ライフサイエンスコーパス: fructose

1 loride anions and promote the dehydration of fructose.

2 ith 14% residual sucrose, 25% glucose and 6% fructose.

3 had fasted or had consumed repeated doses of fructose.

4 overwhelm the intestinal capacity to absorb fructose.

5 issue-specific and sex-specific responses to fructose.

6 The optimum treatment was 15 g/100 g fructose.

7 haride (CPS) when S. pneumoniae was grown on fructose.

8 0, 2, and 4 h); and 6) a high-fat load with fructose.

9 terparts for the isomerization of glucose to fructose.

10 ssed in the intestine but does not transport fructose.

11 Findings were similar for blood fructose.

12 mice fed a western diet enriched in fat and fructose.

13 comparable to the naturally occurring enzyme fructose 1,6 bisphosphate aldolase.

14 The addition of fructose 1,6-biphosphate to the Caco-2 cells increased i

15 ation at phosphofructokinase-1 (PFK1) and/or fructose 1,6-bisphosphatase (FBP1) in association with a

16 te-specific loss of the gluconeogenic enzyme fructose 1,6-bisphosphatase 1 (FBP1) disrupts liver meta

17 We show that the PKM2 activator fructose 1,6-bisphosphate (FBP) alone promotes tetrameri

18 licit major structural reorganization of the fructose 1,6-bisphosphate (FBP), an allosteric activator

19 In vivo phosphorylating agents, such as fructose 1,6-bisphosphate, generate phosphorylated forms

20 ut also requires inhibition by the regulator fructose 1,6-bisphosphate, which senses the upper-glycol

21 ctose uptake mainly results in intracellular fructose 1-phosphate, which is not converted to CPS prec

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

23 -95.5%), followed by glucose (2.9-4.6%), and fructose (1.6-3.7%).

24 pathway were increased in DMG, particularly fructose (1.7-fold).

25 Loss of hepatic fructose-1, 6-bisphosphate aldolase B (Aldob) leads to a

26 and activate gluconeogenesis by stimulating fructose-1,6-bisphophatase; therefore, the decrease in c

27 ssion of the metabolic tumor suppressor gene fructose-1,6-bisphosphatase (FBP1), epigenetically repre

28 nd reexpression of a gluconeogenesis enzyme, fructose-1,6-bisphosphatase (FBP1), was found to inhibit

29 hat co-localized with IVC markers, including fructose-1,6-bisphosphatase (FBPase) and the vacuole imp

30 wnregulated that of a key glycolytic enzyme, fructose-1,6-bisphosphatase 1 (FBP1).

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

32 es for inhibitor alanine (Ala) and activator fructose-1,6-bisphosphate (Fru-1,6-BP) in human liver py

33 phosphorylation, and 3) prevented binding of fructose-1,6-bisphosphate (Fru-1,6-BP).

34 e key processes identified are metabolism of fructose-1,6-bisphosphate, production of glycerol-3-phos

35 Ketohexokinase (KHK) converts fructose to fructose-1-phosphate (F1P) in the first step of the meta

36 Within the tumors, fructose was converted to fructose-1-phosphate, leading to activation of glycolysi

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

38 ade of glucose (30.48%), galactose (33.51%), fructose (16.92%), D-tagatose (10.54%), and lactulose (3

39 y identified mechanism whereby the levels of fructose 2,6-bisphosphate promote mitochondrial PDK4 lev

40 ted levels of the PFK-1 allosteric activator fructose 2,6-bisphosphate.

41 iding with increased 6-phophofructo-2-kinase/fructose-2,6-biphosphatase (PFKFB)-3-mediated glycolysis

42 s, which identified 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (Pfkfb3) as a differentiall

43 6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB3) is an essential gly

44 glycolytic enzyme, 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB3).

45 by inducing the phosphofructokinase PFKFB3 (fructose-2,6-bisphosphatase 3).

