ライフサイエンスコーパス: deoxyglucose

1 a) and viability (insulin-stimulated (18)F-2-deoxyglucose).

2 se that converts UDP-glucose to UDP-4-keto-6-deoxyglucose.

3 glucose analogs alpha-methyl glucoside or 2-deoxyglucose.

4 th of these UOK257 cells by treatment with 2-deoxyglucose.

5 coupled with tracer radioactively labeled 2-deoxyglucose.

6 n the presence of the glycolysis inhibitor 2-deoxyglucose.

7 ravenous injection of the glucopenic agent 2-deoxyglucose.

8 reased in Arabidopsis cells in response to 2-deoxyglucose.

9 e a functional isoform with low affinity for deoxyglucose.

10 e of metabolic inhibition with cyanide and 2-deoxyglucose.

11 s if glucose is replaced with nonmetabolized deoxyglucose.

12 ly different sensitivities to lysozyme and 2-deoxyglucose.

13 We also compared uptake of FLT and deoxyglucose.

14 RNAs inhibits insulin-stimulated uptake of 2-deoxyglucose.

15 e as a function of growth than did uptake of deoxyglucose.

16 S42, UW479 and RES186) using metformin and 2-deoxyglucose.

17 5Y neuroblastoma cells with sodium azide and deoxyglucose.

18 n the presence of the glycolysis inhibitor 2-deoxyglucose.

19 Glucose uptake was measured using (3)H-deoxyglucose.

20 eoxyglucose (5 and 6) > compounds with 2,3,6-deoxyglucose (10).

21 imaging with fluorine-18-labeled 2-fluoro-2-deoxyglucose ((18)FDG) ligand with kinetic analysis demo

22 13)N-ammonia and of the glucose tracer (18)F-deoxyglucose ((18)FDG) was graded on a five-point scale

23 tomography with (11)C-acetate, (18)F-fluoro-deoxyglucose ((18)FDG), and (18)F-fluoro-thiaheptadecano

24 m(-2)), using [(15)O]H(2)O and [(18)F]fluoro-deoxyglucose ([(18)F]FDG) to quantify tissue perfusion a

25 e accumulation of two cytotoxic compounds, 2-deoxyglucose (2-DG) and copper(II)diacetyl-bis(N(4)-meth

26 chment learning and its neural correlates [2-deoxyglucose (2-DG) autoradiography].

27 Treatment with the glycolytic blocker 2-deoxyglucose (2-DG) decreases association of the redox s

28 s glucose (2 g/kg), and was exacerbated by 2-deoxyglucose (2-DG) glycolytic inhibition, despite preve

29 rug metformin and the glycolytic inhibitor 2-deoxyglucose (2-DG) have been used to study the inhibiti

30 gher uptake of radio-labeled [14C]2-fluoro-2-deoxyglucose (2-DG) in the preoptic area (25%) and signi

31 ats show fourth ventricular application of 2-deoxyglucose (2-DG) inhibits NST neurons and activates d

32 Although 2-deoxyglucose (2-DG) is well characterized as a glycolyti

33 e assessed based on LCGU using the [(14)C]-2-deoxyglucose (2-DG) method.

34 ucose utilization (LCGU) using the [(14)C]-2-deoxyglucose (2-DG) method.

35 male, Sprague-Dawley rats using the [(14)C]2-deoxyglucose (2-DG) method.

36 ing the quantitative autoradiographic 2-[14C]deoxyglucose (2-DG) method.

37 glucose utilization (LCGU) using the [14C]2-deoxyglucose (2-DG) method.

38 ponses to glycemic challenges [intravenous 2-deoxyglucose (2-DG) or insulin].

39 , we show that the hexose kinase inhibitor 2-deoxyglucose (2-dG) preferentially kills cancer cells wi

40 Significant differences for 2-deoxyglucose (2-DG) relative recovery at 1.0 microL/min

41 n and does not respond to either Ca(2+) or 2-deoxyglucose (2-DG) stimulation.

