ライフサイエンスコーパス: glucose uptake

1 ed molecular pathway through measurements of glucose uptake.

2 inase B (Akt) pathway, ultimately leading to glucose uptake.

3 t hepatic SCD1 deficiency increases systemic glucose uptake.

4 proves insulin-stimulated vasodilatation and glucose uptake.

5 lucose with or without heparin rapidly cease glucose uptake.

6 ucial in regulating downstream signaling and glucose uptake.

7 in improving the sensitivity to insulin and glucose uptake.

8 tream of AMPK, respectively, in IF1-mediated glucose uptake.

9 , attenuated AGE-ECM inhibition of adipocyte glucose uptake.

10 m) with or without heparin, and analyzed for glucose uptake.

11 lpha and glucose transporter 1 and increased glucose uptake.

12 in functional beta-cell mass plus peripheral glucose uptake.

13 Increased muscle SNA stimulates glucose uptake.

14 ed cellular energetics with anaerobic driven glucose uptake.

15 MPK and mTOR signaling and impaired cellular glucose uptake.

16 promoting both basal and insulin-stimulated glucose uptake.

17 in relative TSCR were associated with raised glucose uptake.

18 from certain nonmalignant tissues with high glucose uptake.

19 triction partially restored the impaired BAT glucose uptake.

20 lines broadly correlates with the amount of glucose uptake.

21 ether GLUT4 is required for overload-induced glucose uptake.

22 re suggested to impact on insulin-stimulated glucose uptake.

23 issue, capable of beta-adrenergic-responsive glucose uptake.

24 sses glucose production without an effect on glucose uptake.

25 e that 2-AG improves insulin sensitivity and glucose uptake.

26 proinflammatory markers and improves IR and glucose uptake.

27 d insulin-stimulated Akt phosphorylation and glucose uptake.

28 ctivated kinase (AMPK), leading to increased glucose uptake.

29 sphorylation towards glycolysis and enhanced glucose uptake.

30 pendent roles of the HM domain in regulating glucose uptake.

31 programs related to Glut4 and Glut1-mediated glucose uptake.

32 act HM domain is required for Glut4-mediated glucose uptake.

33 ssion tomography showed increased myocardial glucose uptake.

34 r enlargement of lysosomes while suppressing glucose uptake.

35 merization, GLUT4 vesicle translocation, and glucose uptake.

36 LUT6, and/or GLUT10 mediate overload-induced glucose uptake.

37 and trailing follower cells rely on elevated glucose uptake.

38 se homeostasis and insulin-stimulated muscle glucose uptake.

39 le respectively impair insulin secretion and glucose uptake.

40 with HFD and is also capable of stimulating glucose uptake.

41 ylazine anesthesia to suppress cardiomyocyte glucose uptake.

42 he role of PAK1 in insulin-stimulated muscle glucose uptake.

43 sociated with suppression of CHI3L1-mediated glucose uptake.

44 ive, meaning it does not require insulin for glucose uptake.

45 ) central memory-like phenotype with reduced glucose uptake (2-NBDG(lo)) and decreased effector funct

46 acological activation of AMPK also increased glucose uptake (3.2 +/- 0.3 vs. 2.3 +/- 0.2 pmol/mg/min;

47 d to electrical stimulation exhibited higher glucose uptake (4.4 +/- 0.55 vs. 2.6 +/- 0.04 pmol/mg/mi

48 The rates of hepatic glucose uptake (5.8 +/- 0.8 vs. 3.2 +/- 0.3 mg kg(-1) mi

49 veness to suppress EGP and stimulate hepatic glucose uptake; activation of glucokinase was restored a

50 ucosidase inhibitory and augmenting cellular glucose uptake activities.

51 henotypes, in which mcDCs exhibit the lowest glucose uptake activity and mcDC survival is the least a

52 Moreover, muscle glucose uptake after contraction was positively associat

53 rom TBC1D1-deficient mice displayed impaired glucose uptake after contraction.