46 ich is regulated by 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 (PFKFB3), and whether this

47 is is controlled by 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 (PFKFB3), the pro-glycolyt

48 n of pfk2 (encoding 6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase; PFKFB in vertebrates) among

49 FKFB3), the pro-glycolytic enzyme that forms fructose-2,6-bisphosphate, a powerful allosteric activat

50 Pfk2 catalyzes the synthesis of fructose-2,6-bisphosphate, which acts as a potent allost

51 or the GAN diet rich in saturated fat (40%), fructose (22%) and cholesterol (2%) for >=38 weeks.

52 nd 4 h); 4) a high-fat load with glucose; 5) fructose (3 doses of 50 g at 0, 2, and 4 h); and 6) a hi

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

54 finities for S7P and the canonical substrate fructose 6-phosphate (F6P).

55 creased expression and activity of glutamine fructose 6-phosphate amidotransferase (GFAT), the enzyme

56 idotransferase 1 (GFAT1), uses glutamine and fructose 6-phosphate to eventually synthesize uridine di

57 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

58 le for members of this family, none exhibits fructose-6-phosphate (F6P) at the active site.

59 athway, which is controlled by the glutamine:fructose-6-phosphate amidotransfera-se (GFAT).

60 Mechanistically, we identify the glucosamine:fructose-6-phosphate amidotransferase (GFPT) among the s

61 Overexpression of Gfat1 (glutamine:fructose-6-phosphate amidotransferase 1), the rate-limit

62 In addition, hGFAT2 is able to isomerize fructose-6-phosphate into glucose-6-phosphate even in th

63 ons for the synthesis of metabolites such as fructose-6-phosphate, glycine, sedoheptulose-7-phosphate

64 atic aldose reductase expression, endogenous fructose accumulation, and fat buildup that was signific

65 We found that fructose acutely and transiently suppressed mTORC1 signa

66 y is enhanced to 24% and 37% for glucose and fructose adulterated honey samples respectively.

67 Recent studies suggest that fructose also can be produced via the polyol pathway in

68 te-limiting enzyme of the pathway, glutamine-fructose amidotransferase 1 (GFAT1), uses glutamine and

69 tulose was determined as 1.28 or 0.74 mol/kg fructose and 0.17 or 0.19 mol/kg lactose with an enzymat

70 hesis reaction containing 40% glucose, 15.8% fructose and 35% of FOS, elimination of the sugars was a

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

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

73 ce were fed the AMLN diet high in trans-fat, fructose and cholesterol for 15 weeks, whereafter they r

74 methods have its own limitations to quantify fructose and d-psicose mixtures.

75 Fructose and exposure to short-chain fatty acids activat

76 imulation, dietary interventions such as low fructose and fibre based diets, and nutraceuticals, whic

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

78 Our results demonstrate that fructose and glucose have a different immediate impact o

79 HFCS increased the concentrations of fructose and glucose in the intestinal lumen and serum,

80 ly decreased; contrary, the concentration of fructose and glucose increased reaching their maximum va

81 Th2-response, de novo cholesterol synthesis, fructose and glucose metabolism, basic amino acid metabo

82 al Bacteroides thetaiotaomicron Silencing by fructose and glucose requires the 5' leader region of th

83 Moreover, the levels of fructose and glucose significantly increased during the

84 nt of a heterologous gene was sufficient for fructose and glucose to turn off expression of the corre

85 fied for the first time in the presence of d-fructose and glucose with a good resolution.

86 ine in primary metabolites content as sugars fructose and glucose, and short-chain organic acids.

87 However, we now report that dietary fructose and glucose, which are prevalent in the Western

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

89 flexibility, involving defects in adenosine, fructose and glycogen metabolism, as well as disruptions

90 To address this question, d-glucose, d-fructose and l-ascorbic acid were incubated with human s

91 queous-phase isomerization of d-glucose to d-fructose and l-sorbose is catalyzed in parallel by Lewis

92 ap and non-invasive procedure for diagnosing fructose and lactose malabsorption (FM/LM) but test accu

93 A mathematical model, incorporating glucose, fructose and maltose and based on known Maillard reactio

94 other non-beta-glucoside PTS sugars, such as fructose and mannose.