42 Patterns of 2-deoxyglucose (2-DG) uptake in the glomerular layer of th

43 The study objective was to determine if 2-deoxyglucose (2-DG), a glucose analogue that blocks its

44 al MAN perfusion of the glucoprivic agent, 2-deoxyglucose (2-DG), under normal and hypoglycemic condi

45 emission maximum 794 nm, was conjugated to 2-deoxyglucose (2-DG).

46 in the nucleus in response to glucose and 2-deoxyglucose (2-DG).

47 ion of an inhibitor of glucose metabolism, 2-deoxyglucose (2-DG).

48 abilities upon glycolysis inhibition with 2-deoxyglucose (2-DG).

49 thoxyphenylhydrazone (FCCP, 50 nmol/L) and 2-deoxyglucose (2-DG, 10 mmol/L), there was a decrease in

50 ficacy of F1,6BP was compared with that of 2-deoxyglucose (2-DG; an inhibitor of glucose uptake and g

51 s is reciprocally regulated by glucose and 2-deoxyglucose (2-DG; inhibitor of cellular glucose metabo

52 The glucose analog 2-deoxyglucose (2-DOG) reduced ROS to levels found in non-

53 059; and (c) effects of AICAR on aPKCs and 2-deoxyglucose (2-DOG) uptake were inhibited by genistein,

54 was assessed via measurement of zero-trans 2-deoxyglucose (2-DOG) uptake.

55 hlearis muscles were incubated with [(3)H]-2-deoxyglucose (2DG) +/- 100 microU/ml insulin.

56 iple brain structures during neglect using 2-deoxyglucose (2DG) as a metabolic marker of neural activ

57 Conversely, 2-deoxyglucose (2DG) blocked glycolysis and partially inhi

58 owing exposure using uptake of 14C-labeled 2-deoxyglucose (2DG) in quiet.

59 The glucose analog 2-deoxyglucose (2DG) inhibits the growth of Saccharomyces

60 After 15 min, the quantified 2-deoxyglucose (2DG) method was carried out in freely beha

61 Then, we used [(14)C]2-deoxyglucose (2DG) uptake and single-neuron recording to

62 ons of primary visual cortex and measuring 2-deoxyglucose (2DG) uptake to assess neural activity in s

63 Rates of muscle 2-deoxyglucose (2DG) uptake were determined by measuring a

64 teral neuronal and hemodynamic changes and 2-deoxyglucose (2DG) uptake, as measured by autoradiograph

65 the impact of glycolysis inhibition, using 2-deoxyglucose (2DG), in combination with cytotoxic agents

66 metabolism with the glycolysis inhibitor, 2-deoxyglucose (2DG), is a viable therapeutic strategy, bu

67 withdrawal or glycolytic inhibition using 2-deoxyglucose (2DG).

68 These effects were mimicked by 8 g/l 2-deoxyglucose (2DOG) (transported, phosphorylated but not

69 We used a 2-deoxyglucose (2DOG) energy clamp to set DeltaPsi at fixe

70 , we used pharmacological agents (insulin, 2-deoxyglucose, 3-nitropropionic acid, and kainic acid) to

71 DP-glucose-4,6-dehydratase and dTDP-4-keto-6-deoxyglucose-3,5-epimerase enzymes respectively.

72 ond gene encodes a bifunctional UDP-4-keto-6-deoxyglucose-3,5-epimerase/-4-reductase that converts UD

73 elated positively with in vitro assays of 3H-deoxyglucose (3H-DG) uptake in cells harvested via bronc

74 -deoxyglucose (8 and 9) > compounds with 2,6-deoxyglucose (5 and 6) > compounds with 2,3,6-deoxygluco

75 cose analogues 3-O-methylglucose (3OMG) or 6-deoxyglucose (6DOG) has been cited as evidence for metab

76 The activity of compounds with 2-deoxyglucose (8 and 9) > compounds with 2,6-deoxyglucose

77 concept the therapeutic potential of using 2-deoxyglucose, a glycolysis inhibitor, to reverse tumorig

78 Similarly, in cancer cells OLIG and 2-deoxyglucose, a glycolytic inhibitor, depolarized mitoch

79 In turn, 2-deoxyglucose, a non-metabolizable glucose analogue, elic

80 RESULTS- We show that 1) 2-deoxyglucose, a nonmetabolizable glucose analog, mimics

81 degrees of overlap in their monomolecular 2-deoxyglucose activation patterns to test the theory in a

82 ly enter torpor in response to fasting and 2-deoxyglucose administration.