54 CLL exhibit impaired activation and reduced glucose uptake after stimulation.

55 Whereas, Glut1-mediated glucose uptake also requires mTORC2 phosphorylation of t

56 air lymphatic contractile status by reducing glucose uptake, altering cellular metabolic pathways, an

57 Increased glucose uptake and aerobic glycolysis are striking featu

58 tes significantly reduced insulin-stimulated glucose uptake and Akt Ser(473) phosphorylation.

59 th static and cycling hypoxia also increased glucose uptake and aldehyde dehydrogenase activity.

60 the heterozygous deletion of Pax5 increased glucose uptake and ATP levels by more than 25-fold.

61 ex vivo contraction-induced AMPK activation, glucose uptake and beclin 1-UVRAG complex assembly.

62 HIF knockdown only affected glucose uptake and bone resorption in hypoxic conditions

63 The nitrate-mediated enhancement of glucose uptake and catabolism in white adipose tissue ma

64 Overexpression of PFKFB3 promoted glucose uptake and cell proliferation, whereas downregul

65 also found evidence of defects in peripheral glucose uptake and concomitant hyperinsulinemia in the a

66 generating high levels of ROS have increased glucose uptake and correspondingly increased glucose met

67 The findings suggest that information on glucose uptake and diffusion coefficient carries complem

68 antly increases adipocyte insulin-stimulated glucose uptake and efficiently promotes white-to-brown a

69 ne (Q282A) doubled the Km(app) for 2-deoxy-d-glucose uptake and eliminated cis-allostery (stimulation

70 en 1 and AGE-modified ECM regulate adipocyte glucose uptake and expression of AGE scavenger receptors

71 Bzeta via IL-17 signaling mediated increased glucose uptake and expression of the gene Cpt1a, encodin

72 velopment of insulin resistance, lower brain glucose uptake and glucose transporters, alterations in

73 egulator of insulin- and exercise-stimulated glucose uptake and GLUT4 trafficking is TBC1D1.

74 of mouse tibialis anterior muscle decreased glucose uptake and glycogen content in vivo, concomitant

75 ells(3) in several ways, including increased glucose uptake and glycolysis even in the presence of ab

76 onstrate the occurrence and functionality of glucose uptake and glycolysis in the cilia.

77 Glucose uptake and glycolysis were increased in platelet

78 1 cells had low ATP levels due to diminished glucose uptake and glycolysis which was rescued by Vitam

79 Inhibition of GLUT1 decreases EC glucose uptake and glycolysis, leading to energy depleti

80 ose transporter in lung SqCC, which augments glucose uptake and glycolytic flux.

81 sporter (GLUT) GLUT1 to facilitate increased glucose uptake and glycolytic metabolism; however, the r

82 Glucose uptake and HDO production by HUH-7 cells showed

83 lationship between the tumor and bone marrow glucose uptake and host systemic inflammation.

84 lationship between the tumor and bone marrow glucose uptake and host systemic inflammatory responses

85 Overload-induced muscle glucose uptake and hypertrophic growth were not impaired

86 Increased glucose uptake and IFN-gamma expression in NKT cells is

87 Maternal WSD reduced insulin-stimulated glucose uptake and impaired insulin signaling at the lev

88 rg effect (WE) is characterized by increased glucose uptake and incomplete oxidation to lactate.

89 acts directly upon adipose tissue to improve glucose uptake and indirectly via insulin signaling.

90 Several studies have linked impaired glucose uptake and insulin resistance (IR) to functional

91 Twelve weeks after surgery, glucose uptake and insulin sensitivity were measured usi

92 ling molecules involved in the regulation of glucose uptake and insulin sensitivity.

