ライフサイエンスコーパス: glucose transport

1 1) mRNA and protein levels and by inhibiting glucose transport.

2 restriction, through impaired transplacental glucose transport.

3 as the virtual absence of insulin-stimulated glucose transport.

4 GLUT4 levels and impaired insulin-stimulated glucose transport.

5 integrity and increase intestinal stress and glucose transport.

6 ed AS160 phosphorylation, thereby regulating glucose transport.

7 160 phosphorylation and subsequent adipocyte glucose transport.

8 3-L1 adipocytes inhibited insulin-stimulated glucose transport.

9 ) in adipocytes decreases insulin-stimulated glucose transport.

10 le cells is the basis for insulin-stimulated glucose transport.

11 ansporter expression and the preservation of glucose transport.

12 e precursor arginine to cells did not affect glucose transport.

13 so failed to affect metformin stimulation of glucose transport.

14 , and the single copy human protein, mediate glucose transport.

15 ocation to the plasma membrane and decreased glucose transport.

16 gnificantly inhibited contraction-stimulated glucose transport.

17 the R125W mutation on contraction-stimulated glucose transport.

18 wn of AMPD obviated metformin stimulation of glucose transport.

19 tes (4P) had no effect on insulin-stimulated glucose transport.

20 12 muscle cells impaired sorbitol-stimulated glucose transport.

21 tion-stimulated, but not insulin-stimulated, glucose transport.

22 auses an ATP deficiency owing to the loss of glucose transport.

23 , interacts with YES1, which plays a role in glucose transport.

24 is AS160, a negative regulator of adipocyte glucose transport.

25 ularly with regard to insulin stimulation of glucose transport.

26 sponse to PGC-1beta-induced insulin-mediated glucose transport.

27 and may play an important role in adipocyte glucose transport.

28 knockdown of ClipR-59 suppresses, adipocyte glucose transport.

29 etic subjects is mostly related to defective glucose transport.

30 as increased by a phorbol ester activator of glucose transport.

31 a postulated mediator for insulin-stimulated glucose transport.

32 ing to actin, and blocked insulin-stimulated glucose transport.

33 ated knockdown attenuates insulin-stimulated glucose transport.

34 n and high-fat diet reduced insulin-mediated glucose transport.

35 g a defect in insulin signaling to stimulate glucose transport.

36 reduced basal and abolished insulin-induced glucose transport.

37 , a pathway that increases fat oxidation and glucose transport.

38 evertheless can function interchangeably for glucose transport.

39 ession, adipogenesis, and insulin-stimulated glucose transport.

40 d insulin-stimulated GLUT4 translocation and glucose transport.

41 , in association with increased capacity for glucose transport.

42 y blunts the ability of insulin to stimulate glucose transport.

43 e and crucial mediator of insulin-stimulated glucose transport.

44 kt is essential for insulin's full effect on glucose transport.

45 important in the physiological regulation of glucose transport.

46 phosphorylation and the possible effects on glucose transport.

47 et GLUT4 preferentially over GLUT1 and block glucose transport.

48 s of exercise on intramuscular signaling and glucose transport.

49 and, together with Rlf, they ensure maximal glucose transport.

50 ose uptake and the membrane translocation of glucose transport 4 (GLUT4)).

51 dual component polyphenols inhibited (14)C-D-glucose transport across differentiated Caco-2/TC7 cell

52 Glucose transport across the blood brain barrier and int

53 e lacking astrocytic IRs indicates a role in glucose transport across the blood-brain barrier (BBB).

54 to mutations in SLC2A1, leads to failure of glucose transport across the blood-brain barrier and ina

55 ng chamber experiments revealed electrogenic glucose transport across the endometrium in wild type (S

56 cally simulate the effect of the hydrogel on glucose transport across the microdialysis membrane usin

57 a the immediate inhibition of amino acid and glucose transport across the plasma membrane.

58 ing of insulin analog to Glut suppresses the glucose transport activity of Glut to attenuate further

59 t positions 176 and 210 are critical for the glucose transport activity of SLC45A1.