83 ose analogs such as 3-O-methyl-glucose and 2-deoxyglucose also caused an induction, suggesting that s

84 The cells were highly sensitive to 2-deoxyglucose, an inhibitor of glycolysis and proposed an

85 Consistent with this, 2-deoxyglucose, an inhibitor of glycolysis, augmented AMPK

86 comitant with enhanced sensitivity towards 2-deoxyglucose, an inhibitor of glycolysis.

87 sing two-photon imaging of a near-infrared 2-deoxyglucose analogue (2DG-IR), that glucose is taken up

88 h glucose deprivation combined with 0.5 mm 2-deoxyglucose and 5 mm azide ("chemical ischemia") to mod

89 Previously, we used deoxyglucose and chilling treatments to implicate Nup170

90 lidinedione-derived ERMA, CG-12, vis-a-vis 2-deoxyglucose and glucose deprivation, we obtain evidence

91 rences in the insulin-stimulated uptake of 2-deoxyglucose and in the activity of carnitine palmitoyl

92 re decreased by the glucose antimetabolite 2-deoxyglucose and increased by high blood glucose concent

93 Secretion was inhibited by 2-deoxyglucose and iodoacetate, confirming active secretio

94 vation, as well as the antimetabolic drugs 2-deoxyglucose and metformin, also promoted the release of

95 ll death in response to the combination of 2-deoxyglucose and metformin.

96 is observed under metabolic inhibition with deoxyglucose and oligomycin, indicating an energy-indepe

97 Moreover, the glycolysis inhibitors, 2-deoxyglucose and oxamate, selectively inhibited the grow

98 ound that ABT-263 increased sensitivity to 2-deoxyglucose and promoted rapid and extensive cell death

99 In vitro, 2-deoxyglucose and radiation synergistically up-regulated

100 n the presence of the glycolysis inhibitor 2-deoxyglucose and radiation treatment followed by PBMC ch

101 e synergy between the glycolytic inhibitor 2-deoxyglucose and rapamycin in decreasing cell viability.

102 be mimicked with the glycolytic inhibitor 2-deoxyglucose and reversed with a pyruvate analogue.

103 rocess, because cells depleted of ATP with 2-deoxyglucose and sodium azide were unable to properly re

104 Using this knowledge we identified 2-deoxyglucose and temsirolimus as agents that can be adde

105 Uptake of 2-deoxyglucose and various indexes of oxidative and glycol

106 lar layer was measured as uptake of [(14)C]2-deoxyglucose and was mapped into anatomically standardiz

107 patterns were measured as uptake of [(14)C]2-deoxyglucose and were mapped into standardized data matr

108 ty (euglycemic-hyperinsulinemic clamp with 2-deoxyglucose) and fat utilization during 1 h of exercise

109 creases in permeability, aliphatic alcohols, deoxyglucose, and chilling trigger the reversible dissoc

110 In HeLa and A549 cells, mannitol, 2-deoxyglucose, and ionomycin, but not 5-aminoimidazole-4-

111 Furthermore, 2-deoxyglucose- and ionomycin-stimulated AMPK activity, al

112 We used 2-deoxyglucose autoradiographic mapping of neural activity

113 min; n = 6) was comparable to that for (14)C-deoxyglucose autoradiographic methods.