93 emonstrate that miR-29a and miR-29c regulate glucose uptake and insulin-stimulated glucose metabolism

94 LA treatment reduced glucose uptake and lactate export during LPS stimulation

95 Hindlimb glucose uptake and lactate output rates were similar bet

96 how that FILNC1 deficiency leads to enhanced glucose uptake and lactate production through upregulati

97 of HIF1alpha by upregulating FIH1, decreases glucose uptake and lactate production, inhibits glioblas

98 dipocytes cultured in darkness had decreased glucose uptake and lower nutrient-induced mitochondrial

99 hysiology and pathophysiologically increased glucose uptake and may have the potential to provide inf

100 The stimulation of glucose uptake and metabolism by a unique microbiome met

101 ar adaptations in skeletal muscle, improving glucose uptake and metabolism in both healthy individual

102 Increased glucose uptake and metabolism is a prominent phenotype o

103 ed mice, including insulin resistance, brain glucose uptake and metabolism, and synaptic function, co

104 Several of the tested compounds increased glucose uptake and metabolism, notably in high glucose-

105 binding domain also exhibited a reduction in glucose uptake and mitochondrial respiration in darkness

106 in terms of (a) insulin signaling, (b) brain glucose uptake and neuronal- and astrocytic metabolism,

107 Cardiac glucose uptake and oxidation are reduced in diabetes des

108 eprivation promoted a tight coupling between glucose uptake and oxidation, G6P reduction, and increas

109 al analysis, we found that nitrate increases glucose uptake and oxidative catabolism in primary adipo

110 ge-determining transcription factors repress glucose uptake and pentose phosphate pathway activity, w

111 t relationship between tumor and bone marrow glucose uptake and poor outcomes.

112 fferentiating into effector T cells increase glucose uptake and shift from quiescent to anabolic meta

113 Muscle glucose uptake and signaling were measured ex vivo in fe

114 a and hepatic steatosis, by enhancing muscle glucose uptake and storage as glycogen.

115 ivates AMPK, its ability to acutely increase glucose uptake and suppress glucose production does not

116 ation of the AHR as measured by decreases in glucose uptake and the production of pyruvate and lactat

117 young hearts (P < 0.05); the AMPK downstream glucose uptake and the rate of glucose oxidation were si

118 The beta-cells are not able to control glucose uptake and they are therefore left vulnerable fo

119 reduced insulin- and contraction-stimulated glucose uptake and to elevated fatty acid (FA) uptake an

120 We found PH PASMCs had increased glucose uptake and utilization by glycolysis and the pen

121 oxygen utilization associated with increased glucose uptake and utilization involving AMPK-TBC1D1 sig

122 tochondrial membrane potential but increased glucose uptake and viability, characteristics of less in

123 Core body temperature, PET imaging of glucose uptake and VO(2) measurements confirm a thermoge

124 vation of SKM G(q) signaling can improve SKM glucose uptake and whole-body glucose homeostasis under

125 tion, muscle MPC disruption increased muscle glucose uptake and whole-body insulin sensitivity.

126 edly improved muscle insulin sensitivity and glucose uptake, and decrease anti-myogenic and inflammat

127 not consume glucose (reduction in myocardial glucose uptake, and glucose-related enzymes) but instead

128 ed the spatial relationship between hypoxia, glucose uptake, and glycolysis in three human pancreatic

129 SIRT6, glucose transporter Glut1 expression, glucose uptake, and glycolysis.

130 vironment and interrelationships of hypoxia, glucose uptake, and glycolysis.

131 ed membranous GLUT1 translocation, elevating glucose uptake, and increased acetyl-CoA levels, leading

132 d Wnt-signaling, enhanced insulin-stimulated glucose uptake, and inhibited the proliferation of DLD-1

133 concomitant reduction in metabolite levels (glucose uptake, and intracellular- lactate, glutamine, a

134 hanisms involving endocannabinoid signaling, glucose uptake, and IR in cardiomyocytes are understudie

135 fission and lysosomal activity, suppressing glucose uptake, and maintaining healthy punctate mitocho

136 n of cell viability, cell cycle progression, glucose uptake, and metabolism.

137 sulin-induced AKT phosphorylation, decreased glucose uptake, and mitochondrial oxygen consumption.

