197 inal tag leads to selective modifications of SGLT1 function; 3) the kinetics of sugar transport can b

198 with the presteady-state charge movement of SGLT1.

199 We monitored SGLT1 kinetics, the number of SGLT1 cotransporters in the plasma membrane, and plasma

200 of the RS1-Reg-blocked exocytotic pathway of SGLT1 between meals.

201 since this is the least conserved portion of SGLT1.

202 DJB induced a 50% reduction of SGLT1-mediated glucose uptake into enterocytes of duoden

203 We conclude that: (i) the regulation of SGLT1 expression in oocytes by protein kinases occurs ma

204 e intestinal sugar sensing and regulation of SGLT1 mRNA and protein.

205 osphorylation, RS1-Reg blocks the release of SGLT1-containing vesicles from the Golgi in a glucose-de

206 ucose-induced acceleration of the release of SGLT1-containing vesicles from the trans-Golgi network (

207 ine by ODC1 at the TGN stimulates release of SGLT1-containing vesicles.

208 Our findings demonstrate a dominant role of SGLT1 in controlling glucose-stimulated GLP-1 release in

209 indirectly, (i) the rate and selectivity of SGLT1 uniport activity and (ii) the apparent affinities

210 tly of influences on the Na+-binding site of SGLT1; and 4) the weak basolateral targeting sequence pr

211 o address different conformational states of SGLT1.

212 glucose (3OMG; a nonmetabolized substrate of SGLT1), or 60 mg sucralose was consumed 15 min before a

213 These data show that 1) the C terminus of SGLT1 is intracellular; 2) disruption of protein structu

214 sorption can be explained solely in terms of SGLT1 and that a passive or paracellular component plays

215 ransport characteristics similar to those of SGLT1 in the absence of Na+: 1) selective (alphaMDG > D-

216 ugar cotransport by blocking the transfer of SGLT1 protein from the endoplasmic reticulum to the plas

217 We showed that upregulation of SGLT1 in the small intestine after glucose ingestion is

218 ough the similarity between the pf values of SGLT1 and aquaporin-1 makes a transcellular pathway plau

219 l, most likely Ca(v)1.3, and is dependent on SGLT1.

220 e ODC1 product putrescine, and/or glucose on SGLT1 expressed in oocytes of Xenopus laevis were invest

221 y the fact that phloridzin inhibits not only SGLT1 but also indirectly that part of the GLUT2-mediate

222 tigated these 7 isoforms and found that only SGLT1 and SMIT1 were expressed in mouse, rat and human h

223 ntestinal mass, without change in maltase or SGLT1 activities per milligram of tissue.

224 Selective inhibition of SGLT2 over SGLT1 is critical for minimizing adverse side effects as

225 Here we overexpressed SGLT1 in MDCK cell monolayers and reconstituted the puri

226 e in the glucose responsiveness of the ovine SGLT1 gene.

227 e identified the minimal region of the ovine SGLT1 promoter able to support transcription.

228 of a glucose-responsive region of the ovine SGLT1 promoter.

229 ine SGLT2 and amino acids 381-662 of porcine SGLT1.

230 In oocytes expressing rabbit SGLT1 8-Br-cAMP increased by 28 +/- 4% (n = 10), and DOG

231 way, a cDNA construct (C5) coding for rabbit SGLT1 amino acids 407-662, helices 10-14, was expressed

232 uggests that protein kinases regulate rabbit SGLT1 activity by controlling the distribution of transp

233 in oocytes expressing rabbit, human, and rat SGLT1 isoforms, but with activation of PKC the response

234 maximum rate of transport by rabbit and rat SGLT1, but increased transport by human SGLT1.

235 During ATP recovery, SGLT1 transport activity remained profoundly depressed e

236 metabolisable and nonmetabolisable, regulate SGLT1 expression.

237 d that increased medium glucose up-regulated SGLT1 abundance and SGLT1 promoter activity, and increas

238 te signaling elements involved in regulating SGLT1 expression could provide novel therapeutic targets

239 To delineate the mechanisms regulating SGLT1, its expression was examined in rats maintained in

240 main sodium-glucose cotransporters (SGLTs), SGLT1 and SGLT2, provide new therapeutic targets to redu

241 Similarly, SGLT1 knockdown improved the glucagon and epinephrine re

242 The specific SGLT1 and GAT1 Lp values were obtained by measuring Lp i

243 n diabetic animals: isoproterenol stimulated SGLT1 migration to luminal membrane, and reduced (50%) t

244 n of the small apical pool of epitope-tagged SGLT1 (by selective inhibition of basolateral epitope-ta

245 terations in sugar transport, epitope-tagged SGLT1 could promote absorptive Na+ currents.

246 bsequent detailed analyses of epitope-tagged SGLT1 using stably transfected clones derived from the C

247 ontrast, the apparent KNa for epitope-tagged SGLT1 was similar to that for native SGLT1.

