ライフサイエンスコーパス: glucose

1 for cell proliferation in low environmental glucose.

2 sterol esters increased linearly up to 25 mm glucose.

3 ng glucose and/or >/=7.8 mmol/L for 2-h post-glucose.

4 to synthesis of trehalose, a disaccharide of glucose.

5 a 1.7% overall yield from d-cellobiose and d-glucose.

6 ntly but only slightly lowered fasting blood glucose (-0.14 mmol/L; 95% CI: -0.24, -0.036 mmol/L), Hb

7 a glucose acceptor, releasing phosphate from glucose 1-phosphate.

8 x basal) hyperglycemic clamp (arterial blood glucose 146 +/- 2 mg/dL) with portal GLC infusion.

9 The glucose analog [(18)F]fluoro-2-deoxy-2-d-glucose ([(18)F]-FDG) is commonly used in PET/CT that is

10 l (1-[(18)F]FDAM), 2-deoxy-2-[(18)F]fluoro-d-glucose (2-[(18)F]FDG), and 6-deoxy-6-[(18)F]fluoro-d-gl

11 nd glucose uptake determined through 2-deoxy glucose 6 phosphate luminescence.

12 2-[(18)F]FDG), and 6-deoxy-6-[(18)F]fluoro-d-glucose (6-[(18)F]FDG) was studied in EMT6 cells, tumors

13 enolpyruvate carboxykinase 1 (PCK1), and the glucose-6-phosphatase catalytic subunit (G6PC).

14 zymes, phosphoenolpyruvate carboxykinase and glucose-6-phosphatase, above the levels in control liver

15 It is caused by the deficiency of glucose-6-phosphatase, an enzyme which catalyses the fin

16 Glucose-6-phosphate dehydrogenase (G6PD) deficiency is b

17 Glucose-6-phosphate dehydrogenase (G6PD) deficiency is t

18 Glucose-6-phosphate dehydrogenase (G6PD) status was dete

19 cal NADPH homeostasis, which is regulated by glucose-6-phosphate dehydrogenase and AMP kinase.

20 sses hexokinase and the rate-limiting enzyme glucose-6-phosphate dehydrogenase.

21 omal-recessive disease caused by mutation of glucose-6-phosphate transporter and characterized by alt

22 e of polymerization of greater than two as a glucose acceptor, releasing phosphate from glucose 1-pho

23 Overall, glucose added at 1.8 wt % and soil inoculum added at 0.1

24 , whereby increased glycolytic flux leads to glucose addiction in cancer cells and a corresponding in

25 Glucose addition to immobilized cells induced pH oscilla

26 e used to test for possible malabsorption of glucose after surgery.

27 The glucose analog [(18)F]fluoro-2-deoxy-2-d-glucose ([(18)F

28 and MYBS2 play opposite roles in regulating glucose and ABA signaling in Arabidopsis during seed ger

29 H there was a substantial net uptake of both glucose and citrate that delivered exogenous energy and

30 real-time monitoring of sucrose, sorbitol, d-glucose and d-fructose concentrations is reported.

31 id program for transcriptional repression of glucose and energy supply.

32 tected an interaction effect between fasting glucose and fasting triglycerides with rs9939609 on BMI

33 ermore, we are able to simultaneously detect glucose and fatty acid uptake directly within the tumor

34 tion was important in the interconversion of glucose and fructose, 5-hydroxymethylfurfural formation

35 together with (13)C stable isotope-labelled glucose and glutamine as metabolic tracers, we probed th

36 ins its ability to significantly lower blood glucose and improve glucose tolerance in diet-induced ob

37 cluded conformations present multiple beta-d-glucose and maltose interaction sites, whereas inward-oc

38 eutral polysaccharides consist of galactose, glucose and mannose whereas the acidic polysaccharides c

39 y, Snrk knockout mouse hearts have increased glucose and palmitate oxidation and UCP3.

40 g (3-dimensional ultrasonography), and blood glucose and plasma gut-hormone concentrations [insulin,

41 ria to define GDM: >/=7.0 mmol/L for fasting glucose and/or >/=7.8 mmol/L for 2-h post-glucose.