138 ging remains the gold standard for measuring glucose uptake, and no optical tools exist for non-invas

139 eam of AMPK, affecting ATP and NADPH levels, glucose uptake, and reactive oxygen species production.

140 tivity, while glycolysis gene expression and glucose uptake are increased, indicative for metabolic r

141 e relationship between PET-CT derived tumour glucose uptake as measured by maximum standard glucose u

142 glucose production and stimulation of muscle glucose uptake) as assessed by using a two-stage hyperin

143 Cell migration and glucose uptake assays combined with protein function inh

144 and the mitochondrial membrane potential and glucose uptake become progressively larger.

145 reases in LSNA to skeletal muscle stimulates glucose uptake, blunted insulin- and leptin-induced symp

146 ration under high-glucose conditions blocked glucose uptake by 1 h into G(1) Of note, glucose transpo

147 lin action by 26% and insulin-stimulated leg glucose uptake by 53% together with increased insulin-st

148 y acids (FFAs) uptake but reduced myocardial glucose uptake by 57% (P < 0.001).

149 ce remained insulin sensitive, had increased glucose uptake by adipose cells and skeletal muscle in v

150 High glucose uptake by cancer compared to normal tissues has

151 l production were reduced cell viability and glucose uptake by D5A and not loss of enzyme activity or

152 s by metabolomics, and significantly reduced glucose uptake by FDG-PET live animal imaging.

153 ng the foundations for how insulin regulates glucose uptake by muscle and fat cells.

154 upin was identified as a potent inhibitor of glucose uptake by selectively targeting and upregulating

155 T2D patients, and as a negative regulator of glucose uptake by skeletal muscle, and of pancreatic bet

156 vasodilator actions of insulin contribute to glucose uptake by skeletal muscle, and previous studies

157 fectively increases the glycogen content and glucose uptake by stimulating the membrane translocation

158 lin secreted into the circulation stimulated glucose uptake by the liver spheroids, while the latter,

159 tolerance tests on different days, promoted glucose uptake by the liver spheroids.

160 ptozotocin prior to increasing cardiomyocyte glucose uptake by transgene induction.

161 The enhanced glucose uptake correlated with increased liver expressio

162 itulating a shift toward noninsulin-mediated glucose uptake could be an early postpartum strategy to

163 AsPC-1 and PANC-1 cells, leading to a lower glucose uptake (deceased > 40%) and glycolysis capacity

164 Adipose tissue triacylglyceride (TAG) and glucose uptake decreased, and the free fatty acid/glycer

165 TFAM enhanced muscle glucose uptake despite increased fatty acid (FA) oxidati

166 ntified using ELISA or radioimmunoassay, and glucose uptake determined through 2-deoxy glucose 6 phos

167 Glucose uptake did not increase in Acsl1(M) (-/-) skelet

168 Here we demonstrate that glucose uptake during exercise/contraction was not compr

169 AMPK has been suggested to regulate muscle glucose uptake during exercise/contraction, but findings

170 and the OGTT and related to IR: peripheral (glucose uptake during the insulin clamp), hepatic (basal

171 rease in offspring muscle insulin-stimulated glucose uptake even in the absence of increased offsprin

172 RMCs entering G(1) in high glucose sustained glucose uptake for the first 3 h, and high-glucose expos

173 Net glucose uptake from the CVVH circuit was 54 +/- 5 mg/min

174 tionally resulted in progressively increased glucose uptake from the medium.

175 body glucose homeostasis, insulin-stimulated glucose uptake, glucose-stimulated insulin secretion, he

176 not alter M1 polarization in the context of glucose uptake, glycolytic metabolism, or cytokine produ

177 the influence of a brief (two weeks) HFD on glucose uptake (GU) +/- insulin in single fibers that we

178 sment of tissue volume, fat content (FF) and glucose uptake (GU) from whole-body [(18)F]FDG-PET/MR im

179 variant (p.P50T/AKT2) on insulin-stimulated glucose uptake (GU) in the whole body and in different t

180 ability of GH to inhibit insulin-stimulated glucose uptake have scarcely been documented.

