ライフサイエンスコーパス: fructose

1 aggregation of the sensor in the presence of fructose.

2 ern" diet containing high amounts of fat and fructose.

3 glucose or sucrose in foods or beverages by fructose.

4 metabolic route able to convert glucose into fructose.

5 o a hydrolysis of the sucrose to glucose and fructose.

6 ssed in the intestine but does not transport fructose.

7 r starting a high-fat diet supplemented with fructose.

8 id base of our bisboronic acids, glucose and fructose.

9 incubated with medium supplemented with 3 mM fructose.

10 nsporters that allow growth on galactose and fructose.

11 with a constant increase in both glucose and fructose.

12 of aldose reductase, sorbitol and endogenous fructose.

13 lators, adenosine 5'-monophosphate (AMP) and fructose 1,6-bisphosphate (FBP), respectively.

14 e, and we can for the first time explain how fructose 1,6-bisphosphate affects the active site.

15 nesis, including bifunctional unidirectional fructose 1,6-bisphosphate aldolase/phosphatase, have bee

16 by thermostability studies, demonstrate that fructose 1,6-bisphosphate binding to the allosteric doma

17 tion leads to the continuous accumulation of fructose 1,6-bisphosphate in a permanently frozen soluti

18 tone phosphate, forming the much more stable fructose 1,6-bisphosphate.

19 Uptake of 1-deoxy-1-[(18)F]fluoro-d-fructose (1-[(18)F]FDF), 6-deoxy-6-[(18)F]fluoro-d-fruct

20 Fructose-1,6-bisphosphatase (FBP1) is a rate-limiting en

21 the enzyme together with the better studied fructose-1,6-bisphosphatase (FBPase), in both cases from

22 three crystal structures of Leishmania major fructose-1,6-bisphosphatase (LmFBPase) along with enzyme

23 ent peaks in the temporal pattern of urinary fructose-1,6-bisphosphatase and glutathione-S-transferas

24 inary excretion of the renal tubular enzymes fructose-1,6-bisphosphatase and glutathione-S-transferas

25 en showed consistently low levels of urinary fructose-1,6-bisphosphatase excretion over comparable pe

26 The gluconeogenic enzyme fructose-1,6-bisphosphatase has been proposed as a poten

27 lmost abolished light-dependent reduction of fructose-1,6-bisphosphatase.

28 s of stress-responsive genes including fbp1 (fructose-1,6-bisphosphatase1).

29 Fructose-1,6-bisphosphate (FBP) aldolase, a glycolytic e

30 rs AMPK activation by sensing the absence of fructose-1,6-bisphosphate (FBP), with AMPK being progres

31 reshold after intake of inulin (13 of 29) or fructose (11 of 29) than glucose (6 of 29).

32 profile is: total sugar (51 +/- 21 g/100g), fructose (17 +/- 9.7 g/100g), glucose (14 +/- 8.6g/100g)

33 ng proteins such as 6-phosphofructo-2-kinase/fructose 2,6-bisphosphatase (PFK2/FBP2), which functions

34 targeting mTORC1 or 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3) ameliorated GVHD m

35 se-2 (PFK2) isoform 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), a rate-limiting e

36 reases the level of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), which activates p

37 and phosphorylates 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase isoform 3 (PFKFB3), a major d

38 bifunctional enzyme 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase-4 (PFKFB4) controls metabolic

39 of mutant forms of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase affect cardiac structure, fu

40 osphatase-deficient 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase in the heart (Glyco(Hi) mice

41 a kinase-deficient 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase transgene (Glyco(Lo) mice) l

42 increased levels of the allosteric regulator fructose-2,6-bisphosphate, leading to increased glycolyt

43 ared: (1) with sucrose, (2) with glucose and fructose, (3) with fructose only and (4) with glucose on

44 ortant in the interconversion of glucose and fructose, 5-hydroxymethylfurfural formation mainly proce

45 phosphate (fructose-6-P) as a substrate to a fructose 6-P-specific enzyme was started by a single ami

46 y covalent binding of the enzyme substrate d-fructose 6-phosphate (F6P).

