ライフサイエンスコーパス: glucose

1 but not ATP and decreased G6pc mRNA at high glucose.

2 ltured in 10 mm glucose compared with 5.5 mm glucose.

3 ated with liver enzymes or non-fasting blood glucose.

4 o many Bgls that are completely inhibited by glucose.

5 ammed cell death pathways, in the absence of glucose.

6 subset of VMN cells that function to elevate glucose.

7 tor for the fused measurement to lactate and glucose.

8 differences with a Bgl3 that is inhibited by glucose.

9 ota increased adiposity but decreased plasma glucose.

10 igration of Schwann cells challenged by high glucose.

11 tin (-0.7 ng/mL; -2.1, 0.8 ng/mL) or fasting glucose (0.2 mmol/L; -0.5, 0.9 mmol/L) in men exposed to

12 In contrast, the reaction intermediate beta-glucose 1,6-bisphosphate, whose concentration depends on

13 ate, whose concentration depends on the beta-glucose 1-phosphate concentration, couples the conformat

14 The ratios of fructose:glucose (1:3, 1:2 and 1:1) and glucose:water (1.7, 1.9 a

15 Glucose-6-phosphatase-alpha (G6Pase-alpha or G6PC) defic

16 hosphate dehydrogenase, pyruvate kinase, and glucose-6-phosphate isomerase showed IgE-binding for 6%-

17 dial responses of blood triglyceride (103%), glucose (68%) and insulin (59%) following identical meal

18 feoylquinic acids and flavones reduced blood glucose, alanine aminotransferase (ALT), aspartate amino

19 On the superior carbon source (glucose), all cells achieve high growth rates, while on

20 ed with fluorescently labeled fatty acids or glucose analog, and analyzed by confocal microscopy.

21 NDH and T2D and improved management of blood glucose and cardiovascular risk factors.

22 e YY in regulating ion-coupled absorption of glucose and dipeptides.

23 e molecules (dopamine, bovine serum albumin, glucose and elongated peptide) was negligible.

24 e sensitivity is enhanced to 24% and 37% for glucose and fructose adulterated honey samples respectiv

25 curve was linear from 0.1 to 15 g L(-1) for glucose and fructose with limits of detection of 0.012 g

26 by increasing the mitochondrial oxidation of glucose and glutamine carbons to support the bioenergeti

27 -value and inversely associated with fasting glucose and HbA(1c) (P < 0.05), whereas BRS was preserve

28 Exposure to PM2.5 impaired glucose and insulin tolerance and reduced energy expendi

29 equires people with diabetes to monitor both glucose and ketone bodies.

30 mice that stress constrains the shuttling of glucose and lactate through astrocyte networks, creating

31 ated in vitro by simultaneous measurement of glucose and lactate, pH, and skin temperature.

32 plays an essential role in the regulation of glucose and lipid homeostasis.

33 y was to investigate the role of fructose in glucose and lipid metabolism in the liver, heart, skelet

34 tory and antidiabetic lipokines that connect glucose and lipid metabolism.

35 , leading to insulin resistance and impaired glucose and lipid metabolism.

36 s generate significantly less phosphorylated glucose and little lactate.

37 ng that the imine formed between circulating glucose and lysine is also stress labile.

38 restores normal electrophysiology, improves glucose and peptide absorption, diminishes diarrhea and

39 CSF glucose and protein levels were normal for 83/116 (75.2%

40 ys mediating the metabolism and transport of glucose and pyruvate.

41 express and secrete glucagon in response to glucose and some glucagon secretagogues, and elevate blo

42 that cAMP synthesis in response to elevated glucose and the selective P2Y(11) agonist NF546 is block

43 hat has a higher reduction state compared to glucose and thereby yields the necessary redox cofactors

44 We used an intragastric infusion of glucose and water to bypass the cephalic phase of food i

45 ch mimic the diabetic milieu, including high glucose and/or fatty levels, and by the ablation of gene

46 de significant associations for T2D, fasting glucose, and fasting insulin, comprising 65, 43, and 13

47 ly suggested causal associations for several glucose- and lipid-related biomarkers with type 2 diabet

48 order cognitive functions critically rely on glucose as a metabolic substrate.