181 e phenolics on carbolytic enzyme inhibition, glucose uptake, hepatic glucose homeostasis and anti-gly

182 dered the possibility that increased hepatic glucose uptake (HGU) contributes to the insulin-independ

183 lucose transporter levels, enhanced cellular glucose uptake, higher cellular oxygen consumption rate

184 However, is increased glucose uptake important for tumor cells, and which tran

185 d lipogenesis but did not alter lipolysis or glucose uptake in 3T3-L1 adipocytes.

186 ould impair insulin action, limiting further glucose uptake in a negative feedback loop of "glucose-d

187 acid uptake and modulated insulin-stimulated glucose uptake in a time-dependent manner.

188 ure experiments showed that ApoA-IV improved glucose uptake in adipocytes in the absence of insulin b

189 sponsive compartment, and insulin-stimulated glucose uptake in adipocytes is suppressed.

190 Delta/+) was resistant to insulin-stimulated glucose uptake in adipose tissue and skeletal muscle com

191 esults suggest that hepatic oleate regulates glucose uptake in adipose tissue either directly or part

192 essential signaling molecules for regulating glucose uptake in adipose tissues upon insulin stimulati

193 DG PET identified intense inter-scapular BAT glucose uptake in all ZL control rats, while no focally

194 ulin action was improved, stimulating muscle glucose uptake in association with decreased intracellul

195 However, in humans basal glucose uptake in BMAT is greater than in axial bones or

196 nd knocking down the expression of DNAJB3 on glucose uptake in C2C12 as well as the molecular determi

197 both WT and diabetic KKAy mice by increasing glucose uptake in cardiac muscle, white adipose tissue,

198 tients, we model the stimulation by RdCVF of glucose uptake in cones and glucose metabolism by aerobi

199 SF and GM-CSF generated comparable levels of glucose uptake in cultured macrophages and murine athero

200 te that silencing MondoA expression improves glucose uptake in EndoC-betaH1 cells.

201 PAHSA treatment augmented insulin-stimulated glucose uptake in glycolytic muscle and heart in HFD-fed

202 Loss of Rab20 impairs insulin-stimulated glucose uptake in human and mouse skeletal muscle by blo

203 esents an important alternative to stimulate glucose uptake in insulin-resistant muscle.

204 s exercise an effective stimulus to increase glucose uptake in insulin-resistant skeletal muscle.

205 partially reduced (-20%) insulin-stimulated glucose uptake in isolated mouse soleus muscle (P < 0.00

206 , PAK1 is dispensable for insulin-stimulated glucose uptake in mouse muscle.

207 Glucose uptake in muscle and adipose did not show simila

208 IRS1 and stimulates Akt- and Glut4-mediated glucose uptake in muscle cells.

209 esis which proposes that the reduced adipose glucose uptake in obesity is a physiological down-regula

210 activation of G(q) signaling also stimulated glucose uptake in primary human SKM cells.

211 glycolysis, despite an inability to increase glucose uptake in response to IGF-1.

212 ose-handling proteins for insulin-stimulated glucose uptake in skeletal muscle and insulin-stimulated

213 cise bypasses insulin resistance to increase glucose uptake in skeletal muscle and therefore represen

214 extent insulin-induced hypoglycemia affects glucose uptake in skeletal muscle and whether hypoglycem

215 sults expand the model of insulin-stimulated glucose uptake in skeletal muscle cells by implicating p

216 Exercise increases glucose uptake in skeletal muscle independently of insul

217 CHI3L1 was associated with increased glucose uptake in skeletal muscles in an AMP-activated p

218 We investigated the effect of ApoA-IV on glucose uptake in the adipose and muscle tissues of mice

219 usion in both legs and abrogated the greater glucose uptake in the exercised compared with the rested

220 nducible factor 1alpha (HIF-1alpha) controls glucose uptake in the hypothalamus and that it is upregu

221 get TBC1D1 are involved in regulating muscle glucose uptake in the immediate period after exercise/co

222 tomography scan demonstrated a reduction in glucose uptake in the left thalamus and bilateral inferi

223 y due to decreased (~37%) insulin-stimulated glucose uptake in the nonexercised muscle.