114 sing c-Fos early gene expression and (14)C 2-deoxyglucose autoradiography during mother-to-infant fea

115 14C-deoxyglucose autoradiography was performed 45 min after

116 tumors had similar uptake of [(18)F]fluoro-2-deoxyglucose before and after 2 weeks of 2-DG treatment

117 Inhibition of hexokinase with 2-deoxyglucose blocked the transforming activity of CBL mu

118 ntroduced for the glycosylation of 2-azido-2-deoxyglucose building blocks.

119 lucosensors detect mannose, d-glucose, and 2-deoxyglucose but not galactose, l-glucose, alpha-methyl-

120 Hydralazine activated more neurons than 2-deoxyglucose but similar numbers of catecholaminergic ne

121 by the non-metabolizable glucose analogue 2-deoxyglucose, but not by stimulating intracellular ATP p

122 bles that of cortical metabolism seen with 2-deoxyglucose, but the increase in vascular density prece

123 erregulatory responses to hypoglycemia and 2-deoxyglucose, but the mechanisms that mediate these resp

124 nine dye scaffold for signal generation, a 2-deoxyglucose cancer localization moiety, and a boronic e

125 neurons shortly after vascular insulin and 2-deoxyglucose challenges.

126 7-nitrobenz-2-oxa-1, 3-diazol-4-yl) amino)-2 deoxyglucose compared with those from HIV(-) controls.

127 ing intact Mpi(-/-) fibroblasts with 2-[(3)H]deoxyglucose confirmed mannose-dependent hexokinase inhi

128 low uptake activity for the glucose analog 2-deoxyglucose, consistent with a role in the transport of

129 Systemic administration of 2-deoxyglucose depleted ADR content in control rats, and C

130 ulin-stimulated glucose uptake ((18)F-fluoro-deoxyglucose) during euglycemic (5.6 mmol/l), physiologi

131 he presence of an inhibitor of glycolysis, 2-deoxyglucose, enhanced the generation of memory cells an

132 quantitatively by measuring uptake of [14C]2-deoxyglucose evoked by each odorant.

133 pare the neuronal populations activated by 2-deoxyglucose evoked glucoprivation.

134 [18F]2-fluoro-2-deoxyglucose (FDG) -positron emission tomography (PET) h

135 in metabolism and volume using [(18)F]fluoro-deoxyglucose (FDG) and simultaneous time-of-flight (TOF)

136 heterogeneity in the uptake of [(18)F]fluoro-deoxyglucose (FDG) in single cells, which was found cons

137 ism was assessed with (18)F-labeled fluoro-2-deoxyglucose (FDG) positron emission tomography in 236 y

138 nd response monitoring by using (18)F-fluoro-deoxyglucose (FDG) positron emission tomography.

139 ositron emission tomography with fluorine-18-deoxyglucose (FDG-PET) detects active lymphoid tissues d

140 by positron emission tomography using (18)F-deoxyglucose (FDG-PET) has not been established after sa

141 n vitro work and confirms the selectivity of deoxyglucose for viable cells over necrotic regions and

142 sures derived from the comparison of [14C]-2-deoxyglucose glomerular activity pattern data yielded a

143 ia and knob can incorporate and accumulate 2-deoxyglucose (glucose analog), but not when blocking GLU

144 sitivity to radiation with or without 25mM 2-deoxyglucose (glycolytic inhibitor) was evaluated in clo

145 diopharmaceutical used in PET imaging - [18F]deoxyglucose - has a limited role in diagnosing primary

146 SF188 cells were highly sensitive to 2-deoxyglucose however, combination of metformin with 2-de

147 C-fos immunohistochemistry and [14C]2-deoxyglucose imaging identified brain structures involve

148 conversion of CDP-D-glucose to CDP-4-keto-6-deoxyglucose in an NAD(+)-dependent manner.

149 of excised plaques confirmed accumulation of deoxyglucose in macrophage-rich areas of the plaque.