95 ent scores were not associated with maternal fructose and SSB + J consumption at 6 postnatal months.

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

97 induced obesity mouse model by substituting fructose and sucrose with NCS in the drinking water.

98 However, in comparison to fructose and sucrose, Rebaudioside A significantly impro

99 4 are the STs with most affinity for glucose/fructose and SUT1_T1 has the highest affinity to sucrose

100 perceived intensity of 2 sugars (glucose and fructose) and 2 high-potency sweeteners (neohesperidin d

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

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

103 rs consumed 1656 +/- 470 kcal, 21.8 +/- 12 g fructose, and 2.5 +/- 2.6 servings SSBs + J, and reporte

104 igarette smoke exposure and WD (rich in fat, fructose, and cholesterol) could induce a more reliable

105 he administration of high-fat load, glucose, fructose, and combinations thereof affects HFC measured

106 sumption of energy-dense foods, particularly fructose, and consequent obesity and insulin resistance

107 ifferent carbohydrates, such as d-glucose, d-fructose, and d-xylose, and their typical degradation pr

108 ation and elevated AR metabolites (sorbitol, fructose, and uric acid), which correlated significantly

109 icrobe, Oh et al. (2018) reveal that dietary fructose- and microbiota-derived short-chain fatty acids

110 ion factors respond to two distinct ligands, fructose (anti-FruR) or D-ribose (anti-RbsR); and were c

111 AR, the only endogenous enzyme that produces fructose) are strongly associated with the development o

112 We used blood fructose as a validation exposure.

113 5 x 10(-6)) associated with blood sucrose or fructose as instrumental variables and applied them to s

114 pic enrichment techniques further identified fructose as the main precursor of RCS, indicating the im

115 ng of the mechanisms by which consumption of fructose, as part of a mixed meal, may alter hepatic fat

116 size (length and width), sugars (glucose and fructose), ascorbic acid content, cyanidin derivatives (

117 on, Salmonella utilizes the Amadori compound fructose-asparagine (F-Asn) as a nutrient through the su

118 fructosyl transfer event and, together with fructose, because of the inherent hydrolytic activity of

119 c regulation of phosphofructokinase-1 and/or fructose bisphosphatase-1, as supported by increased met

120 teric effectors of phosphofructokinase-1 and fructose bisphosphatase-1, including AMP, P(i), and glyc

121 of these targets were the glycolytic enzymes fructose bisphosphate aldolase (FBPA) and glyceraldehyde

122 y identified candidate biomarkers (myosin-9, fructose-bisphosphate aldolase and plectin).

123 tulose 7-phosphate (S7P) to SBP, after which fructose-bisphosphate aldolase cleaves SBP into dihydrox

124 rose (a disaccharide composed of glucose and fructose), but not in mice fed a complex polysaccharide-

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

126 Combining the intake of glucose plus fructose can further increase total exogenous carbohydra

127 Ingesting a mixture of both glucose and fructose can improve endurance exercise performance comp

128 nism whereby soft drinks rich in glucose and fructose can induce NAFLD.

129 Fructose co-ingestion can also accelerate post-exercise

130 Furthermore, fructose co-ingestion can lower gastrointestinal distres

131 anine and total monosaccharides (glucose and fructose) compared to controls, suggesting a further sta

132 The influence of lactose and fructose concentration as well as enzymatic activity of

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

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

135 Increased fructose consumption and its subsequent metabolism have

136 Increased fructose consumption and its subsequent metabolism have

137 al months correlated inversely with maternal fructose consumption at 1 postnatal month (B = -0.08; 95

138 Fructose consumption in FRU increased postprandial net c

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

140 Current fructose consumption levels often overwhelm the intestin

141 t cognitive development scores with maternal fructose consumption was no longer significant after adj

142 Dietary, fructose-containing sugars have been strongly associated

143 Soluble sugar (glucose and fructose) contents were enhanced during germination in t

144 and substantial accumulation of glucose and fructose contributed to obtaining robust FT during field

145 consumption of beverages sweetened with high-fructose corn syrup (HFCS) is associated with obesity an

146 steviol glycoside (rebaudioside A), and high fructose corn syrup (HFCS) were examined and compared wi

147 single sugars, mixtures of sugars, and high-fructose corn syrup (HFCS).

