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 is a sodium/glucose cotransporter that moves two N

6 SGLT1 mRNA expression was determined by quantitative rev

7 SGLT1 mRNA levels varied significantly, with the maximum

8 SGLT1 was located in luminal membranes of cells immunopo

9 SGLT1-dependent glucose uptake occurs at the attachment

10 SGLT1-mediated glucose transport was assessed using ever

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

12 marily absorbed by Na-glucose cotransport 1 (SGLT1) and coupled NaCl by the dual operation of Na-H ex

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 propose that sodium-glucose cotransporter 1 (SGLT1) senses increases in luminal glucose at the macula

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

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

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

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

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

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

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

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

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

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

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

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

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 al levels of sodium hydrogen exchanger 3 and SGLT1, which regulate transport of sodium, glucose, and

36 via glucose transporter isoforms GLUT1-5 and SGLT1.

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

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

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

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

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

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

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

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

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

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

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

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

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

50 Maltase and SGLT1 capacities increased only sublinearly with load du

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

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

53 the sodium-glucose cotransporters SGLT2 and SGLT1 in the proximal tubule.

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

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

56 favorable transcellular Na gradient for BBM SGLT1 and NHE3.

57 lls resulted in selective stimulation of BBM SGLT1 and DRA or PAT1 but not NHE3.

58 TPase led to compensatory stimulation of BBM SGLT1 and DRA or PAT1, whereas NHE3 was unaffected.

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

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

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

62 intestinal GLUTs were inhibited by teas, but SGLT1 was not.

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

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

65 In addition, sodium-glucose cotransport by SGLT1 on macula densa cells triggers the production of n

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

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

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

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

70 ys a critical role in sugar translocation by SGLT1.

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

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

73 thout affecting intestinal glucose uptake by SGLT1.

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

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

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

77 e abundance of Na(+)-d-glucose cotransporter SGLT1 by blocking the exocytotic pathway at the trans-Go

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

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

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

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

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

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

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

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

86 the intestinal sodium/glucose cotransporter SGLT1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 10-13 form the sugar permeation pathway for SGLT1.

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

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

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

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

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

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

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

126 a densa; in the presence of tubular glucose, SGLT1 inhibits TGF and NO generation, but this action is

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

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

129 rat SGLT1, but increased transport by human SGLT1.

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

131 nvestigated whether QEP down-regulates human SGLT1 (hSGLT1) like hRS1-Reg(S20E) and whether human Na(

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

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

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

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

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

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

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

139 partners contributes to circadian changes in SGLT1 transcription.

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

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

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

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

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

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

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

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

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

149 d to inhibit GLUT2 and phloridzin to inhibit SGLT1.

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

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

152 ssive urea or water transport through intact SGLT1.

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

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

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

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

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

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

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

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

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

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

163 No SGLT1 charge movements were observed with the mutant pro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 ects of the epitope on critical functions of SGLT1.

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

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

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

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

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

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

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

189 3 nM) were considerably weaker inhibitors of SGLT1 (IC50 = 10-19 muM).

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

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

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

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

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

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

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

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

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

199 with the presteady-state charge movement of SGLT1.

200 0E) down-regulates the exocytotic pathway of SGLT1 at the trans-Golgi by inhibiting ODC.

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

202 QEP down-regulates the exocytotic pathway of SGLT1 similar to hRS1-Reg(S20E).

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

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

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

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

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

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

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

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

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

212 o address different conformational states of SGLT1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 rption from the novel coupling of stimulated SGLT1 with DRA or PAT1.

245 of the intestinal glucose transport system (SGLT1).

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

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

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

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

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

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

252 We also showed that SGLT1 is expressed at the macula densa; in the presence

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

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

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

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

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

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

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

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

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

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

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

264 cells, individual tea catechins reduced the SGLT1 gene, but not protein expression levels.

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

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

267 eration, but this action is blocked when the SGLT1 inhibitor KGA-2727 is present.

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

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

270 a follow the sugar transport pathway through SGLT1.

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

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

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

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

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

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

277 2 inhibition (phloretin), but in contrast to SGLT1 inhibition, phloretin did not eliminate the respon

278 as it largely depends on GLUT5 as opposed to SGLT1 transporters.

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

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

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

282 effect on the intestinal glucose transporter SGLT1.

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

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

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

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

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

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

289 on the small intestinal sugar transporters, SGLT1 and GLUTs (GLUT1, 2 and 5).

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 late the expression and activity of NOS1 via SGLT1, blunting the TGF response and promoting glomerula

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

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

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

298 imizing adverse side effects associated with SGLT1 inhibition.

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

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