42 holesterol, triglycerides, and fasting blood glucose) and identified several cis-eGenes (ALDH2 for sy

43 nyl transfers (IPP), glucosyl transfers (UDP-glucose), and electron and ADP-ribosyl transfers (NAD(P)

44 olism-an exaggerated spike in triglycerides, glucose, and insulin-increases cardiovascular disease ri

45 : waist circumference, triglycerides, HDL-c, glucose, and systolic and diastolic blood pressure.

46 , in the absence of insulin, did not consume glucose as efficiently.

47 sphorylase that is capable of generating GDP-glucose as well as GDP-mannose.

48 interference from external factors, such as glucose, ascorbic acid human serum protein, immunoglobul

49 cells to achieve meticulous control of blood glucose (BG) would revolutionize diabetes care.

50 polypyrrole (PPy)-based bilayer amperometric glucose biosensor integrated with a permselective layer

51 smic NAD(+) regeneration that sustains rapid glucose breakdown through glycolysis.

52 pletion from a mixture of 19 amino acids and glucose by two Pseudomonas and one Bacillus species isol

53 Alternatively, glucose can be catabolized anaerobically via glycolysis

54 our results suggest that, in the presence of glucose, carbon/nitrogen cross-talk is likely involved i

55 howed that Pkm2 deletion reduced the flow of glucose carbons into lactate and glutamate without marke

56 Moreover, chronically elevated glucose causes beta-cell dysfunction, but little is know

57 Subsequent C5aR1 activation controlled UDP-glucose ceramide glucosyltransferase production, thereby

58 ed by feeding time and could underpin plasma glucose changes.

59 Based on review of the insulin/glucose chart in the electronic medical record, recommen

60 Muscle autophagy deficiency did not affect glucose clearance and exercise capacity in lean adult mi

61 The C-statistics were 0.662 for ADA fasting glucose clinical concentration categories and 0.672 for

62 lbumin and fructosamine levels with the mean glucose concentration (P > 0.20 for both comparisons).

63 arterial disease, and 0.683 for ADA fasting glucose concentration clinical categories and 0.688 for

64 ardiovascular disease, 0.701 for ADA fasting glucose concentration clinical categories and 0.722 for

65 1050 curves of glucose concentration of type 1 and type 2 diabetics wer

66 Empagliflozin reduced the plasma glucose concentration threshold for glucose spillage in

67 nmark, we found that impaired fasting plasma glucose concentration was associated with 44% (9-91%) la

68 hich is well below the normal fasting plasma glucose concentration.

69 ase insulin in response to changes in plasma glucose concentration.

70 omeostasis model assessment index (+54%) and glucose concentrations after lunch (+46%) were, however,

71 In contrast, low glucose concentrations did not affect exosialidase activ

72 an +/- SEM pre- and postfilter venous plasma glucose concentrations in the aggregate group were 152 +

73 ale Sprague-Dawley rats with different blood glucose concentrations were utilized to demonstrate the

74 ase expression is downregulated under a high glucose condition both in vitro and in vivo.

75 Caco-2 models treated with EGF had increased glucose consumption, production of lactate, and presence

76 Glucose-containing formulation resulted in the highest c

77 ion dehydration rather than 3-deoxglucosone, glucose contributed more than fructose and fructofuranos

78 rid closed-loop insulin delivery can improve glucose control while alleviating the risk of hypoglycae

79 sure, physical inactivity, smoking, and poor glucose control) are associated with incident HF in blac

80 preliminary investigation of the blood/sweat glucose correlation.

81 Carbasugar sodium-glucose cotransporter 2 (SGLT2) inhibitors are highly pr

82 Empagliflozin, a sodium-glucose cotransporter 2 inhibitor, reduced cardiovascula

83 Dapagliflozin is a sodium-glucose cotransporter-2 inhibitor approved for the treat

84 Finally, to demonstrate this applicability, glucose could be detected in synthetic urine samples dow

85 A truncated form of human glucose-dependent insulinotropic polypeptide (GIP), GIP(

86 ed in immediate and reversible intracellular glucose depletion and lactate accumulation.

87 nscript levels of MSN2/MSN4 are increased in glucose-depletion conditions and that during growth in n

88 el, ER stress markers, and cell death during glucose deprivation, which could be rescued by inhibitio

89 TCA intermediates, with no compensation from glucose-derived anaplerosis.

90 TRPC3) channels are involved in hypothalamic glucose detection and the control of energy homeostasis.

91 apoptosis when a combined high-fat and high-glucose diet was given, seemingly due to suppression of

92 markedly more sensitive than for stimulating glucose disposal (Rd).