49 ctor performed after beta-elimination showed glucose as the major component in the O-glycans of the t

50 ompound K (CK), containing a monosaccharide (glucose) attached at carbon-20.

51 BP flux does not respond to acute changes in glucose availability or cardiac workload.

52 and concentration and (ii) determine whether glucose availability or workload regulate cardiac HBP fl

53 cts of estrogen on SF1 neuronal activity and glucose balance control to paradoxical and detrimental.

54 The current understanding of glucose-based energetics in vivo is based on the quantif

55 s protect against infection; competition for glucose between host and pathogen; significance of infec

56 eta2p = 0.29] and skeletal muscle uptake of glucose [between-group difference (95% CI): 4266 (261, 8

57 The electrochemical measurements for glucose binding on the AuNP-MIP sensor revealed a high a

58 The glucose biosensor presents a linear range of response wi

59 Other parameters, such as glucose, BMI, insulin, HOMA-IR and lipid profile, were a

60 Interrupting glucagon signaling lowers blood glucose but also results in hyperglucagonemia and alpha-

61 uced cell death is driven not by the lack of glucose, but rather by l-cystine import.

62 , a key regulatory enzyme encoded by the UDP-glucose ceramide glucosyltransferase (UGCG) gene.

63 of early vertebrate development, connecting glucose, cholesterol and steroid hormone metabolism with

64 Under glucose clamp conditions (study 2), the change in plasma

65 ifting training profound improved whole-body glucose clearance and skeletal muscle insulin sensitivit

66 Sodium-glucose co-transporter-2 inhibitors and the risk of diab

67 e point-of-care (POC) device for whole blood glucose colorimetric detection.

68 RNA levels in mouse islets cultured in 10 mm glucose compared with 5.5 mm glucose.

69 glycerides and 0.2 mmol/l higher non-fasting glucose, compared with mothers of AGA offspring.

70 r array for electrical conductivity, pH, and glucose concentration measurement was developed.

71 Unlike admission glucose concentration, stress hyperglycemia ratio was si

72 s promote glycosuria, thereby reducing blood glucose concentrations and often resulting in modest wei

73 tric variations in response to environmental glucose concentrations-these are efficiently converted t

74 ss the whole range of maternal mid-gestation glucose concentrations.

75 onged exposure to hypoxia with physiological glucose concentrations.

76 Under high glucose conditions, PKM2 is a target of OGA-associated a

77 in yeast cells grown under steady-state low-glucose conditions, with the largest group being involve

78 Glucose conjugation nevertheless increases nuclear deliv

79 ific differences in the rate and kinetics of glucose consumption and glycolysis throughout IVM.

80 ramicro electrode (UME) to measure the local glucose consumption of Streptococcus mutans (S. mutans)

81 eld, as well as improved cellular growth and glucose consumption, compared with strains without biode

82 47 (31.1%) vs 42 (28.3%) needed insulin for glucose control, and 5 (3.3%) vs 9 (6.1%) experienced ot

83 y involved in disease progression and proper glucose control.

84 the proximal tubule, which (alongside sodium-glucose cotransport) further limits urinary glucose loss

85 The sodium glucose cotransporter 2 (SGLT2) inhibitor empagliflozin

86 ence of new glucose-lowering agents - sodium-glucose cotransporter 2 inhibitors and incretin therapie

87 Sodium-glucose cotransporter 2 inhibitors reduce the risk of he

88 SGLT2 (sodium-glucose cotransporter 2) inhibitors have been shown to l

89 cts of ertugliflozin, an inhibitor of sodium-glucose cotransporter 2, have not been established.

90 Sodium-glucose cotransporter-2 (SGLT-2) inhibitors reduced hear

91 Inhibition of the sodium-glucose cotransporter-2 (SGLT2i) improves outcomes in pa

92 storage level showed increased tolerance to glucose deficiency among the studied melanoma phenotypes

93 artially impairing vascular permeability and glucose delivery to beta-cells.

94 dopsis (Arabidopsis thaliana) CSLD3 is a UDP-glucose-dependent beta-1,4-glucan synthase that forms pr

95 h day, whereas levels of the other incretin, glucose-dependent insulinotropic polypeptide, were not a

96 sulin secretion machinery, which enables the glucose-dependent secretion of protective immunomodulato

97 of lipopolysaccharide (LPS), KCl and oxygen/glucose deprivation (OGD) that reflect inflammation, dep

98 Following glucose deprivation, the import of l-cystine and its sub

99 Building on this observation, we show that glucose deprivation-induced cell death is driven not by

100 metabolic plasticity, evidenced by increased glucose-derived lactate production upon ROS inhibition.