248 ive inhibition of basolateral epitope-tagged SGLT1) revealed that, despite the documented kinetic alt

249 to 7.37 mM for native versus epitope-tagged SGLT1).

250 as synthesized in 20-fold higher levels than SGLT1.

251 Our data indicate that SGLT1 activity is the driving force for glucose-stimulat

252 The data indicate that SGLT1 is 1) pivotal for intestinal mass absorption of d-

253 We have previously proposed that SGLT1 contains separate Na(+)- and glucose-binding domai

254 periments on mouse small intestine show that SGLT1 accounts for two-thirds of the passive water flow

255 These findings suggest that SGLT1 in the VMH plays a significant role in the detecti

256 The SGLT1 transcription rate was 7-fold higher in the mornin

257 cretion, and the response was blocked by the SGLT1 inhibitor phlorizin or by replacement of extracell

258 ssociated viral vector containing either the SGLT1 short hairpin RNA (shRNA) or a scrambled RNA seque

259 llows us to propose a testable model for the SGLT1 sugar binding site.

260 the study were to identify mutations in the SGLT1 gene and to determine the defect in sugar transpor

261 ters with GGM had a missense mutation in the SGLT1 gene.

262 clear factor 1 (HNF-1) was identified in the SGLT1 promoter that formed different complexes with smal

263 nding diminution in apical GLUT2 levels: the SGLT1 component and its level were unaltered by stress.

264 However, genetic testing of the SGLT1 (SLC5A1) gene was negative and, indeed, feeding ma

265 ifferentiating the eukaryotic members of the SGLT1 family from bacterial homologues.

266 ted that cAMP-dependent stabilization of the SGLT1 message was correlated with the protein phosphoryl

267 Glucose-induced activation of the SGLT1 promoter was mimicked by the protein kinase A (PKA

268 nce changes (milliseconds) were close to the SGLT1 capacitive charge movements.

269 ed by choline, which is not transported, the SGLT1 Lp was indistinguishable from that in Na+ or Li+,

270 (alpha-MGP), stimulated release, whereas the SGLT1 inhibitor phloridzin (luminally) abolished respons

271 glucose transportation into the cell through SGLT1 cotransporters can induce Ca(2+) influx and releas

272 a follow the sugar transport pathway through SGLT1.

273 Water permeation through SGLT1 and other transporters bears directly on the struc

274 thway activated by glucose transport through SGLT1 and also involves mitogen-activated protein kinase

275 for passive Na+ and water transport through SGLT1 were 21 and 5 kcal mol-1, respectively.

276 Passive Na+ and water transport through SGLT1 were blocked by phlorizin with the same sensitivit

277 rdiomyocytes, galactose (transported through SGLT1) did not activate NOX2.

278 symporters, three aromatic residues in TM6 (SGLT1 W289, Y290, and W291) are conserved in only those

279 2 inhibition (phloretin), but in contrast to SGLT1 inhibition, phloretin did not eliminate the respon

280 Similar to SGLT1, the C5-urea uptake was cation independent, linear

281 rmine whether the sodium-glucose transporter SGLT1 in the ventromedial hypothalamus (VMH) plays a rol

282 ltase in series with the glucose transporter SGLT1, for comparison with previous studies of sucrase a

283 effect on the intestinal glucose transporter SGLT1.

284 namics of the sodium glucose co-transporter (SGLT1) upon substrate and inhibitor binding on the singl

285 ts in the Na+-dependent glucose transporter (SGLT1) are associated with the disorder glucose-galactos

286 The Na+-dependent glucose transporter (SGLT1) mediates absorption of luminal glucose by the int

287 n the expression of the glucose transporters SGLT1 and SGLT2 under hypoxic conditions which implies a

288 f HIF-1alpha and of the glucose transporters SGLT1, SGLT2, and GLUT1.

289 ssenger RNAs encoding the sugar transporters SGLT1, GLUT1, GLUT2, GLUT3, GLUT4, and GLUT5.

290 s in the oocyte were comparable to wild-type SGLT1, but no complex glycosylation was detected.

291 d despite glucose constituting the load upon SGLT1.

292 e absorption comprises active absorption via SGLT1 and facilitated absorption via GLUT2 in the apical

293 n across the brush-border membrane (BBM) via SGLT1 and GLUT2 were analyzed.

294 The shRNA reduced VMH SGLT1 expression by 53% in nondiabetic rats, and this au

295 The glucose-induced component was SGLT1-dependent and nifedipine-sensitive.

296 ted at the basolateral, vascular side, while SGLT1 is exposed to luminal glucose at the apical side o

297 imizing adverse side effects associated with SGLT1 inhibition.

298 in wild type and G457E-mSGLT3b compared with SGLT1 and the sugar-activated cation transport without s

299 tially uncoupled stoichiometry compared with SGLT1, suggesting that mSGLT3b is also a sugar sensor.