60 Intracellular glucose transport activity of the p.Arg176Trp and p.Ala2

61 d physical state of the membrane bilayer and glucose transport activity via the glucose transporter G

62 relationship was established that indicated glucose transport activity was dependent on the presence

63 increased the ability of insulin to augment glucose transport activity, and the mechanism involved i

64 cle stems from defects in insulin-stimulated glucose transport activity.

65 to inhibit sodium-dependent and facilitative glucose transport activity.

66 sayed for their resistance to B. cinerea and glucose transport activity.

67 1 4P mutant decreased contraction-stimulated glucose transport, an effect prevented by concomitant di

68 ing consistent with reduced transendothelial glucose transport and a diagnostic criterion for the Glu

69 le IR in T2D involves a severe impairment of glucose transport and additional impairment in the effic

70 Intestinal glucose transport and blood glucose were elevated due to

71 Glucose transport and consumption were assayed using ex

72 hesized that via control of transendothelial glucose transport and contributing paracrine mechanisms

73 Metformin stimulated both glucose transport and fatty acid oxidation.

74 As metabolic pathway markers, we focused on glucose transport and fatty acid oxidation.

75 signaling is critical to insulin-stimulated glucose transport and GLUT4 translocation.

76 ative myosin 5a attenuate insulin-stimulated glucose transport and GLUT4 translocation.

77 h that of human erythrocytes, and identified glucose transport and glyceraldehyde-3-phosphate dehydro

78 sulin-resistant individuals, impaired muscle glucose transport and glycogen synthesis redirect energy

79 AMP-activated protein kinase (AMPK) promotes glucose transport and glycolysis for ATP production, whi

80 Glucose transport and glycolysis in activated CD4(+) T c

81 a cell function, including those involved in glucose transport and glycolysis, and isolated betaVhlKO

82 Conversely, cardiac glucose transport and glycolytic genes were activated in

83 Glucose transport and glycolytic metabolism carry the ri

84 overed that two metabolic regulatory points, glucose transport and HMS enzyme trafficking, are affect

85 ,8-tetrachlorodibenzo-p-dioxin (TCDD) alters glucose transport and increases serum lipid levels and b

86 m chow-fed lean mice to compound A increased glucose transport and insulin signaling.

87 nthesis that was accompanied by increases in glucose transport and intracellular [G6P].

88 The underlying mutations altered glucose transport and led to major shifts between homofe

89 sfunctional state 3 respiration, and altered glucose transport and lipolysis.

90 s indicate that HGF is a potent activator of glucose transport and metabolism and also a strong inhib

91 HGF, through its ability to stimulate glucose transport and metabolism and to impair FAO, may

92 Although striking similarities exist in glucose transport and metabolism between tumor cells and

93 Cells use complex mechanisms to regulate glucose transport and metabolism to achieve optimal ener

94 regulation of water homeostasis, blood flow, glucose transport and metabolism, the blood-brain barrie

95 riggers a signaling pathway independently of glucose transport and metabolism.

96 T1DM to assess regional differences in brain glucose transport and metabolism.

97 d molecular mechanisms perturbed by impaired glucose transport and metabolism.

98 fetal growth partially by altering placental glucose transport and mTOR signalling.

99 reduced the ability of insulin to stimulate glucose transport and phosphorylate Insulin receptor sub

100 We addressed the questions of how cerebral glucose transport and phosphorylation change under acute

101 hese data suggest that 1) insulin stimulates glucose transport and phosphorylation of AS160 and TBC1D

102 Insulin-stimulated glucose transport and phosphorylation of both AS160 and

103 Alterations in glucose transport and phosphorylation, as well as intrac

104 e phosphorylation of GLUT1 on S226 regulates glucose transport and propose that this modification is

105 Muscle contraction increases glucose transport and represents an alternative signalin

106 nergistic interaction between GLUT1-mediated glucose transport and the cell-cycle checkpoint kinases

107 nction underscores the rate-limiting role of glucose transport and the critical minute-to-minute depe

108 Glucose transport and translocation of glucose transport

109 ally substantial role of functional SGLTs in glucose transport and use.

110 ally substantial role of functional SGLTs in glucose transport and utilization.