47 r that could phosphorylate either glucose or fructose 6-phosphate (fructose-6-P) as a substrate to a

48 Diabetes elevated glucose 6-phosphate, fructose 6-phosphate and oxidised (NAD+ and NADP+) and r

49 accumulation of the glycolytic intermediate fructose 6-phosphate, leading to engagement of the hexos

50 se (1-[(18)F]FDF), 6-deoxy-6-[(18)F]fluoro-d-fructose (6-[(18)F]FDF), 1-deoxy-1-[(18)F]fluoro-2,5-anh

51 late either glucose or fructose 6-phosphate (fructose-6-P) as a substrate to a fructose 6-P-specific

52 P, resulted from a decrease in the Khalf for fructose-6-P, which likely influences both gluconeogenes

53 pair, which enhances methanol conversion to fructose-6-phosphate (F6P).

54 P) via regulation of expression of glutamine:fructose-6-phosphate amidotransferase 1 (GFAT1), the rat

55 donor substrates, namely l-erythrulose and d-fructose-6-phosphate.

56 Fructose, a major component of SSBs, may acutely trigger

57 binds to fructose transporters and promotes fructose absorption by the small intestine.

58 e abolished the diabetes-induced increase in fructose absorption.

59 ity of fructose supports the contention that fructose accelerates subcellular hexose sugar-related pr

60 ze, decreased number of pauses), relative to fructose, across training.

61 We found that fructose acutely and transiently suppressed mTORC1 signa

62 Fructose administration over a 10-hour period stimulated

63 hepatic lipogenesis was stimulated with oral fructose administration.

64 oholic proof, l-lactic acid content, glucose+fructose and acetic acid content.

65 ljungdahlii was grown organotrophically with fructose and also lithotrophically, either with syngas -

66 teatohepatitis associated with diets high in fructose and fat.

67 deoxglucosone, glucose contributed more than fructose and fructofuranosyl cation to the early stage o

68 (up to 70 degrees C) of aqueous solutions of fructose and glucose (up to 10% w/v), with significantly

69 Fructose and glucose accumulation were linear in 'Ntopia

70 uces lipogenesis, we compared the effects of fructose and glucose on mammalian target of rapamycin co

71 t flour with different molar ratios of total fructose and glucose to asparagine were investigated.

72 ifferences in the signaling pathways used by fructose and glucose to regulate lipid metabolism.

73 Results of this study indicated that fructose and glucose undergo oxidation during thermal tr

74 The relative importance of fructose and glucose, released from wheat fructan and su

75 of various samples with different ratios of fructose and glucose.

76 ng for sucrose, a disaccharide consisting of fructose and glucose.

77 naffected by treatment although fetal plasma fructose and hepatic lactate dehydrogenase activity were

78 Fructose and inulin increased breath hydrogen levels in

79 ucose conjugates, generating 1-amino-1-deoxy-fructose and its derivatives.

80 glucose increased in a high C/N ratio, while fructose and mannitol decreased.

81 BIO apples had consistently higher levels of fructose and monomeric phenolic compounds but lower leve

82 Overconsumption of fructose and other sugars has been linked to nonalcoholi

83 mined the association between maternal serum fructose and placental uric acid levels in humans.

84 abinose, glucose, rhamnose, xylose, mannose, fructose and ribose) plus inositol as internal standard

85 ast, today, the combination of diets high in fructose and salty foods, increasing temperatures, and d

86 in Jam 4 sucrose was completely replaced by fructose and stevioside, making this formulation suitabl

87 region between 1175 and 950cm(-1) (glucose, fructose and sucrose absorption bands).

88 most abundant sugars were xylose, arabinose+fructose and sucrose, presenting dried samples with high

89 SuS can be controlled by the availability of fructose and UDP, depending on the metabolic status of a

90 f sucrose and uridine diphosphate (UDP) into fructose and UDP-glucose, is a key enzyme in sucrose met

91 Gene expression with fructose and with H2/CO2 was compared by RNA-Seq.

92 rs to resolve glucose in high backgrounds of fructose and, in combination with multivariate statistic

93 a range of carbohydrates (glucose, sucrose, fructose) and nitrogen sources (urea, NH4Cl) at various

94 mide formation, reducing sugars (glucose and fructose) and ten major amino acids, were quantified dur

95 that certain hormones (vasopressin), foods (fructose), and metabolic products (uric acid) function a

96 T) mice were fed chow or high saturated fat, fructose, and cholesterol (FFC) diet.

97 f mice fed a diet rich in trans-fatty acids, fructose, and cholesterol.

98 nd to contain significantly higher levels of fructose, and lower levels of potassium and glutamine.