93 cle is the major site for insulin-stimulated glucose disposal, and muscle insulin resistance confers

94 fferent substrates (muscle proteins, lipids, glucose, DNA (satellite cells)) can be monitored simulta

95 LC/MS) techniques to investigate the role of glucose during ammonia detoxification.

96 nditions of high fat diet (HFD) consumption, glucose dyshomeostasis develops when beta-cells are unab

97 prevalence and levels of fasting and 2-hour glucose (each P < 0.008).

98 clusion, SGLT2-I treatment improves impaired glucose effectiveness in the liver and insulin sensitivi

99 Acylsugars are composed of either sucrose or glucose esterified with varying numbers of acyl chains o

100 We report a novel system for glucose estimation in model and real samples, utilizing

101 In conclusion, insulin and glucose exposure acutely alter the DNA methylation profi

102 The mice also had elevated fasting blood glucose, fatty liver, and insulin resistance.

103 l (random blood glucose [RBG], fasting blood glucose [FBG], and glycated hemoglobin [HbA1c]) and surv

104 preprandial lipid oxidation and postprandial glucose flux in ZDF rats.

105 es linearly with increasing concentration of glucose from 0.03mmol/L to 3mmol/L, which covers the ran

106 hose polar metabolites (L-serine, L-leucine, glucose, fructose, myo-inositol, citric acid and 2, 3-hy

107 on proton leak but instead via modulation of glucose-fueled respiration.

108 v2 interact with calnexin cycle proteins UDP-glucose:glycoprotein glucosyltransferase 1 (UGGT1), whic

109 SFP1 is induced in stressed glucose-grown cells, whereas RTG3 is upregulated in stre

110 Glucose has been quantified by measuring hydrogen peroxi

111 : 0.2% polidocanol diluted in 70% hypertonic glucose (HG) (group 1) vs 75% HG alone (group 2).

112 We examined glucose homeostasis and beta-cell function of these mice

113 cate aPKC as a novel regulator of energy and glucose homeostasis downstream of the leptin-PI3K pathwa

114 Control of glucose homeostasis plays a critical role in health and

115 ways in skeletal muscle to maintain systemic glucose homeostasis remains largely unexplored.

116 knockout mice exhibited paradoxical superior glucose homeostasis resulting from an enhanced insulin s

117 oncentrations were inversely associated with glucose homeostasis variables and inflammation variables

118 ermore, the adverse effects of ATB2 cells on glucose homeostasis were partially dependent upon T cell

119 e and control db/db mice were phenotyped for glucose homeostasis, insulin sensitivity, insulin secret

120 binding to the Mas receptor (MasR) improves glucose homeostasis, partly by enhancing glucose-stimula

121 as an important target of insulin action on glucose homeostasis.

122 y in hepatocytes did not show any changes in glucose homeostasis.

123 eta cells producing glucagon and insulin for glucose homeostasis.

124 porter and characterized by altered glycogen/glucose homeostasis.

125 mselves by differential actions on lipid and glucose homeostasis.

126 1), a critical incretin that regulates blood glucose homeostasis.

127 g physiological roles in insulin release and glucose homeostasis.

128 mechanism is essential for insulin-regulated glucose homeostasis.

129 chitin as a carbon source in the absence of glucose, importing it via the chitin-uptake channel EcCh

130 ormalize activation of VMH GI neurons by low glucose in STZ rats after RH.

131 ve layer has been developed for detection of glucose in the presence of interferences.

132 sensor towards the determination of H2O2 and glucose in the real samples have been demonstrated.

133 owered insulin levels while increasing blood glucose in vivo.

134 ibition, while lung ADC exhibits significant glucose independence.

135 We found that glucose-induced insulin secretion declined by 50% in rat

136 human beta-cells, barr2 knockdown abolished glucose-induced insulin secretion.

137 hed the ameliorative effects of NaHS on high glucose-induced NOX4 expression, reactive oxygen species

138 antioxidant system through up-regulation of glucose influx, the pentose phosphate pathway, and NAD s

139 nts performed following [U-(2)H7, U-(13)C]-D-glucose injections.

140 ed meal induced a greater increase in plasma glucose, insulin, and GIP concentrations after surgery,

141 Metabolic variables, including glucose, insulin, insulin-like growth factor I, triglyce

142 However, a high-glucose intake alone did increase beta cell mass and ins

143 d conformations present only a single beta-d-glucose interaction site.