150 The uptake of 2-deoxyglucose in MIN6 cells was similarly inhibited (IC(5

151 tic agents (ERMAs) such as resveratrol and 2-deoxyglucose in suppressing carcinogenesis in animal mod

152 catalyzes C-3 deoxygenation of CDP-4-keto-6-deoxyglucose in the biosynthesis of 3,6-dideoxyhexoses,

153 The tumor microdistribution of deoxyglucose in viable, hypoxic, and necrotic regions sh

154 Uptake of 2-[(14)C]deoxyglucose in vivo was reduced by a high-fat diet in a

155 Injection of 2-deoxyglucose induced a very rapid sympathoadrenal respon

156 In contrast, the glycolytic inhibitor 2-deoxyglucose induced prosurvival autophagy.

157 Addition of 2-deoxyglucose inhibited seed germination, but did so less

158 re layer was assessed by mapping uptake of 2-deoxyglucose into anatomically standardized data matrice

159 ation of AMPK in response to ionomycin and 2-deoxyglucose is not impaired in LKB1(-/-) murine embryo

160 animals studied using the metabolic marker 2-deoxyglucose, layer 4 was 25% denser than the other laye

161 ng p53, we showed that CR mimetics such as 2-deoxyglucose led to a decrease in Mcl-1 expression and s

162 nd pdk1, lung fluorine-18-labeled 2-fluoro-2-deoxyglucose ligand uptake was significantly increased i

163 nthesis (oligomycin, 2,4-dinitrophenol, or 2-deoxyglucose) made them more susceptible to cell death b

164 sults fail to confirm predictions based on 2-deoxyglucose maps of bulbar activity that enantiomers of

165 [(14)C] 2-deoxyglucose maps to investigate patterns of glucose uti

166 avioral abnormalities, we applied the [(14)C]deoxyglucose method for the determination of cerebral me

167 To this end, we used the [14C]2-deoxyglucose method to determine glomerular responses to

168 uctures in this system, we used the [(14)C]2-deoxyglucose method to determine glomerular responses to

169 sured in the same monkeys using the 2-[(14)C]deoxyglucose method.

170 and glycolysis (as measured by (18)fluoro-2-deoxyglucose microPET) of glioblastoma xenografts engine

171 ffects of metabolic blockade (cyanide plus 2-deoxyglucose) on Ca2+ release from the sarcoplasmic reti

172 Compounds, such as 2-deoxyglucose or 6-aminonicotinamide, that reduced the fr

173 rintuitively, restricting glycolysis using 2-deoxyglucose or by limiting glucose supply strongly impr

174 directly inhibited glycolysis using either 2-deoxyglucose or iodoacetic acid.

175 aspase-dependent cell death in response to 2-deoxyglucose or its combination with metformin.

176 s, Thr49 was phosphorylated in response to 2-deoxyglucose or phenformin, stimuli that activate the AM

177 This increase was blocked by either 2-deoxyglucose or the protein phosphatase inhibitor, calyc

178 ysis brought about by glucose deprivation, 2-deoxyglucose, or Akt inhibition.

179 were exposed to the glycolytic inhibitor, 2-deoxyglucose, or fatty acid synthase inhibitors to pertu

180 cell lines, 5 small-molecule perturbagens (2-deoxyglucose, oxamate, oligomycin, rapamycin, and wortma

181 between increased normalized (18)F fluoro-2-deoxyglucose PET SUVmax, outcome, and EMT in NSCLC.

182 glucose metabolism (imaged with [(18)F]fluro-deoxyglucose PET), and structural atrophy (imaged by MRI

183 urrent prostate cancer than (18)F-2-fluoro-D-deoxyglucose-PET and monoclonal antibody imaging with th

184 lity, validity and reproducibility of fluoro-deoxyglucose-PET/CT for imaging of atherosclerotic plaqu

185 Fluoro-deoxyglucose-PET/CT imaging is currently used to improve

186 Fluoro-deoxyglucose-PET/CT imaging is demonstrated to have the

187 18-Fluoro-deoxyglucose positron emission tomography (FDG-PET) is a

188 We retrospectively evaluated (18)fluoro-2-deoxyglucose positron emission tomography (FDG-PET) scan

189 [18F]-deoxyglucose positron emission tomography (PET) and matc

190 that contained fluorine 18 ((18)F) fluoro-2-deoxyglucose positron emission tomography (PET) and mess