101 Interestingly, both l-glucose-derived ligands are partial agonists: they are a

102 l-Glucose-derived ligands, methyl alpha-l-glucopyranoside

103 The results herein reported for corrected glucose detection during on-body measurements are suppor

104 However, the glucose-driven phosphate flush occurred despite inositol

105 e contribution of central K(ATP) channels to glucose effectiveness.

106 expressing (CCKBR-expressing) VMN targets of glucose-elevating parabrachial nucleus neurons.

107 e shift but are less fit in a constant, high-glucose environment, and we observe natural variation in

108 locks beta-cell proliferation in response to glucose ex vivo and in vivo in transplanted glucose-infu

109 flozin promotes osmotic diuresis via urinary glucose excretion and therefore, might offer a novel tre

110 e study highlights the importance of chronic glucose exposure on cell phenotype and emphasises the ne

111 [(13)C(6)]-glucose feeding revealed that GCBCs generate significant

112 Brain glucose-sensing neurons detect glucose fluctuations and prevent severe hypoglycemia, bu

113 dge, this is the first direct measurement of glucose flux through the HBP in any organ.

114 of nondiabetic human islets cultured at 5 mm glucose for 72 h and exacerbated the negative effect of

115 c approach for targeting tumors dependent on glucose for survival.

116 ify neurons that specifically increase blood glucose from among the diversely functioning cell types

117 ty to uncouple the glycolytic utilization of glucose from mitochondrial respiration, allowing for the

118 fect of ethanol, glycerol, tartaric acid and glucose/fructose on the refractive index in model aqueou

119 Using a library of fluorinated glucose (Glc), mannose (Man), and galactose (Gal) derive

120 In TGF-beta-treated PASMCs, glucose, glutamine and fatty acids all contributed carbo

121 l for the development of obesity or impaired glucose handling due to HFD, and advance understanding o

122 no changes in energy expenditure or systemic glucose handling.

123 was negatively correlated with fasting blood glucose, HbA1c and diastolic blood pressure (DBP), and p

124 Glucose homeostasis and growth essentially depend on the

125 ciation between 9p21.3 and MI is modified by glucose homeostasis and lifestyle.

126 Disturbances in glucose homeostasis and low-grade chronic inflammation c

127 nts been shown to have protective effects on glucose homeostasis during high-fat overfeeding.

128 r the P2 isoform alone in the liver improves glucose homeostasis in dietary and genetic mouse models

129 e adipose tissue is associated with improved glucose homeostasis in mice.

130 in adipose tissue is crucial for whole-body glucose homeostasis, with insulin resistance being a maj

131 ic beta-cells is essential to maintain blood glucose homeostasis.

132 regulation of energy metabolism and systemic glucose homeostasis.

133 rides, reduced levels of HDL cholesterol and glucose impairment) on the phenotype of LRRK2 and GBA Pa

134 id not match the relevant clinical range for glucose in blood.

135 WAT inversely correlated with fasting plasma glucose in both obese mice and humans.

136 subpopulations, and 20 free amino acids and glucose in EV subpopulations were identified and quantif

137 oximately a hundred times less abundant than glucose in human blood.

138 within the expected physiological levels of glucose in sweat (10-200 muM), and the calibration param

139 ying the failure of beta-cells to respond to glucose in T2D remains unknown.

140 ectral measurements of proteins, lipids, and glucose in the short-wavelength IR region, performed at

141 We found that glucose increases lipolysis in non-diabetic human islets

142 itional need of HLCs and HepG2 cells induces glucose independence, mitochondrial function, and the ac

143 dies further show that TG2 inhibition blocks glucose-induced fibrogenesis and cell proliferation.

144 tion of LncRNA MALAT1 by its siRNA prevented glucose-induced increase in Keap1 and facilitated Nrf2 n

145 High glucose-induced remodeling of microtubule network facili

146 glucose ex vivo and in vivo in transplanted glucose-infused rats.