148 decades owing to the use of sucrose and high-fructose corn syrup in beverages and processed foods(1),

149 However, fructose decreased significantly only in RPF (11.29%).

150 The contribution of fructose dehydration through fructofuranosyl cation on t

151 suggest that the formation of complexes with fructose derivatives contribute to increase the iron bio

152 enotyping prior to and 8 wk following a high-fructose diet (150 g daily).

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

154 Mesenteric lymphatic vessels from high-fructose diet-induced metabolic syndrome (MetSyn) rats e

155 During consumption of a high-sugar (fructose) diet, which induced 10% weight gain, animals w

156 Fructose (dietary or endogenous), its metabolite uric ac

157 high trans-fat diet (HTFD) supplemented with fructose, either ad libitum or restricting their food in

158 uction is further increased in response to a fructose-enriched diet.

159 that the combination of dietary glucose and fructose, even at a moderate dose, can enhance tumorigen

160 e highland honeys; the highest color (a) and fructose, F/G ratio, proline, pH, conductivity, Fe, Cu,

161 Here the effect of fructose, fat-rich and western diet (WD) feeding was stu

162 communities, both at baseline and following fructose feeding, including increased abundance of Bacte

163 produced hypotriglyceridemia after 1 week of fructose feeding.

164 Ingestion of a high dose of fructose for 8 wk was not associated with relevant metab

165 %RMSEP values of 11.3%, 11.1% and 11.7% for fructose, glucose and sucrose respectively.

166 ifferences in primary metabolites, including fructose, glucose, sorbitol, malic acid were recorded am

167 loric effect of substituting dietary sugars (fructose, glucose, sucrose) with other sugars or starch

168 med to understand the interactive effects of fructose, glucose, sucrose, maltose and water on crystal

169 he measured T(gs) (P < 0.05) and sugaring of fructose-glucose-water model solutions.

170 e DNL area under the curve 6 hours following fructose/glucose bolus (R(2) = -0.554, P = 0.005).

171 ic DNL was measured before and after an oral fructose/glucose bolus using isotopic labeling with 1-(1

172 honey to three honey samples with different fructose/glucose ratio, the key characteristic for honey

173 The ratios of fructose:glucose (1:3, 1:2 and 1:1) and glucose:water (1

174 ompson, Flame and Golden raisins differed in fructose:glucose and glucose:water ratios, impacting on

175 bility of honey crystallization depending on Fructose:Glucose and Glucose:Water ratios.

176 Post-simulation analysis showed that Fructose:Glucose of 1.18 formed the most stable crystal

177 Results indicated that not only Fructose:Glucose ratio but also sucrose, maltose and wat

178 Consumption of fructose has risen markedly in recent decades owing to t

179 Considering that fructose has the capacity to upregulate hepatic glycogen

180 ter being fed a high-fat, -cholesterol, and -fructose (HFCF) diet.

181 mped for 1 hour in rats fed a high-fat, high-fructose (HFHF) diet for 5, 10, or 15 weeks.

182 baseline and after 4 weeks of high-fat high-fructose (HFHF) feeding.

183 diets, including HFD, HFD supplemented with fructose, high trans-fat diet (HTFD) supplemented with f

184 , pH, ash, electrical conductivity, glucose, fructose, hydroxymethylfurfural (HMF), CIE L(*)a(*)b(*)

185 iptional program is activated in response to fructose in a manner that is independent of acetyl-CoA m

186 s influenced by fructose in breast milk, and fructose in breast milk is increased in response to mate

187 that infant somatic growth is influenced by fructose in breast milk, and fructose in breast milk is

188 As for sugar compounds, it was found that fructose in buds (1.56-3.23 g/100 g DW) and glucose in b

189 of this study was to investigate the role of fructose in glucose and lipid metabolism in the liver, h

190 the detection of adulteration of glucose and fructose in pure honey.