111 anied by an impairment in insulin-stimulated glucose transport and, after prolonged silencing, a redu

112 glucose delivery), kinetics of bidirectional glucose transport, and glucose phosphorylation to interr

113 f FDG accumulation include tumor blood flow, glucose transport, and glycolytic rate, but the underlyi

114 a within 60 min, enhanced insulin-stimulated glucose transport, and improved glucose disposal without

115 s in glycolytic intermediates, reductions in glucose transport, and in levels of ATP, NADPH, and ulti

116 ucose tolerance, restored insulin-stimulated glucose transport, and increased insulin signaling in so

117 ciated with increased 18F-FDG incorporation, glucose transport, and lactate production.

118 mice, mice with genetically impaired muscle glucose transport, and monkeys with diet-dependent long-

119 accumulation of lipid droplets, induction of glucose transport, and secretion of adipokines signaling

120 tes both insulin- and contraction-stimulated glucose transport, and this occurs via distinct mechanis

121 , although AICAR-stimulated AMPK activation, glucose transport, and total glucose utilization were no

122 slocation to the cell surface and subsequent glucose transport are impaired in Tfam knockdown cells.

123 down in myocytes, wherein insulin effects on glucose transport are particularly relevant for understa

124 Finally, glucose-transport assay demonstrated that the KCl-F2 fra

125 ease is characterized by early reductions in glucose transport associated with diminished GLUT1 expre

126 e with the alternating conformer carrier for glucose transport but are consistent with either a multi

127 Complex I inhibitor rotenone also stimulated glucose transport but it inhibited fatty acid oxidation,

128 ter SGLT1 mediated efficient plasma membrane glucose transport but no detectable ER uptake, probably

129 randial glycemia independently on intestinal glucose transport but rather inhibiting gastric emptying

130 and 3) contraction stimulates PAS-TBC1D1 and glucose transport (but not PAS-AS160) in an AMPK-depende

131 generator 3-morpholinosydnonimine stimulated glucose transport, but inhibited fatty acid oxidation.

132 ed pACC and PAS-TBC1D1 and partially blocked glucose transport, but it did not significantly alter pA

133 Transplacental glucose transport by glucose transporter isoform 1 (GLUT

134 el syndrome-associated mutations invalidated glucose transport by hGLUT2 either through absence of pr

135 Insulin stimulates glucose transport by recruiting the GLUT4 glucose transp

136 Insulin signaling augments glucose transport by regulating glucose transporter 4 (G

137 Insulin increases glucose transport by stimulating the trafficking of intr

138 Insulin stimulates muscle glucose transport by translocation of GLUT4 to sarcolemm

139 Insulin stimulates glucose transport by triggering regulated delivery of in

140 Glucose transported by GLUT2 may act after metabolizatio

141 SGLT-mediated glucose transport can be estimated using alpha-methyl-4-

142 SGLT-mediated glucose transport can be estimated using alpha-methyl-4-

143 in adipose tissue, which has a 3-fold-higher glucose transport capacity.

144 to the fetus, despite an increased placental glucose transport capacity.

145 On a molecular basis, the glucose transport carried out by glucose transporter 3 (

146 n the R125W mutant reversed this decrease in glucose transport caused by the R125W mutant.

147 range in excess of water and had the desired glucose-transport characteristics.

148 nnels of uniform diameter, with reproducible glucose transport-characteristics.

149 nsistent with that determined previously for glucose transport, confirming the central role of this r

150 generation, that the EIIA(Glc) component of glucose transport could enhance cAMP production and that

151 The gene was heterologously expressed in a glucose transport-deficient Escherichia coli strain, whe

152 d cells, suggesting a possible alteration in glucose transport during infection.

153 e that GLUTs are sufficient for mediating ER glucose transport en route to the plasma membrane.