147 avenous arginine bolus before and after 72-h glucose infusion.

148 mediated LincIRS2 loss causes elevated blood glucose, insulin resistance and aberrant glucose output

149 , weight, waist circumference, blood lipids, glucose, insulin, and blood pressure were measured.

150 years, and ages 6.5-11.5 years) with fasting glucose, insulin, insulin resistance, beta-cell function

151 HF diet caused greater weight gain and glucose intolerance in middle-aged females than males.

152 lenge, FtMT-Adip mice are leaner but exhibit glucose intolerance, low adiponectin levels, increased r

153 glucose to ethanol and respire ethanol once glucose is consumed.

154 o not rise with increased respiration unless glucose is present; and (c) mitochondrial oxidative stre

155 Glucose isomerization rates (per Ti, 373 K) are undetect

156 Net cerebral glucose/lactate exchange, and biomarkers of oxidative an

157 es vary significantly, irrespective of blood glucose level or diabetic status.

158 hypoglycemia with severity of level 2 (blood glucose level, <54 mg per deciliter) or level 3 (severe

159 exhibited significantly higher fasting blood glucose levels and produced more glucose than floxed AMP

160 y facilitates the maintenance of circulating glucose levels by decreasing the rate of blood sugar abs

161 ut retained its ability to lower circulating glucose levels in the absence of GDF15 activity.

162 to secrete insulin in response to increased glucose levels that occur with eating.

163 ER) stress related gene expressions, fasting glucose levels, insulin sensitivity and restored pancrea

164 as those guided by physicians in controlling glucose levels.

165 (AMPK) is a key energy sensor, activated by glucose limitation to resolve nutrient supply-demand imb

166 Importantly, upon glucose limitation, Vitamin K2-upregulated glycolysis ma

167 us wild-type; (2) Aberrant activation of the glucose/lipid metabolism regulator peroxisome proliferat

168 d with excessive levels of nutrients such as glucose, lipids, and amino acids.

169 -glucose cotransport) further limits urinary glucose loss.

170 rkinson's disease of users of any other oral glucose lowering drugs.

171 The emergence of new glucose-lowering agents - sodium-glucose cotransporter 2

172 s for longer durations, considering studying glucose-lowering therapies as first-line management of t

173 to diagnose hypertension and a single blood glucose measurement to diagnose diabetes.

174 coli by successively adapting it to defined glucose media without and with the antibiotic rifampicin

175 li population during adaptation to a minimal glucose medium containing citrate (DM25).

176 cs in vivo is based on the quantification of glucose metabolic rates with 2-FDG PET, a method that pe

177 Glucose metabolism and calcium influx are involved in pr

178 cess functionally distinct from conventional glucose metabolism and leads to distinct metabolic requi

179 ein instability was associated with impaired glucose metabolism and lower glycolytic enzyme expressio

180 sterone ((18)F-FFNP) PET/CT imaging of tumor glucose metabolism and progesterone receptor (PR) expres

181 for genes encoding other enzymes involved in glucose metabolism compared to follower cells.

182 ting evidence suggests that individuals with glucose metabolism disorders are susceptible to mortalit

183 ocumented that 5-PAHSA primes adipocytes for glucose metabolism in a different way from insulin, prom

184 phosphate receptor-1 (S1PR1) expression and glucose metabolism in CD4(+) T cells as potential mechan

185 d key biomarkers of inflammation, lipid, and glucose metabolism in the blood of patients with moderat

186 ecular pathways that respond to the state of glucose metabolism to drive the morula to blastocyst tra

187 Mitochondrial function and fatty acid and glucose metabolism were impaired in HF-patients compared

188 o how TIH, prevalent in people with impaired glucose metabolism, contributes to cardiovascular diseas

189 Among genes involved in glucose metabolism, hexokinase domain containing 1 (HKDC

190 d, thus, obesity-associated deterioration of glucose metabolism.

191 und pregnancy-related physiologic changes in glucose metabolism.

192 inflammation, as well as improved lipid and glucose metabolism.

193 id, which is enabled by the reprogramming of glucose metabolism.

194 tic pancreatic cancers were dependent on the glucose-metabolizing enzyme phosphogluconate dehydrogena

195 less than 9% when compared with a commercial glucose meter.