144 creating an alternative route for directing glucose into the pentose phosphate pathway that bypasses

145 S. pombe Gcd1 and Idn1 act together to shunt glucose into the pentose phosphate pathway, creating an

146 lta subunit in pancreatic islets, results in glucose intolerance and diabetes without affecting insul

147 ion in both white and brown adipose tissues, glucose intolerance and insulin resistance while exhibit

148 vents may be enhanced when heart failure and glucose intolerance coexist and may be attenuated when d

149 with CF may contribute to the development of glucose intolerance in the CF pediatric population, and

150 studies, we found no consistent evidence of glucose intolerance or insulin resistance during pregnan

151 y, DHHC7 KO mice developed hyperglycemia and glucose intolerance, thereby confirming that DHHC7 repre

152 nt obesity-related hypertension and impaired glucose intolerance.

153 idation; and ameliorated liver steatosis and glucose intolerance.

154 study indicated CRP gene is associated with glucose intolerance.

155 Since 2-hour glucose is an indicator of glucose tolerance, this study

156 Under aerobic conditions, glucose is generally assumed to be burned fully by tissu

157 Although glucose is known to stimulate insulin secretion by beta

158 Glucose is the primary driver of hypothalamic proopiomel

159 this, with a steeper increase of the fasting glucose level (beta=131; 95% CI 38-225) during follow-up

160 rate of documented hypoglycemia with a blood glucose level of 55 mg per deciliter (3.1 mmol per liter

161 2.2 +/- 0.44 kg/m(2) in persons with fasting glucose levels below and above the median, respectively.

162 Only 8% monitored their blood glucose levels daily, 15% monitored weekly, and 10% repo

163 L to 3mmol/L, which covers the range of tear glucose levels for both diabetics and healthy subjects.

164 ssfully normalized and maintained host blood glucose levels for over 370 days in the absence of immun

165 e non-invasive and on-body quantification of glucose levels in human perspiration.

166 We could show that glucose levels influenced the extent of induction of the

167 DNA (pDNA) encoding GLP-1 decreased diabetic glucose levels to the normoglycemic range with significa

168 As expected, pre-diagnostic blood glucose levels were inversely related to glioma risk (AM

169 h lowered insulin secretion, increases serum glucose levels, which stimulates de novo lipogenesis (DN

170 al for use as dietary ingredients with serum glucose lowering activity in humans.

171 Glucose lowering remains important for the prevention of

172 betic sulfonylurea drugs to exert their full glucose-lowering effects.

173 having blood pressure <120/80 mm Hg, fasting glucose <100 mg/dl, glycosylated hemoglobin <5.7%, and t

174 the effect of the presence of xylose during glucose measurements.

175 ivation may protect against DN by increasing glucose metabolic flux, inhibiting the production of tox

176 1 in mice with diet-induced obesity impaired glucose metabolism and AKT activation.

177 es.Several metabolic factors affect cellular glucose metabolism as well as the innate inflammatory re

178 d that differential regulation of macrophage glucose metabolism by macrophage colony-stimulating fact

179 ally, CTRP6 regulates local inflammation and glucose metabolism by targeting macrophages and adipocyt

180 a mechanism by which alterations in cellular glucose metabolism can influence cellular inflammatory r

181 Perturbation of glucose metabolism or disruption of Myc function or ster

182 Both treatments had neutral effects on glucose metabolism parameters.

183 Parameters of glucose metabolism were analyzed according to the oral m

184 eveals the mechanism by which YAP reprograms glucose metabolism, but also highlights the therapeutic

185 se model whether early or late components of glucose metabolism, exemplified by fluorine 18 ((18)F) f

186 t in the intestine and to partially modulate glucose metabolism.

187 on is an important step in the regulation of glucose metabolism.

188 lic flux, inhibiting the production of toxic glucose metabolites and inducing mitochondrial biogenesi

189 d mouse podocytes had higher levels of toxic glucose metabolites, mitochondrial dysfunction and apopt

190 l (rapid polymyxin NP test) in 2016, detects glucose metabolization in the presence of polymyxin E (P

191 published new, more stringent guidelines for glucose meter manufacturers to evaluate the performance

192 cturers to evaluate the performance of blood glucose meters in critically ill patient settings.