154 oduce truncated protein variants impaired in glucose transport, exhibited no significant defects in A

155 or accuracy is the physiological time lag of glucose transport from the vascular to the interstitial

156 n healthy adults, the physiological delay of glucose transport from the vascular to the interstitial

157 This glucose transport function was replaced by increased exp

158 and long-chain acyl-CoA synthetase (3), and glucose transport genes (glucose transporter-2 and insul

159 proteins involved in insulin signalling and glucose transport (GLUT4, Akt1 and Akt2) were unaffected

160 However, atazanavir, which does not inhibit glucose transport, had no effect.

161 d concomitantly inhibited insulin-stimulated glucose transport; here again, these depleting/inhibitor

162 methyl-D-glucose incorporation (a measure of glucose transport), hexokinase activity and subcellular

163 spanning membrane protein regulates cellular glucose transport illuminated a novel adaptation of the

164 ntrahippocampal inhibition of GluT4-mediated glucose transport impaired memory acquisition, but not m

165 and activate the insulin receptor, stimulate glucose transport in adipocytes, and reduce blood glucos

166 s a positive regulator of insulin-stimulated glucose transport in adipocytes.

167 Glucose transport in adipose cells is regulated by chang

168 When we found changes in adipocyte glucose transport in altered metabolic states, we were h

169 ylase (pACC; AMPK substrate), PAS-TBC1D1, or glucose transport in contraction-stimulated muscle.

170 Insulin stimulates glucose transport in fat and muscle cells by regulating

171 sults in an inhibition of insulin-stimulated glucose transport in fat cells, and likely contributes t

172 d did not significantly inhibit facilitative glucose transport in human adipocytes.

173 ment of Rac1 and its downstream signaling in glucose transport in insulin-sensitive and insulin-resis

174 ificity by using Akt2-specific regulation of glucose transport in insulin-stimulated adipocytes as a

175 ity of contraction and exercise to stimulate glucose transport in isolated muscles with AMPK loss of

176 of physiologically relevant phospholipids on glucose transport in liposomes containing purified GLUT4

177 ne whether Rac1 regulates insulin-stimulated glucose transport in mature skeletal muscle.

178 ed, and tested for their ability to increase glucose transport in mouse 3T3-L1 adipocytes, a surrogat

179 and KO of Rac1 decreased insulin-stimulated glucose transport in mouse soleus and extensor digitorum

180 h partially decreased contraction-stimulated glucose transport in mouse soleus and extensor digitorum

181 increases ROS, AMPKalpha phosphorylation and glucose transport in murine extensor digitorum longus (E

182 Insulin stimulates glucose transport in muscle and adipose tissue by produc

183 Insulin stimulates glucose transport in muscle and adipose tissue by transl

184 aPKC and Akt mediate the insulin effects on glucose transport in muscle and synthesis of lipids, cyt

185 the importance of aPKC in insulin-stimulated glucose transport in muscles of intact mice and show tha

186 rotein kinase C (aPKC) in insulin-stimulated glucose transport in myocytes and adipocytes is controve

187 at aPKCs are required for insulin-stimulated glucose transport in myocytes and adipocytes.

188 eptin 7 may participate in the regulation of glucose transport in podocytes.

189 ired insulin sensitivity in skeletal muscle, glucose transport in response to submaximal insulin (450

190 important effects of contraction to increase glucose transport in skeletal muscle are not well unders

191 Insulin stimulates glucose transport in skeletal muscle by GLUT4 translocat

192 ice also had impaired contraction-stimulated glucose transport in skeletal muscle, and knockdown of S

193 dy was to determine whether TBC1D1 regulates glucose transport in skeletal muscle.

194 a unique mediator of contraction-stimulated glucose transport in skeletal muscle.

195 D1, has been implicated in the regulation of glucose transport in skeletal muscle.

196 t significantly decreased insulin-stimulated glucose transport in the absence of changes in TBC1D1 PA

197 ted in a full blunting of insulin-stimulated glucose transport in the alpha2i TG mice.

198 a methodology for the noninvasive imaging of glucose transport in vivo with PET and (18)F-labeled 6-f

199 eding partially decreased insulin-stimulated glucose transport in wild-type mice, while high-fat feed

200 stimulates PAS-AS160 (but not PAS-TBC1D1 or glucose transport) in a PI 3-kinase/Akt-dependent manner

201 tochondrial function, insulin signaling, and glucose transport, in which impaired respiratory chain a

202 with functional A. thaliana SWEET1 inhibited glucose transport, indicating that homooligomerization i

203 yopathy, HIV protease inhibitors that impair glucose transport induce acute, decompensated heart fail

204 orylation, Glut4 membrane translocation, and glucose transport induced by insulin in 3T3-L1 adipocyte

205 ased state can be rescued by administering a glucose transport inhibitor.