196 glycemic responses as measured by continuous glucose monitors (CGMs).

197 diversity of oral bacteria, and pH, lactate, glucose, nitrate and nitrite concentrations.

198 and exacerbated the negative effect of 20 mm glucose on the cell viability during culture period.

199 ood glucose, insulin resistance and aberrant glucose output in lean mice.

200 (SECM) probe by covalently immobilizing the glucose oxidase (GOD) enzyme onto an ultramicro electrod

201 Enzymes including papain, alpha-amylase, glucose oxidase and phytase stabilized dough structure t

202 abolism toward oxygen-sparing glycolysis and glucose oxidation and to increase cAMP levels is depende

203 NADH homeostasis and proliferation even when glucose oxidation is increased.

204 resent evidence for the alternation of brain glucose oxidation.

205 whereas deficiency of the glycolytic enzyme glucose phosphate isomerase (Gpi1) selectively eliminate

206 Hub cells appear to be enriched for the glucose phosphorylating enzyme glucokinase and for genes

207 Polydextrose (PDX) is a branched glucose polymer, utilized as a soluble dietary fiber.

208 Starch granules are composed of two distinct glucose polymers - amylose and amylopectin.

209 tand the consequences of GLP-1 resistance on glucose portal signaling.

210 mphasises the need to pay close attention to glucose preconditioning in interpreting results under cu

211 glycemia is a potent regulator of endogenous glucose production (EGP).

212 a through significant suppression of hepatic glucose production.

213 the novel findings that loss of LacR altered glucose-PTS activity and expression of the gene for gluc

214 spend >50% of their time outside the optimal glucose range.

215 By inhibiting glucose reabsorption in the proximal tubule, these agent

216 Glucose-regulated protein 78 is reduced in AT2 cells fro

217 Individuals have widely varying glucose responses to different meals, and precision nutr

218 Glucose-responsive INS-1 beta-cells were incubated with

219 A series of glucose-responsive insulin delivery mechanisms and devic

220 Glucose-responsive insulin delivery systems that mimic p

221 human islets, INS1 cells showed visible LDs, glucose-responsive lipolysis, and impairment of GSIS aft

222 sulin is achieved highlighting an autonomous glucose-responsive microdevice operating as an "artifici

223 Feeding males with stable-isotope-labelled glucose revealed that the males produced these five comp

224 nsumed fatty acids and, unexpectedly, little glucose; secreted glutamine and other nitrogen-rich amin

225 We have developed a new dual-tip glucose sensing scanning electrochemical microcopy (SECM

226 but mechanisms mediating functions of these glucose-sensing neurons are unclear.

227 Brain glucose-sensing neurons detect glucose fluctuations and

228 e detection limit of the new 25 mum diameter glucose sensor is 10.0 muM with a linear range up to 4.0

229 of two key glycolytic genes, suggestive of a glucose shortage during disease.

230 Moreover, the levels of fructose and glucose significantly increased during the elaboration p

231 In contrast, glucose starvation or hyperosmotic shock causes cell shr

232 Glucose starvation suppressed H2Aub levels independently

233 tes Pontin chromatin-remodeling factor under glucose starvation, and methylated Pontin binds Forkhead

234 ts the same metabolic pathways necessary for glucose stimulated insulin secretion for protection from

235 ) channels is a key determinant of beta-cell glucose-stimulated Ca(2+) entry and thus the set-point o

236 duced mitochondrial oxygen consumption rate, glucose-stimulated Ca(2+) flux, and reduced insulin cont

237 ey regulator in determining the set-point of glucose-stimulated Ca(2+) influx and insulin secretion.

238 Glucose-stimulated insulin secretion (GSIS) is regulated

239 cultured male and female islets, T enhanced glucose-stimulated insulin secretion (GSIS).

240 rc -/- mice, which correlated with decreased glucose-stimulated insulin secretion (GSIS).

241 isplay improved glucose tolerance, increased glucose-stimulated insulin secretion, and hyperglucagone

242 cyclophilin D (CypD) promotes NGSIS, but not glucose-stimulated insulin secretion, by increasing mito

243 ents with HNF1A diabetes via potentiation of glucose-stimulated insulin secretion.