99 glucose, sucrose, rhamnose, xylose, mannose, fructose, and ribose were quantified in packed roast-and

100 Although calorically equivalent to glucose, fructose appears to be more lipogenic, promoting dyslipi

101 Hypercaloric fructose ( approximately 25% excess of energy compared w

102 ecent findings to synthesize a novel view of fructose as a cardiopathogenic agent in diabetes and to

103 rates a role for fructokinase and endogenous fructose as mediators of acute renal disease.

104 e enzymatic generation of lactulose requires fructose as nucleophilic acceptor.

105 of mixtures and their combination including fructose, asparagine and different molecular weight chit

106 onella enterica fra locus, which encodes the fructose-asparagine (F-Asn) utilization pathway, are hig

107 for the Salmonella-specific nutrient source fructose-asparagine (F-Asn), to the probiotic bacterium

108 Fructose, at a moderate dose, did not significantly elev

109 t activity is associated with cell growth in fructose-based media or assayed by fructose uptake in wh

110 to 10 wk (mean: 28 d) and included doses of fructose between 40 and 150 g/d (mean: 68 g/d).

111 scence increase is not fully associated with fructose binding, but instead disaggregation of the sens

112 the high activities of glycogen synthase and fructose bisphosphatase in tumors as potential targets f

113 s revealed that it inhibits E. coli class II fructose bisphosphate aldolase, but not RNA polymerase.

114 to blood (13)C glucose (gluconeogenesis from fructose), blood VLDL-(13)C palmitate (a marker of hepat

115 E678, F680, and E686 affected the binding of fructose, but not of UDP.

116 gluconeogenesis intermediates (e.g., glucose/fructose, C6H12O6, keto-hexose, deoxy-hexose, (P < 0.01)

117 rsion into glucose and VLDL-triglyceride and fructose carbon storage into hepatic glycogen and lipids

118 Alternative sugars, such as fructose, circumvent metabolic control systems and exace

119 s analysed using the developed assay and the fructose concentration was calculated to be 477mM with a

120 toring of sucrose, sorbitol, d-glucose and d-fructose concentrations gave unique results for each sol

121 cytosolic ATP and phosphate induced by high fructose concentrations in the medium.

122 etween asparagine and the sum of glucose and fructose concentrations in the wheat flour.

123 toring of sucrose, sorbitol, d-glucose and d-fructose concentrations is reported.

124 in before fructose ingestion [exercise, then fructose condition (ExFru)] or 90 min after fructose ing

125 protein together with 4.4 g/kg fructose (the fructose condition; FRU) or glucose (the glucose conditi

126 Increased fructose consumption and its subsequent metabolism have

127 High fructose consumption has been suggested to contribute to

128 ndings suggest that in mice, excess maternal fructose consumption impairs placental function via a xa

129 Fructose consumption in FRU increased postprandial net c

130 onflicting evidence exists on the effects of fructose consumption in people with type 1 and type 2 di

131 In mice, maternal fructose consumption led to placental inefficiency, feta

132 Excess fructose consumption may confer metabolic risks for both

133 ing evidence exists on the role of long-term fructose consumption on health.

134 Short-term fructose consumption, in isocaloric exchange or in hyper

135 metabolic outcomes resulting from long-term fructose consumption.

136 choice between the 20% glucose- and the 20% fructose-containing food.

137 arch substituted for sugar, yielding a final fructose content of 4% of total kilocalories.

138 Fructose contributed considerably to acrylamide formatio

139 e ingestion minus (13)C-fructose oxidation), fructose conversion into blood (13)C glucose (gluconeoge

140 otein (VLDL) triglycerides by decreasing the fructose conversion into glucose and VLDL-triglyceride a

141 Fructose conveys orosensory (ie, taste) reinforcement bu

142 centage of fructose in three samples of high fructose corn syrup (<4% error).

143 ther beverages sweetened with fructose, high-fructose corn syrup (HFCS), and glucose differentially i

144 a control diet or an HFD coupled with a high fructose corn syrup equivalent.

145 In addition, glucose and fructose could be distinguished up to 1:9 molar ratio in

146 eoxy-d-glucose uptake was not inhibited by d-fructose, demonstrating that the fructose-transporting G

147 Fructose-derivative 6-[(18)F]FDF revealed greater tumor

148 d nearly identically to 3 in the presence of fructose, despite having no functional group with which

149 ) coordinates an adaptive response to a high-fructose diet in mice and that loss of this transcriptio

150 We assessed the impact of a maternal high-fructose diet on the fetal-placental unit in mice in the

151 s and in livers of rats fed a high-fat, high-fructose diet.