206 y for glucose, and is inhibited by the human glucose transport inhibitors cytochalasin B, phloretin,

207 mal models by inducing glucosuria with renal glucose transport inhibitors.

208 robe as a tool for the identification of new glucose transport inhibitors.

209 Glucose-transport inhibitors killed trypanosomes without

210 ocused on understanding how insulin promotes glucose transport into adipocytes, a classic model of hi

211 discovery that adipocytes, and specifically glucose transport into adipocytes, regulate whole-body g

212 However, whether increasing glucose transport into either of these cell types offers

213 skeletal muscle, concomitant with increased glucose transport into extensor digitorum longus and gas

214 Insulin stimulates glucose transport into fat and muscle cells by increasin

215 GLUT4 controls glucose transport into fat and muscle tissues in respons

216 Glucose transport into mammalian cells is mediated by a

217 for improved insulin sensing with increased glucose transport into skeletal muscle and also reduced

218 T1 at the blood-brain barrier (BBB) mediates glucose transport into the brain.

219 fuse with the plasma membrane, facilitating glucose transport into the cell.

220 Glc-6-P), the first metabolite produced upon glucose transport into the cell.

221 bited expression of Glut1, which facilitated glucose transport into the cytoplasm; glyceraldehyde 3-p

222 rence signal and provide critical control of glucose transport into the particle.

223 Glucose transport is regulated by GLUT4 translocation in

224 ays jointly account for the entire signal to glucose transport is unknown.

225 The impact of glycemic variability on brain glucose transport kinetics among individuals with type 1

226 data suggest that whole-body alterations in glucose transport may be organ specific and facilitate n

227 Intramuscular signaling and glucose transport mechanisms contribute to improvements

228 d concomitantly inhibited insulin-stimulated glucose transport; more importantly, these depleting/inh

229 ous acetate can amend the lytic cycle of the glucose transport mutant.

230 A glucose transport-null strain of Saccharomyces cerevisia

231 and GLUT2 glucose transporters, reduced the glucose transport of almost 10 times.

232 the fructose transport of human GLUT2 or the glucose transport of human GLUT1-4 or bacterial GlcPSe.

233 t oxygen transport has a greater effect than glucose transport on the distribution of quiescent cells

234 AHR, inhibition of glycolysis, inhibition of glucose transport, or inhibition of enolase, increased S

235 ther by activation of the AHR, inhibition of glucose transport, or inhibition of enolase, was depende

236 cose relationship or the kinetics describing glucose transport over the blood-brain barrier differ be

237 t is consistent with the known properties of glucose transport, particularly with regard to insulin s

238 Results support use of the glucose transport pathway by cy-2-glu and fatty acid tra

239 th lower content/activity of key proteins in glucose transport/phosphorylation and storage.

240 The human blood-brain barrier glucose transport protein (GLUT1) forms homodimers and h

241 containing DNA encoding the wild-type human glucose transport protein (GLUT1), mutant GLUT1 (GLUT1(3

242 7 inhibits the erythrocyte sugar transporter glucose transport protein 1 (GLUT1) and examines the tra

243 Sodium-glucose transport protein 2 (SGLT2) inhibitors are a cla

244 ythrocyte hexose transfer is mediated by the glucose transport protein GLUT1 and is characterized by

245 e mutagenesis studies suggest that the human glucose transport protein GLUT1 and its distant bacteria

246 rification and characterization of an active glucose transport protein member of the TC 2.1.7 subgrou

247 The insulin-sensitive isoform of the glucose transporting protein, Glut4, is expressed in fat

248 n conjugates that are putative substrates of glucose transport proteins (GLUTs) and possess hypoxia-s

249 omotes recovery by stopping the synthesis of glucose transport proteins, which in turn limits the acc

250 There also is limited evidence for a role of glucose transport proteins.

251 action-stimulated PAS-AS160, PAS-TBC1D1, and glucose transport, rat epitrochlearis was incubated with

252 nied by a decrease in the insulin-stimulated glucose transport rate, and neither response was affecte

253 and also causes a large decrease in the net glucose transport rate.