244 es exhibited first- and second-phase dynamic glucose-stimulated insulin secretion.

245 Glucose stimulation significantly enhances L-DOPA uptake

246 the saccharide hydration properties (xylose, glucose, sucrose) in pure water are determined.

247 sting blood glucose levels and produced more glucose than floxed AMPK catalytic alpha1 and alpha2 mic

248 his yeast has evolved the ability to ferment glucose to ethanol and respire ethanol once glucose is c

249 The isomerisation of glucose to fructose is a critical step towards manufactu

250 ajority of their energy via the breakdown of glucose to lactate.

251 provide evidence that a metabolic shift from glucose to lipid is a key mechanism in neurodegeneration

252 Mice lacking TrkB.T1 show impaired glucose tolerance and insulin secretion.

253 icipants (N = 973) with different weight and glucose tolerance categories were recruited.

254 y weight by 3-17% and significantly improved glucose tolerance in aged mice fed a chow (~30% vs. sali

255 Antibody injection improved glucose tolerance in D734A INSR-expressing mice and redu

256 opositivity and different BMI categories, or glucose tolerance status.

257 amily history of T2DM (FH+) received an oral glucose tolerance test and two-step hyperglycemic clamp

258 signaling, insulin sensitivity, and systemic glucose tolerance was consistent with functional MRI dat

259 ed the L lactis subsp cremoris had increased glucose tolerance while on the Western-style diet compar

260 tational diabetes mellitus and have impaired glucose tolerance whilst cholestatic.

261 6a-(KGKY-knockin) mice demonstrated improved glucose tolerance, despite impaired insulin sensitivity

262 nd DLL4 in adult beta-cells display improved glucose tolerance, increased glucose-stimulated insulin

263 in females and was associated with improved glucose tolerance, increased metabolism, energy expendit

264 ngagement on ILC2s significantly ameliorates glucose tolerance, protects against insulin-resistance o

265 defect in insulin action to maintain normal glucose tolerance.

266 uded 256 with diabetes and 133 with a normal glucose tolerance.

267 n via an anti-alpha-klotho antibody impaired glucose tolerance.

268 d (P = 0.026) placental mRNA expression of a glucose transporter (GLUT-3) and increased (P = 0.037) p

269 Glycogen and glucose transporter GLUT4 are decreased.

270 ortant for both flagellar trafficking of the glucose transporter GT1 and for successful cytokinesis a

271 nd plasma membrane localization of the GLUT4 glucose transporter in skeletal muscle, but are not defi

272 has been proposed to function in delivery of glucose transporter type 4 (GLUT4)-containing vesicles t

273 of potent, orally bioavailable inhibitors of glucose transporters, targeting both GLUT1 and GLUT3.

274 with increasing concentrations of [U-(13)C] glucose under conditions where GSIS was not affected (2-

275 me glucagon secretagogues, and elevate blood glucose upon transplantation in mice.

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

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

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

279 Cardiac glucose uptake and oxidation are reduced in diabetes des

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

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

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

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

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

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

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

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

288 The glucose, used as an initiator, was tracked through the s

289 explaining why short-term, insulin-dependent glucose utilization does not promote insulin resistance.

290 n the improvement of insulin sensitivity and glucose utilization in extrahepatic tissues.

291 ances, the 2-FDG LC used to quantify in vivo glucose utilization should not be expected to remain con

292 in A1c) levels, which poorly reflects direct glucose variation.

293 Expression of FLCN in response to glucose was greater in individuals with diabetic retinop

294 d K(ATP) channel opened more frequently when glucose was high.

295 s measured by chemiluminescence, and fasting glucose was measured with the enzymatic colorimetric met

296 In contrast, glucose was required for insulin to increase mitochondri

297 ed T(gs) (P < 0.05) and sugaring of fructose-glucose-water model solutions.

298 s of fructose:glucose (1:3, 1:2 and 1:1) and glucose:water (1.7, 1.9 and 2.1) also influenced the mea

299 ealed that the MpBgl3 was highly tolerant to glucose, which is in contrast to many Bgls that are comp

300 P-MIP sensor revealed a high affinity toward glucose with a dissociation constant (K(d)) of 3 x 10(-8

301 hibitor-1, was depressed by exposure to high glucose, with the reduction in nitric oxide production b