152 sis, which is exacerbated by a high-transfat/fructose diet.

153 titration calorimetry, it was confirmed that fructose does indeed bind to the sensor.

154 Fructose-driven glycolytic respiration in naked mole-rat

155 Interference by glucose, fructose, ethanol, and acetic acid in glycerol detection

156 nduction of hepatic de novo lipogenesis with fructose feeding.

157 produced hypotriglyceridemia after 1 week of fructose feeding.

158 or soluble sugar identified in the berry was fructose, following by glucose, and the main organic aci

159 ase.Strong evidence exists that substituting fructose for glucose or sucrose in food or beverages low

160 e evidence suggests that the substitution of fructose for glucose or sucrose in food or beverages may

161 mutarotation velocity and HPLC analyses of d-fructose formation during thermal treatment indicated a

162 enzyme that hydrolyzes sucrose and releases fructose from various fructooligosaccharides (FOS) and f

163 re composed of arabinose, rhamnose, glucose, fructose, galactose and xylose.

164 decreasing lipid and sucrose, and increasing fructose, glucose and acetaldehyde levels, which are pot

165 Fructose, glucose and sucrose were identified in all the

166 Changes in the concentrations of sucrose, fructose, glucose, amino acids, 3-deoxyglucosone, 1-deox

167 by the presence of biological diols such as fructose, glucose, and catechol, and the thiosemicarbazi

168 n contrast, the total monomeric anthocyanin, fructose, glucose, Ca, Na values were higher in the ripe

169 Fructose, glucose, sucrose, maltose, and total sugar con

170 Participants drank 4 servings/d of fructose-, glucose-, or HFCS-sweetened beverages account

171 Fructose had a significantly lower insulin response than

172 Excessive amounts of fructose, HFCS, and glucose from SSBs consumed over 8 d

173 o determine whether beverages sweetened with fructose, high-fructose corn syrup (HFCS), and glucose d

174 replacement of glucose, sucrose, or both by fructose in adults or children with or without diabetes

175 Consistent with elevated urinary fructose in AKI patients, mice undergoing iAKI show sign

176 ) or a high-fat diet supplemented with 30% d-fructose in drinking water (obesogenic diet) for 25-33 w

177 eplacement of glucose, sucrose, or both with fructose in healthy adults or children with or without d

178 dence reveals that while binding occurs with fructose in the aqueous solvent system used, it is not r

179 f carbohydrate (glucose in the first period, fructose in the second, and inulin in the third, in a ra

180 used to accurately measure the percentage of fructose in three samples of high fructose corn syrup (<

181 hich was repressed by FruR in the absence of fructose, in addition to being under carbon catabolic re

182 mmonly consumed monosaccharides, glucose and fructose, in obese and lean adolescents.

183 Both glucose and fructose increased during ripening and demonstrated a po

184 Fructose increased small-bowel water content in both pat

185 Changes in the concentrations of glucose, fructose, individual free amino acids, lysine and argini

186 In the placenta, fructose induced de novo uric acid synthesis by activati

187 We found that fructose-induced G6PC activity is a major determinant of

188 sessed the hypothesis that exercise prevents fructose-induced increases in very-low-density lipoprote

189 most effective strategy to prevent or treat fructose-induced metabolic diseases.

190 To better understand how fructose induces lipogenesis, we compared the effects of

191 ls underwent a 2-hour control period with no fructose infusion followed by a 2-hour hyperinsulinemic/

192 ormed a 60-min exercise either 75 min before fructose ingestion [exercise, then fructose condition (E

193 fructose condition (ExFru)] or 90 min after fructose ingestion [fructose, then exercise condition (F

194 tion ((13)CO2 production), fructose storage (fructose ingestion minus (13)C-fructose oxidation), fruc

195 Compared with glucose, fructose ingestion results in lower postprandial glucose

196 rose from baseline, peaking at 45 min after fructose ingestion, whereas breath hydrogen peaked later

197 ildren with habitual high sugar consumption (fructose intake >50 g/d).

198 However, the direct consequences of fructose intake per se are unknown.

199 d low carbon substrate concentrations (<1 mM fructose) into site wells.

