ライフサイエンスコーパス: glucose transport

1 ed AS160 phosphorylation, thereby regulating glucose transport.

2 160 phosphorylation and subsequent adipocyte glucose transport.

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

4 ) in adipocytes decreases insulin-stimulated glucose transport.

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

6 ansporter expression and the preservation of glucose transport.

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

8 so failed to affect metformin stimulation of glucose transport.

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

10 ocation to the plasma membrane and decreased glucose transport.

11 gnificantly inhibited contraction-stimulated glucose transport.

12 the R125W mutation on contraction-stimulated glucose transport.

13 wn of AMPD obviated metformin stimulation of glucose transport.

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

15 12 muscle cells impaired sorbitol-stimulated glucose transport.

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

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

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

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

20 ularly with regard to insulin stimulation of glucose transport.

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

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

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

24 etic subjects is mostly related to defective glucose transport.

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

26 a postulated mediator for insulin-stimulated glucose transport.

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

28 ated knockdown attenuates insulin-stimulated glucose transport.

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

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

31 reduced basal and abolished insulin-induced glucose transport.

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

33 evertheless can function interchangeably for glucose transport.

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

35 d insulin-stimulated GLUT4 translocation and glucose transport.

36 te microsomal membrane transport pathway for glucose transport.

37 o effect on contraction- or sorbitol-induced glucose transport.

38 l for some, but not all, insulin-independent glucose transport.

39 , in association with increased capacity for glucose transport.

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

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

42 important in the physiological regulation of glucose transport.

43 phosphorylation and the possible effects on glucose transport.

44 et GLUT4 preferentially over GLUT1 and block glucose transport.

45 s of exercise on intramuscular signaling and glucose transport.

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

47 restriction, through impaired transplacental glucose transport.

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

49 GLUT4 levels and impaired insulin-stimulated glucose transport.

50 integrity and increase intestinal stress and glucose transport.

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

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

53 Glucose transport across the blood brain barrier and int

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

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

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

57 solic levels, suggesting rapid bidirectional glucose transport across the ER membrane.

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

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

60 they are in the lumen; (e) characterized UDP-glucose transport activities in Golgi apparatus and endo

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

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

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

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

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

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

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

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

69 1 4P mutant decreased contraction-stimulated glucose transport, an effect prevented by concomitant di

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

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

72 Intestinal glucose transport and blood glucose were elevated due to

73 Glucose transport and consumption were assayed using ex

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

75 Metformin stimulated both glucose transport and fatty acid oxidation.

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

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

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

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

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

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

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

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

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

85 Glucose transport and glycolytic metabolism carry the ri

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

87 ,8-tetrachlorodibenzo-p-dioxin (TCDD) alters glucose transport and increases serum lipid levels and b

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

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

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

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

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

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

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

95 Nitric oxide (NO) inhibits myocardial glucose transport and metabolism, although the underlyin

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

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

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

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

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

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

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

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

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

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

106 Muscle contraction increases glucose transport and represents an alternative signalin

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

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

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

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

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

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

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

116 ration, cell survival, membrane trafficking, glucose transport, and membrane ruffling.

117 lization of fatty acid substrate, diminished glucose transport, and mitochondrial dysfunction.

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 th mouse and human resistins directly impair glucose transport; and in contrast to effects on the liv

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

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

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

126 bservations in vitro, contraction-stimulated glucose transport, assessed in vivo by 2-deoxy-d-[(3)H]g

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

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

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

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

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

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

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

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

135 Transplacental glucose transport by glucose transporter isoform 1 (GLUT

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

137 K)-independent pathway of insulin-stimulated glucose transport by recruiting CAP and c-Cbl.

138 Insulin stimulates glucose transport by recruiting the GLUT4 glucose transp

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

140 Insulin increases glucose transport by stimulating the trafficking of intr

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

142 Glucose transported by GLUT2 may act after metabolizatio

143 2-deoxy-d-glucose, 3-O-methylglucose, and d-glucose transport capacity to RE700A.

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

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

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

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

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

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

150 This increase in glucose transport correlated with enhanced insulin-stimu

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

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

153 Plasma membrane and ER membrane glucose transport differed regarding sensitivity to cyto

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

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

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

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

158 This glucose transport function was replaced by increased exp

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

164 not significantly affect insulin-stimulated glucose transport in 3T3-L1 adipocytes, it significantly

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

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

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

171 ion of p38 MAPK by anisomycin also increased glucose transport in heart muscles.

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

180 and KO of Rac1 decreased insulin-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 y insulin in part through the stimulation of glucose transport in muscle and fat cells.

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

186 Thus, the markedly reduced glucose transport in muscle results in increased glycoge

187 Here we show that despite markedly reduced glucose transport in muscle, muscle glycogen content in

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

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

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

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

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

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

194 Insulin stimulates glucose transport in skeletal muscle by GLUT4 translocat

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

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

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

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

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

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

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

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

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

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

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

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

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

208 Measurements in the presence of a well-known glucose transport inhibitor indicate that variations in

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

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

211 Glucose-transport inhibitors killed trypanosomes without

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

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

214 Glucose transport into mammalian cells is mediated by a

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

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

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

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

219 Here we show that insulin-stimulated glucose transport is increased in the skeletal muscle an

220 n content in muscle in the fasted state when glucose transport is reduced.

221 Glucose transport is regulated by GLUT4 translocation in

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

223 AMP-activated protein kinase (AMPK) promotes glucose transport, maintains ATP stores, and prevents in

224 cle contraction- and hyperosmolarity-induced glucose transport may be regulated by a redundant mechan

225 Intramuscular signaling and glucose transport mechanisms contribute to improvements

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

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

228 A glucose transport-null strain of Saccharomyces cerevisia

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

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

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

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

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

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

235 These findings suggest that inhibition of glucose transport plays an important role in the therape

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

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

238 7 inhibits the erythrocyte sugar transporter glucose transport protein 1 (GLUT1) and examines the tra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

260 The presence of a high-capacity glucose transport system on the ER membrane is consisten

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

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

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

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

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

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

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

268 ions as a suppressor of insulin signaling to glucose transport through the PI 3-kinase pathway in cul

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

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

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

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

273 s demonstrated that TNFalpha increased basal glucose transport via GLUT1, nitric oxide synthase and p

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

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

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

277 ing the downstream action of AMPK to promote glucose transport was also assessed.

278 Glucose transport was assayed following expression of SL

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

280 AICAR- and rotenone-stimulated glucose transport was fully inhibited in alpha2i TG mice

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

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

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

284 Glucose transport was measured in vitro using isolated E

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

286 Glucose transport was moderately though significantly in

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

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

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

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

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

292 MP-activated protein kinase (AMPK) in muscle glucose transport, we generated muscle-specific transgen

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

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

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

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

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

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

299 sed the effects of microtubule disruption on glucose transport with divergent results.

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