193 In vitro evaluation of dual lactate-glucose microbiosensor revealed an extended linear range

194 otential for the use as the enzyme for blood glucose monitor enzyme sensor strips was evaluated, espe

195 tients with type 1 diabetes using continuous glucose monitoring (CGM) has not been studied.

196 to evaluate the clinical accuracy of a blood glucose monitoring system in critically ill patients.

197 egnant, 110 planning pregnancy) to capillary glucose monitoring with CGM (108 pregnant and 53 plannin

198 pharmacologically in vitro and in vivo using glucose, nifedipine (VDCC blocker), the sulfonylureas to

199 lusion criteria (NAFLD with impaired fasting glucose or impaired glucose tolerance) and were randomly

200 C. perfringens can grow by utilizing either glucose or sialic acids, such as N-acetylneuraminic acid

201 highly sensitive to external signals such as glucose oscillations and stress cues.

202 discern the concentration of average plasma glucose over a long-drawn-out period.

203 biosensor, horseradish peroxidase (HRP) and glucose oxidase (GOD) were electrodeposited within the h

204 Glucose oxidase (GOx) was immobilized on a modified indi

205 erometry at -0.35V (vs pseudo-Ag/AgCl) using glucose oxidase immobilized on Pt-decorated graphite.

206 vitro with nitrating nitrite/myeloperoxidase/glucose oxidase.

207 utant mice also exhibited increased rates of glucose oxidation with increased energy expenditure, des

208 tail a mediator- and membrane-free enzymatic glucose/oxygen biofuel cell based on transparent and nan

209 and Foxo3alpha expression in IRPTCs by high glucose plus palmitate.

210 suppressive actions of insulin on endogenous glucose production (EGP) are markedly more sensitive tha

211 Insulin inhibits hepatic glucose production and promotes lipogenesis by suppressi

212 ss gluconeogenic gene expression, and reduce glucose production in hepatocytes.

213 that TCF19 overexpression represses de novo glucose production in HepG2 cells.

214 actate likely contributes to high endogenous glucose production in seals.

215 to-minute regulation of postprandial hepatic glucose production, although conditions of glucagon exce

216 The liver is the primary site of endogenous glucose production, especially during states of prolonge

217 insulin-stimulated suppression of endogenous glucose production.

218 SVEN_3027 is a UDP-glucose pyrophosphorylase, SVEN_3972 is an unusual ITP-m

219 interval [CI], 1.04-1.16), low CSF to blood glucose ratio (HR, 1.16 per 0.10 decrease; 95% CI, 1.04-

220 nship between glycemic control (random blood glucose [RBG], fasting blood glucose [FBG], and glycated

221 nes involved in control of bone homeostasis, glucose regulation, satiety, and gastro-intestinal funct

222 e traits) or glycemic (associated with other glucose-related traits).

223 Regulation of blood glucose requires precise coordination between different

224 uctosyl residue to either C6-OH group of the glucose residues in Tre.

225 Glucose-responsive delivery of insulin mimicking the fun

226 principle used to endow insulin analogs with glucose responsivity.

227 ense system would prevent HAAF and normalize glucose sensing after RH in diabetes.

228 in islet physiology, including regulators of glucose sensing and hormone secretion, are differentiall

229 Furthermore, deficiencies in beta cell glucose sensing are likely to contribute to defective in

230 sisted method and examined for non-enzymatic glucose sensing in ionic liquids by cyclic voltammetry a

231 A glucose-sensitive signal transduction circuit involving

232 ECG abnormalities but not with higher blood glucose, serum cholesterol, or serum homocysteine levels

233 e plasma glucose concentration threshold for glucose spillage in the urine similarly in individuals w

234 deletion of StarD10 in mice led to impaired glucose-stimulated Ca(2+) dynamics and insulin secretion

235 While it is known that ghrelin inhibits glucose-stimulated insulin secretion (GSIS), the effect

236 ves glucose homeostasis, partly by enhancing glucose-stimulated insulin secretion (GSIS).

237 n clonal MIN6 beta-cells increases basal and glucose-stimulated insulin secretion and Ca(2+) uptake i

238 ivity were reduced by approximately 60%, and glucose-stimulated insulin secretion was eliminated.

239 a-cells, mitochondrial bioenergetics control glucose-stimulated insulin secretion.

240 intermediates and ATP during large shifts in glucose supply or demand.