200 sorptive capacity of the small intestine for fructose is limited, though the molecular mechanisms con

201 conveys orosensory reinforcement but unlike fructose, it is a major metabolic energy source, underli

202 day, the men ingested an oral (13)C-labeled fructose load (0.75 g/kg), and their total fructose oxid

203 Under such conditions, fructose lowers whole-body glycogen synthesis and impair

204 n of corticotropin-releasing factor (CRF) on fructose malabsorption and the resulting volume of water

205 CRF constricts the small bowel and increases fructose malabsorption, as shown by increased ascending

206 provides very specific spectral patterns for fructose, mannose, glucose, and galactose.

207 were quantified: 4 monosaccharides (glucose, fructose, mannose, rhamnose), 11 disaccharides (sucrose,

208 perometry with a 40microl mixture containing fructose, mediator and FDH, deposited onto the SPCE-G-CO

209 KHK) is the principal enzyme responsible for fructose metabolism, identification of a selective KHK i

210 Our data suggest that tumor uptake of fructose metabolism-targeting radiotracers 1-[(18)F]FDF,

211 e were identified as molecular signatures of fructose metabolism.

212 LD: mice on a high-fat diet (with or without fructose), mice on a Western-type diet, mice on a methio

213 r metabolites (L-serine, L-leucine, glucose, fructose, myo-inositol, citric acid and 2, 3-hydroxyprop

214 eta-analyses have investigated the effect of fructose on insulin sensitivity in nondiabetic subjects.

215 ose, (2) with glucose and fructose, (3) with fructose only and (4) with glucose only.

216 ed meals containing fat, protein, and either fructose or glucose elicit similar repletion of IMCLs an

217 ed meals containing fat, protein, and either fructose or glucose on the repletion of muscle energy st

218 ilar physiological responses after intake of fructose or inulin; patients reported symptoms more freq

219 yield a content of either 20% glucose or 20% fructose, or a treatment consisting of choice between th

220 iven the preference of yeast for glucose and fructose over maltose.

221 d fructose load (0.75 g/kg), and their total fructose oxidation ((13)CO2 production), fructose storag

222 tose storage (fructose ingestion minus (13)C-fructose oxidation), fructose conversion into blood (13)

223 nes with both syngas and H2/CO2 (compared to fructose) point to the urea cycle, uptake and degradatio

224 evels in both groups, compared with glucose; fructose produced an earlier increase than inulin.

225 e we show the detrimental role of endogenous fructose production by the polyol pathway and its metabo

226 Since the fructose PTS has been shown to impact virulence in sever

227 sts, and their activities were determined by fructose radiotracer flux.

228 Arils from SDI experienced glucose/fructose ratio loss (19%) lower than that of the control

229 iew has addressed the effect of isoenergetic fructose replacement of glucose or sucrose on peak postp

230 iew has addressed the effect of isoenergetic fructose replacement of other sugars and its effect on g

231 strate binding assays indicated that UDP and fructose, respectively, were the leading substrates in t

232 Short-term (9 days) isocaloric fructose restriction decreased liver fat, VAT, and DNL,

233 etermined the effect of 9 days of isocaloric fructose restriction on DNL, liver fat, visceral fat (VA

234 assessments were performed before and after fructose restriction.

235 .Replacement of either glucose or sucrose by fructose resulted in significantly lowered peak postpran

236 We show that myocytes from fructose-rich diet (FRD) animals exhibit arrhythmias pro

237 most of the metabolic disorders induced by a fructose-rich diet and could be the most effective strat

238 : C (control diet and sedentary), F (fed the fructose-rich diet and sedentary), FA (fed the fructose-

239 uctose-rich diet and sedentary), FA (fed the fructose-rich diet and subject to aerobic exercise), FS

240 ject to strength exercise), and FAS (fed the fructose-rich diet and subject to combined aerobic and s

241 nd subject to aerobic exercise), FS (fed the fructose-rich diet and subject to strength exercise), an

242 ulum (SR) Ca(2+) release events increased in fructose-rich diet mouse (FRD) myocytes vs. control diet

243 training on metabolic disorders induced by a fructose-rich diet.

244 gnals of carbohydrates (sucrose, glucose and fructose) seemed to play the most important role in the

245 Fructose showed a lower insulin response, which may be b

246 nificantly higher concentrations observed in fructose solutions.

247 Fructose-specific facilitative hexose transporter GLUT5

248 Human GLUT5 is a fructose-specific transporter in the glucose transporter

249 tal fructose oxidation ((13)CO2 production), fructose storage (fructose ingestion minus (13)C-fructos

250 Fructose substitution in some subgroups resulted in sign

251 r the radiolytic induced rupture of glucose, fructose, sucrose and vitamin C have been proposed.