191 al blood to clinical outcomes and (18)fluoro-deoxyglucose positron emission tomography combined with

192 icient rationale given the utility of fluoro-deoxyglucose positron emission tomography in diagnostic

193 cs, magnetic resonance imaging and 18-fluoro-deoxyglucose positron emission tomography results, and n

194 lizing on the diagnostic utility of 18fluoro-deoxyglucose positron emission tomography that relies on

195 on magnetic resonance imaging and 18-fluoro-deoxyglucose positron emission tomography.

196 High-resolution (18)F-labelled deoxyglucose positron-emission tomography (FDG-PET) was

197 Using 18FDG (18fluoro-2-deoxyglucose) positron emission tomography, we found tha

198 n brain glucose metabolism (measured by [18F]deoxyglucose-positron emission tomography) and on its re

199 ular responses relative to resveratrol and 2-deoxyglucose, respectively.

200 In addition, treatment of NOD mice with 2-deoxyglucose resulted in improved beta cell granularity.

201 tudies using intrinsic optical imaging and 2-deoxyglucose) resulted in increased detection thresholds

202 Regionally, F-18 deoxyglucose score was highest in segments with late gad

203 ose however, combination of metformin with 2-deoxyglucose significantly reduced cell proliferation co

204 ndent manner, whereas oxidative stress and 2-deoxyglucose stimulated phosphorylation at this site via

205 2-deoxyglucose stimulated Thr49 phosphorylation of endogen

206 is, functional magnetic resonance imaging, 2-deoxyglucose studies, and induction of gene expression h

207 results are consistent with a previous (14)C-deoxyglucose study of the isoflurane-anesthetized rat.

208 of pyruvate or alpha-ketocaproate, but not 2-deoxyglucose, suggesting that mitochondrial metabolism w

209 We demonstrate that the parthenolide, 2-deoxyglucose, temsirolimus (termed PDT) regimen is a pot

210 determined by NMR spectroscopy, including 2-deoxyglucose, the glucose analogue used for tumor detect

211 as little change in the microdistribution of deoxyglucose throughout this time course.

212 hen prediabetic NOD mice were treated with 2-deoxyglucose to block aerobic glycolysis, there was a re

213 of ATP by the addition of sodium azide and 2-deoxyglucose to block ATP production by oxidative phosph

214 positron emission tomography (PET) and [18F] deoxyglucose to compare the brain metabolic responses (m

215 er, we used the quantitative method of (14)C-deoxyglucose to reveal changes in activity, in the corte

216 rase/-4-reductase that converts UDP-4-keto-6-deoxyglucose to UDP-rhamnose.

217 e, we show that low doses of verapamil and 2-deoxyglucose, to accentuate the cost of resistance and t

218 ies examining the LC values for radiolabeled deoxyglucose tracers used to estimate the glucose metabo

219 dipocytes also attenuated insulin-stimulated deoxyglucose transport and Myc-GLUT4-EGFP translocation

220 pha (GSK-3alpha) phosphorylation, as well as deoxyglucose transport in 3T3-L1 adipocytes.

221 onse relationship for insulin stimulation of deoxyglucose transport in primary adipocytes derived fro

222 was screened for their ability to inhibit 2-deoxyglucose transport in primary rat adipocytes.

223 Deoxyglucose transport mediated by GLUT9 was not inhibit

224 cells failed to attenuate insulin-stimulated deoxyglucose transport or Myc-tagged GLUT4-GFP transloca

225 HLDB2 failed to attenuate insulin-stimulated deoxyglucose transport.

226 me- and concentration-dependent decline in 2-deoxyglucose transport.