224 muscles displayed normal insulin-stimulated glucose uptake in vivo and in isolated muscle, insulin-s

225 late insulin-stimulated muscle perfusion and glucose uptake in vivo.

226 exposure promoted mitochondrial activity and glucose uptake in WT adipocytes but not in Opn3-KO cells

227 Increased glucose uptake induced direct O-GlcNAcylation of many el

228 lated glycogen synthesis, glucose oxidation, glucose uptake, insulin signal transduction (IRS1, Akt,

229 nt in teas were the predominant inhibitor of glucose uptake into Caco-2 cells, and gallated catechins

230 Through regulating GLUT1 level, GLD4 affects glucose uptake into cells and lactate levels.

231 modulated (14)C-D-glucose and (14)C-deoxy-D-glucose uptake into hepatic HepG2 cells.These data indic

232 ic function of insulin is the stimulation of glucose uptake into muscle and adipose tissues.

233 Insulin controls glucose uptake into muscle and fat cells by inducing a n

234 inhibition of insulin secretion and enhances glucose uptake into skeletal muscle cells.

235 ich promotes GLUT4 vesicle translocation and glucose uptake into skeletal muscle cells.

236 ation of SKM G(q) signaling greatly promoted glucose uptake into SKM and significantly improved gluco

237 t (OT), and black tea extract (BT) inhibited glucose uptake into the intestinal Caco-2 cells with GT

238 Muscle insulin sensitivity for stimulating glucose uptake is enhanced in the period after a single

239 that muscle insulin sensitivity to stimulate glucose uptake is enhanced several hours after an acute

240 RgA was found to inhibit glucose uptake, leading to a decrease in cellular ATP sy

241 us via enhanced beta-oxidation and decreased glucose uptake, leading to flux-redirection away from re

242 rophages require metabolic reprogramming and glucose uptake mediated by hypoxia-inducible factor (HIF

243 es (TSCR) from IRT and the metabolic rate of glucose uptake (MR(gluc)) from PET/CT were determined.

244 Glucose uptake on MR(gluc)MIP was found to correlate pos

245 molecules in mice has revealed the impact of glucose uptake on whole-body metabolism.

246 ons and the information gained is limited to glucose uptake only.(13)C magnetic resonance spectroscop

247 Common glucose-imaging techniques report glucose uptake or catabolism activity, yet do not trace

248 Furthermore, mutants defective in glucose uptake or dependent upon peptides for growth als

249 is not necessary for overload-induced muscle glucose uptake or hypertrophic growth and suggest that G

250 We did not observe significant changes in glucose uptake or lactate secretion in senescent HMECs.

251 Insulin-stimulated glucose uptake partly relies on PAK2 in glycolytic exten

252 on, glucose tolerance and insulin-stimulated glucose uptake partly rely on PAK2 in glycolytic mouse m

253 aphy tracers and validate the bioluminescent glucose-uptake probe as a tool for the identification of

254 e report the development of a bioluminescent glucose-uptake probe for real-time, non-invasive longitu

255 mechanisms that enable the tradeoff between glucose uptake rate and growth yield.

256 ides, the proposed model was able to predict glucose uptake rate at given external glucose concentrat

257 An improvement in skeletal glucose uptake rate was also observed in obese-stimulate

258 was lower by 34% (P < 0.01) and the hepatic glucose uptake rate was lower by 33% (P < 0.01) in obese

259 yield and (B) a tradeoff between substrate (glucose) uptake rate and growth yield.