252 The radiolytic decomposition of glucose, fructose, sucrose, ascorbic acid (H2A) and dehydroascorb

253 The content of glucose, fructose, sucrose, maltose and water were determined for

254 ch of seven saccharides (glucose, galactose, fructose, sucrose, trehalose, raffinose, and stachyose)

255 The high reactivity of fructose supports the contention that fructose accelerat

256 ared to a previous study conducted using the fructose system, the novel findings of this research dem

257 ncubated with medium supplemented with 20 mM fructose than in hepatocytes incubated with medium suppl

258 Symptoms peaked sooner after intake of fructose than inulin.

259 kely to give rise to metabolisms viable on D-fructose than on acetate.

260 hibited a higher amount of free radicals for fructose than the other sugars, and more for DHAA than H

261 the content of reducing sugars (glucose and fructose) that dominate the honey matrix, and of the min

262 iding fat and protein together with 4.4 g/kg fructose (the fructose condition; FRU) or glucose (the g

263 Following fortification (477mM fructose) the mean recovery was found to be 97.12% with

264 (ExFru)] or 90 min after fructose ingestion [fructose, then exercise condition (FruEx)].

265 d postprandially by portal hyperglycemia and fructose through dissociation from GKRP, translocation t

266 The conversion of fructose to fat in liver (de novo lipogenesis [DNL]) may

267 Asparagine reacted with fructose to form a Schiff base before decarboxylation to

268 ty by shifting Glut5-mediated transport from fructose to glucose.

269 the discovery of compounds that modulate the fructose transport activity of GLUT5.

270 gh this chimera was inactive, we demonstrate fructose transport after introduction of four amino acid

271 Deletion of Txnip in mice reduced fructose transport into the peripheral bloodstream and l

272 MSNBA is a selective and potent inhibitor of fructose transport via GLUT5, and the first chemical pro

273 Global expression of the GLUT5 fructose transporter and high levels of ketohexokinase w

274 tes glucose homeostasis in mammals, binds to fructose transporters and promotes fructose absorption b

275 ibited by d-fructose, demonstrating that the fructose-transporting GLUT2, GLUT5, GLUT8, and GLUT12 do

276 mained lying down throughout the experiment [fructose treatment alone with no exercise condition (NoE

277 ing sucrose, potentially via sucrose/glucose/fructose/trehalose 6-phosphate signaling.

278 p in the small intestine as well as enhanced fructose uptake and transport into the hepatic portal ci

279 growth in fructose-based media or assayed by fructose uptake in whole cells.

280 Intestinal fructose uptake is mainly mediated by glucose transporte

281 All fragments that yielded reduced fructose uptake were analyzed further by assessing the r

282 ll line, MSNBA competitively inhibited GLUT5 fructose uptake with a KI of 3.2 +/- 0.4 muM.

283 system based on a yeast strain deficient in fructose uptake, in which GLUT5 transport activity is as

284 ere identified as being important for proper fructose uptake.

285 noamperometric assay, for the measurement of fructose, using a graphite-nanoparticle modified screen-

286 es, d-glucose, d-galactose, d-mannose, and d-fructose, using only mass spectrometry with no prior sep

287 n conclusion, this study highlights enhanced fructose utilization as a metabolic feature of AML and a

288 the GLUT5-encoding gene SLC2A5 or increased fructose utilization have poor outcomes.

289 Formation of 5-hydroxymethyl-2-furfural from fructose was found to be a key step.

290 s not aggregate, no fluorescence response to fructose was observed.

291 Fructose was the major sugar in pulp, seeds and peel (22

292 When fructose was titrated into a solution of 3 in 2:1 water/

293 lucose or sucrose in foods or beverages with fructose.We searched the Cochrane Library, MEDLINE, EMBA

294 ntly, we observed that glucose, sucrose, and fructose were inhibitory for biofilm formation, whereas

295 Glucose, sorbitol and fructose were markedly elevated in all AD brain regions,

296 Additionally, binary mixtures of glucose and fructose were studied.

297 on products was lower with glucose than with fructose when they were used as reducing sugars in food

298 t switches to anaerobic metabolism fueled by fructose, which is actively accumulated and metabolized

299 ve control responses to drinking glucose and fructose, while their homeostatic and hedonic responses

300 nerea is able to actively absorb glucose and fructose with equal capacities.