227 on preconditioning (1 h of antimycin A and 2-deoxyglucose treatment followed by 1 h of recovery), ade

228 g p38 vectors reduced apoptosis induced by 2-deoxyglucose treatment, whereas overexpression of wild-t

229 [(14)C]glucose into glycogen (60%) and [(3)H]deoxyglucose uptake (40%) but did not inhibit phosphoryl

230 ose incorporation into glycogen (60%), [(3)H]deoxyglucose uptake (60%), and protein kinase B phosphor

231 We therefore examined the effects of HGF on deoxyglucose uptake (DOGU), glucose utilization, and fat

232 lted in increased glycolysis and increased 2-deoxyglucose uptake (P < 0.05).

233 ice, caCaMKKalpha increased in vivo [(3)H]-2-deoxyglucose uptake 2.5-fold and AMPKalpha1 and -alpha2

234 ocytes, and their membrane concentrations, 2-deoxyglucose uptake activities, and sensitivities to pCM

235 s N terminus suppressed insulin-stimulated 2-deoxyglucose uptake and Glut4 translocation to roughly t

236 n insulin signaling and insulin-stimulated 2-deoxyglucose uptake and glycogen synthesis.

237 bitor LY-294002 display a decrease in both 2-deoxyglucose uptake and hexokinase activity as compared

238 , is required for insulin-stimulated 2-[(3)H]deoxyglucose uptake and metabolism.

239 significant correlation between posterior 2-deoxyglucose uptake and molecular properties associated

240 is manifested as improved insulin-mediated 2-deoxyglucose uptake and suppression of lipolysis.

241 aCaMKKalpha increased basal in vivo [(3)H]-2-deoxyglucose uptake approximately twofold, insulin incre

242 t with DMOG or DHB reverses the decline in 2-deoxyglucose uptake caused by NGF withdrawal and suppres

243 ron emission tomography of 2-[(18)F]fluoro-2-deoxyglucose uptake combined with computed tomography.

244 Cip4-null mice exhibited increased [(14)C]2-deoxyglucose uptake compared with cells from wild-type m

245 by individual odorant chemicals, we mapped 2-deoxyglucose uptake during exposures to vapors arising f

246 les with the greatest UBX-Cter expression, 2-deoxyglucose uptake during fasting was similar to that i

247 nfusion rate and 90% greater muscle [(3)H]-2-deoxyglucose uptake during hyperinsulinemic-euglycemic c

248 Metabolic mapping of 2-deoxyglucose uptake during odor-shock conditioning in po

249 evious studies, we mapped glomerular layer 2-deoxyglucose uptake evoked by hundreds of both systemati

250 In past studies in which we mapped 2-deoxyglucose uptake evoked by systematically different o

251 d with c-Fos immunohistochemistry and [14C]2-deoxyglucose uptake implicate a prominent involvement of

252 nduced PPAR gamma-dependent adipogenesis and deoxyglucose uptake in 3T3-L1 preadipocytes at a potency

253 on of [(14)C]glucose into glycogen and [(3)H]deoxyglucose uptake in L-CPT I-transduced, palmitate-tre

254 rogressive but similar levels of increased 2-deoxyglucose uptake in macrophages that reached up to si

255 first investigated glomerular patterns of 2-deoxyglucose uptake in response to aromatic compounds th

256 ent with the 2.5- to threefold increase in 2-deoxyglucose uptake in skeletal muscle, heart, and white

257 ytokine, increases macrophage glycolysis and deoxyglucose uptake in vitro and acutely enhances (18)F-

258 ke in transfected muscles, we measured [3H]2-deoxyglucose uptake in vivo following intravenous glucos

259 tified activity patterns by mapping [(14)C]2-deoxyglucose uptake into anatomically standardized data

260 In vivo 2-[(18)F]fluoro-2-deoxyglucose uptake into brown adipose tissue (BAT) was

261 glucose infusion rate and markedly reduced 2-deoxyglucose uptake into skeletal muscle (85-90%) and wh

262 tive to WL5, submaximal insulin-stimulated 2-deoxyglucose uptake into the epitrochlearis muscle was l

263 rug triester 70 did induce enhancements in 2-deoxyglucose uptake into two different cell lines with c

264 e together with impaired exercise-mediated 2-deoxyglucose uptake into white but not red muscles.