241 In addition to high sensitivity to glucose, the grik1-2 grik2-1 mutant was sensitive to hig

242 effect on serum so as conventional pasta and glucose, thus suggesting greater effectiveness of lipoph

243 te and glutamate without markedly increasing glucose-to-ribose flux.

244 nd categorized into quartiles) with impaired glucose tolerance (IGT) and gestational diabetes mellitu

245 a large group of subjects with NGT, impaired glucose tolerance (IGT), and T2DM.

246 evels are observed in subjects with impaired glucose tolerance (IGT).

247 l littermates, knockout mice showed impaired glucose tolerance and circulating leptin, GLP-1, and ins

248 ly, ATM Exos obtained from lean mice improve glucose tolerance and insulin sensitivity when administe

249 ng that even 1 night of shift work decreases glucose tolerance and that circadian disruption is linke

250 reated participants (63.8%) developed normal glucose tolerance compared with 8 placebo-treated partic

251 dams produced female offspring with impaired glucose tolerance compared with offspring of chow-fed da

252 ats housed at 5 degrees C for 28 h, and yet, glucose tolerance did not change, owing to a doubling of

253 ignificantly lower blood glucose and improve glucose tolerance in diet-induced obese mice.

254 in either group, but did transiently improve glucose tolerance in high fat-fed mice.

255 ult mice greatly impairs insulin release and glucose tolerance in mice fed with a calorie-rich diet.

256 e and that circadian disruption is linked to glucose tolerance in mice.

257 9(-/-) mice displayed normal body weight and glucose tolerance on a regular chow (RC) diet.

258 olar bone volume changes and increased BW or glucose tolerance response.

259 irst-phase insulin release on an intravenous glucose tolerance test that was higher than the threshol

260 postchallenge change in glucagon during oral glucose tolerance tests (OGTTs), hypothesizing that high

261 nts with coronary heart disease and impaired glucose tolerance were randomly assigned (1:1), in block

262 -10 g/L (95% CI: -12.90, -7.10 g/L; impaired glucose tolerance) and -6 g/L (95% CI: -8.47, -3.53 g/L;

263 LD with impaired fasting glucose or impaired glucose tolerance) and were randomly assigned into exerc

264 nts with coronary heart disease and impaired glucose tolerance, acarbose did not reduce the risk of m

265 normoglycemia and vascularization, improved glucose tolerance, and increased insulin content.

266 sulted in decreased beta cell mass, impaired glucose tolerance, defective insulin secretion, and incr

267 Since 2-hour glucose is an indicator of glucose tolerance, this study indicated CRP gene is asso

268 body-positive at-risk children with impaired glucose tolerance.

269 insulin sensitivity, insulin secretion, and glucose tolerance.

270 temically to promote insulin sensitivity and glucose tolerance; as a class, these lipids are referred

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

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

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

274 Glucose-transport inhibitors killed trypanosomes without

275 tion based on addiction to the high-affinity glucose transporter, Glut3.

276 alcineurin inhibitor rescued cells from high-glucose triggered oxidative stress and apoptosis.

277 atment conditions, showed strongly increased glucose (up to +81%) and xylose (up to +153%) release, s

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

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

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

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

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

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

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

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

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

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

288 in relative TSCR were associated with raised glucose uptake.

289 from certain nonmalignant tissues with high glucose uptake.

290 and the activation of VMH GI neurons in low glucose using membrane potential sensitive dye in vitro

291 Thus, therapy with 2DG to limit glucose utilization caused mice to become susceptible to

292 sulin resistance are associated with reduced glucose utilization in the muscle and poor exercise perf

293 Synechococcus elongatus PCC 7942 to improve glucose utilization, enhance CO2 fixation and increase c

294 However, glucose utilization, glycerol release, triglyceride and

295 including aerobic production of lactate from glucose (Warburg effect), extensive glutamine utilizatio

296 s to produce [2,3,4,6,6-(2)H5, 3,4-(13)C2]-D-glucose was developed to improve the (13)C signal-to-noi

297 Besides being oxidized, glucose was mainly metabolized via glycerol production a

298 s activates AMPK even in cells with abundant glucose, whereas the catalysis-defective D34S aldolase m

299 ex) by UV crosslinking immediately following glucose withdrawal (0, 4, and 8 min).

300 nd nutrient stresses caused by amino acid or glucose withdrawal.