254 hole-brain CMRglc (along with blood-to-brain glucose transport rates and brain glucose concentrations

255 at aPKCs are required for insulin-stimulated glucose transport, recent findings in studies of aPKC kn

256 ceptor coactivator (PGC)-1alpha, involved in glucose transport regulation and mitochondrial biogenesi

257 At day 19, placental glucose transport remained high in C9 mice while MeAIB t

258 ng of the structural biology of facilitative glucose transport remains elusive.

259 vents following Akt activation which mediate glucose transport stimulation remain relatively unknown.

260 s of novel compounds were prepared and their glucose transport stimulatory activities were measured u

261 loyl-alpha-D-xylopyranose (59), also possess glucose transport stimulatory activity suggests that 2 m

262 yranose (80) exhibits a significantly higher glucose transport stimulatory activity than 2.

263 carbohydrate digestion and enteral or renal glucose transport, suggesting that genetic variants asso

264 showing no effect on contraction-stimulated glucose transport, suggests that one or more AMPK-relate

265 ual targeting of the DNA damage response and glucose transport synergistically induces apoptosis in K

266 be limited by the capacity of the intestinal glucose transport system (SGLT1).

267 n source via the binding of EIIA(Glc) of the glucose transport system to the GGDEF-EAL domain protein

268 at are homologous to an ATP-binding cassette glucose transport system, although the PBP sequence is h

269 This is due in part to an increase in glucose transport that occurs in the working skeletal mu

270 results identify PON2 as a new modulator of glucose transport that regulates a pharmacologically tra

271 ur negative regulators of insulin-responsive glucose transport: the protein kinases PCTAIRE-1 (PCTK1)

272 IVAS stimulated a dose-dependent increase in glucose transport through glucose transporter GLUT4- and

273 found that prolonged hippocampal blockade of glucose transport through GluT4-upregulated markers of h

274 In addition, microsphere swelling reduced glucose transport through the coatings in PBS media and

275 T2DM had significantly greater maximal renal glucose transport (TmG) compared with subjects without d

276 ernal hepatic glucose handling and placental glucose transport together with insulin signalling in th

277 strated that the uptake of nonphosphorylated glucose transport tracer (18)F-6FDG is sensitive to insu

278 When brain regions were compared, glucose transport under hypoglycemia was lowest in the h

279 With glucose transport via GLUT1, the higher maximal rate and

280 ase 2 (PON2), which regulates GLUT1-mediated glucose transport via stomatin.

281 beta2 KO or alpha2KD, contraction-stimulated glucose transport was almost completely inhibited.

282 Glucose transport was assayed following expression of SL

283 SGLT1-mediated glucose transport was assessed using everted rings of di

284 sulin sensitive than controls, and augmented glucose transport was identified in both adipose and ske

285 The increase in insulin-stimulated glucose transport was less (P < 0.01) in T2D (twofold) t

286 In incubated muscle, glucose transport was measured by 2-deoxy-D-[(3)H]-gluco

287 eins in mouse tibialis anterior muscles, and glucose transport was measured in vivo.

288 Glucose transport was moderately though significantly in

289 Further evidence for UDP-glucose transport was obtained by expression of ZK 896.9

290 in S21A-C/EBPalpha cells, insulin-responsive glucose transport was reconstituted, suggesting that the

291 On the control diet, insulin-stimulated glucose transport was reduced by approximately 50% in al

292 Discovery of intestinal sodium-glucose transport was the basis for development of oral

293 keletal muscle, whereas insulin signaling in glucose transport was unaffected by hypoglycemia.

294 The effects of apelin on (14)C-labeled glucose transport were determined in jejunal loops and i

295 )F-FDG uptake, hexokinase (HK) activity, and glucose transport were measured in each clone and in the

296 yed severely impaired contraction-stimulated glucose transport, whereas exercise-stimulated glucose u

297 ntire ex vivo contraction response in muscle glucose transport, whereas only Rac1, but not alpha2 AMP

298 W mutation of TBC1D1 impairs skeletal muscle glucose transport, which could be a mechanism for the ob

299 forkhead box O transcriptional signaling or glucose transport, which may also impair cardiac metabol

300 ently, suppression of GLUT4 or inhibition of glucose transport with the HIV protease inhibitor ritona