260 Finally, lower insulin-stimulated SCAT glucose uptake rates in obese individuals are proportion

261 Lower insulin-stimulated glucose uptake rates in obese versus lean individuals we

262 ereas their glycolytic flux and 2-deoxy-(3)H-glucose uptake rates were largely unaffected.

263 have decreased saturation or activity at low glucose uptake rates.

264 d cells simulated at different glutamine and glucose uptake rates.

265 (GLUT1), which sustains an elevated level of glucose uptake required to maintain proliferation.

266 show that insulin-stimulated Glut4-mediated glucose uptake requires PDPK1 phosphorylation of the kin

267 P2Y(6)R deletion in skeletal muscle reduced glucose uptake, resulting in impaired glucose homeostasi

268 ucose uptake as measured by maximum standard glucose uptake (SUVmax) and total lesion glycolysis (TLG

269 NKT cells are less efficient in glucose uptake than CD4 T cells with or without activati

270 orted by microvessels and has markably lower glucose uptake than clear cell RCC and papillary RCC.

271 Leader cells exhibit higher glucose uptake than follower cells.

272 Additionally, CHI3L1 was found to influence glucose uptake through the PI3K/AKT pathway.

273 ion of LDHA in a PA cell line (GH3) promoted glucose uptake through the upregulation of glucose trans

274 Deuterium mass balance of [(2)H(7)]glucose uptake to (2)H-lactate and HDO production is qua

275 Growth factors also enhance glucose uptake to fuel an anabolic metabolism required f

276 ficient skeletal muscle, whereas reversal of glucose uptake toward resting levels after exercise/cont

277 IF1 stimulates glucose uptake via AMPK in skeletal muscle cells and pri

278 oxygen utilization efficiency and augmented glucose uptake via AMPK-TBC1D1 signaling nexus.

279 Mechanistically, glucose uptake via GLUT (glucose transporter)-1 and enha

280 Insulin-stimulated SkM glucose uptake was approximately twofold greater in mdKO

281 CAR stimulation, enhanced insulin-stimulated glucose uptake was evident in muscle from wild-type mice

282 iltration and inflammation was decreased and glucose uptake was increased in PU.1 AKO mice compared w

283 se homeostasis and insulin-stimulated muscle glucose uptake was investigated.

284 Overload-induced [(3)H]-2-deoxy-d-glucose uptake was not inhibited by d-fructose, demonstr

285 However, PF-induced glucose uptake was not prevented in primary muscle cells

286 GT and OT inhibition of glucose uptake was partial non-competitive, with an inhi

287 The stimulatory effect of PF on glucose uptake was partially reduced by expression of th

288 In juvenile offspring, insulin-stimulated glucose uptake was similarly reduced by both maternal an

289 o and in isolated muscle, insulin-stimulated glucose uptake was slightly reduced in isolated glycolyt

290 e transcriptional targets are suppressors of glucose uptake, we propose that MondoA is critical for r

291 muscle weights and ex vivo [(3)H]-2-deoxy-d-glucose uptake were assessed.

292 nuclear exclusion, GLUT4 translocation, and glucose uptake were attenuated upon loss of Ser(474) pho

293 d increases in sarcolemmal GLUT4 content and glucose uptake were lower in the white gastrocnemius of

294 Myocardial palmitate and glucose uptake were measured with (11)C-palmitate and (1

295 473) phosphorylation, and insulin-stimulated glucose uptake were significantly reduced in FIT2 knockd

296 onstrate that Glut1 and Glut3 loss decreases glucose uptake, which is mainly dependent on Glut1.

297 IUGR at birth have higher rates of hindlimb glucose uptake, which may compensate for myocyte deficie

298 ocytes, cyclin D1 depletion led to increased glucose uptake, which was negated if HNF4alpha was deple

299 atic gluconeogenesis and inhibits peripheral glucose uptake, while adipose Tmem127 downregulates adip

300 at BMAT resists insulin- and cold-stimulated glucose uptake, while further in vivo studies showed tha

301 We observed increased glucose uptake with SOD1(G93A) expression in all co-cult