265 robust and surprisingly focal patterns of 2-deoxyglucose uptake involving clusters of neighboring gl

266 Ischemia stimulated a 2.5-fold increase in 2-deoxyglucose uptake over base line in WT, whereas the in

267 ozygote matings exhibited reduction of the 2-deoxyglucose uptake rate: one by 50% (presumed heterozyg

268 ly active cdc42 (CA-cdc42; V12) stimulated 2-deoxyglucose uptake to 56% of the maximal insulin respon

269 Muscle 2-deoxyglucose uptake was similarly reduced under these co

270 activity of the alpha2 isoform of AMPK and 2-deoxyglucose uptake were assessed in incubated rat exten

271 no significant changes in AMPK activity or 2-deoxyglucose uptake were detected.

272 q), and CA-cdc42 on GLUT4 translocation or 2-deoxyglucose uptake were inhibited by microinjection of

273 osely with decreases in glucose transport (2-deoxyglucose uptake), measured during a subsequent 20-mi

274 testing, measurement of in vivo myocardial 2-deoxyglucose uptake, and echocardiography were performed

275 FosB immunoreactivity, 2-deoxyglucose uptake, and firing activity of LHb were stu

276 ipocytes, we analyzed Akt phosphorylation, 2-deoxyglucose uptake, and Glut4 translocation by immunofl

277 ults in decreased insulin-stimulated 2-[(3)H]deoxyglucose uptake.

278 ng a hyperinsulinemic-euglycemic clamp and 2-deoxyglucose uptake.

279 porter-4 accumulation, and enhanced [(3)H]-2-deoxyglucose uptake.

280 dose-response curve for insulin stimulated 2-deoxyglucose uptake.

281 adiponectin secretion and insulin-stimulated deoxyglucose uptake.

282 correlation between tumor blood flow and 18F-deoxyglucose uptake.

283 -stimulated GLUT4 translocation as well as 2-deoxyglucose uptake.

284 ion, gACRP30 caused a 1.5-fold increase in 2-deoxyglucose uptake.

285 M2), resulted in a 2.5-fold increase in (3)H-deoxyglucose uptake.

286 tory activation and uptake of radiolabeled 2-deoxyglucose was assessed before and after GM-CSF exposu

287 Rather, IRF3 activation by tunicamycin and 2-deoxyglucose was inhibited by 4-(2-aminoethyl)-benzenesu

288 administration of the glycolysis inhibitor 2-deoxyglucose was sufficient to rescue animals from HLH.

289 2[14C]deoxyglucose was used to assess MGU.

290 depletion, equivalent ATP loss induced by 2-deoxyglucose was without toxicity, arguing that bioenerg

291 cancer cells to ERMAs, including CG-12 and 2-deoxyglucose, we demonstrated that this beta-TrCP accumu

292 7-nitrobenz-2-oxa-1, 3-diazol-4-yl) amino)-2 deoxyglucose were analyzed by flow cytometry on monocyte

293 Glycogen synthesis and uptake of 2-deoxyglucose were reduced in skeletal muscle, suggesting

294 ked by the energy poisons sodium azide and 2-deoxyglucose, whereas staining of the nucleus (nucleolus

295 rated by using an inhibitor of glycolysis, 2-deoxyglucose, which almost totally abolished low-dose ar

296 lucose-inhibited neurons were activated by 2-deoxyglucose, which also activates counterregulatory res

297 form glucose, the nonmetabolizable sugars 2-deoxyglucose, which is still converted to G-6-P as well

298 adiotracer for oncologic PET is (18)F-fluoro-deoxyglucose, which measures glucose accumulation as a s

299 radiation response after administration of 2-deoxyglucose, which significantly (p<0.05) potentiated e

300 Using F-18 deoxyglucose with heparin pretreatment, metabolic rate o