191 ily high concentration of the monosaccharide fructose in semen contributes significantly to the effec

192 We discovered that the sugar fructose in semen decreases the activity of a broad and

193 ORD is an enzyme that converts sorbitol into fructose in the two-step polyol pathway previously impli

194 Fructose increases hepatic de novo lipogenesis via numer

195 bly, the selectivity toward l-sorbose over d-fructose increases systematically as spatial constraints

196 soluble sugars (notably sucrose, maltose and fructose) increasing and most amino acids (including asp

197 s conferred transmissible protection against fructose-induced hepatic steatosis in association with a

198 d Mttp-IKO mice were still protected against fructose-induced hepatic steatosis, suggesting that chan

199 e normally but are protected against dietary fructose-induced hepatic steatosis, without weight loss

200 letion of Acly in mice is unable to suppress fructose-induced lipogenesis.

201 or in determining the metabolic responses to fructose ingestion, and saturation of hepatic glycogen s

202 Both increased fructose intake (P = 0.01) and endotoxin level (P = 0.02

203 Dietary modifications through decreasing fructose intake and addressing systemic endotoxemia are

204 The role of fructose intake and metabolic endotoxemia has gained att

205 recipients (KTRs), focusing particularly on fructose intake and systemic endotoxemia.

206 Increased fructose intake has been associated with metabolic conse

207 nths can be adversely influenced by maternal fructose intake in early lactation, and this could be at

208 High fructose intake resulted in lower intake of other dietar

209 Fructose intake triggers de novo lipogenesis in the live

210 Specifically, increased fructose intake was associated with the central obesity

211 independently associated with MS; and higher fructose intake was independently associated with obesit

212 , as well as relationships between increased fructose intake, inflammation, and blood glucose (r > 0.

213 the negative metabolic effects of excessive fructose intake.

214 t least temporarily compensate for increased fructose intake.

215 potently suppresses the conversion of bolus fructose into hepatic acetyl-CoA and fatty acids.

216 Fructose is a commonly ingested dietary sugar which has

217 The isomerisation of glucose to fructose is a critical step towards manufacturing petrol

218 d host colonization capacity when glucose or fructose is available for metabolism.

219 When fructose is consumed more gradually to facilitate its ab

220 Dietary fructose is converted to acetate by the gut microbiota(9

221 Fructose is primarily metabolised by the liver in humans

222 ypically includes a composite of glucose and fructose) is associated with an increased risk of develo

223 littermate mice were used and received a 20%-fructose (KHK-F and WT-F) or 20%-glucose diet.

224 onents related to isopropylidene-protected d-fructose, l-sorbose, d-galactose, and d-allose.

225 This effect of semen fructose likely reduces the efficacy of such inhibitors

226 towards the higher resistance of galactosyl-fructose linkages during its intestinal degradation.

227 mplete absorption of the orally administered fructose load.

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

229 wer this question, a mouse model of moderate fructose malabsorption [ketohexokinase mutant (KHK)(-/-)

230 Fructose malabsorption induces cholecystokinin expressio

231 We investigated the impact of fructose malabsorption on intestinal endocrine function

232 Antibiotic treatment abolished fructose malabsorption-dependent induction of cecal Cck

233 oposed for the hydration numbers of glucose, fructose, maltose and glycerol.

234 ition, we found alterations in the levels of fructose metabolism enzymes and a reduction in the methy

235 To date, the study of fructose metabolism has primarily focused on the liver,

236 This review summarises what is known about fructose metabolism in the liver and adipose tissue and

237 ency of TKFC causes disruption of endogenous fructose metabolism leading to generation of by-products

238 ults suggest that uric acid generated during fructose metabolism may act as a positive feedback mecha

239 FC encodes a bifunctional enzyme involved in fructose metabolism through its glyceraldehyde kinase ac

240 Moreover, fructose metabolism yields uric acid, which is highly as

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

242 Mttp-IKO mice absorb fructose normally but are protected against dietary fruc

243 enols, flavonoids, anthocyanins, glucose and fructose of methanolic extracts from ripe fruits of each

244 ethanol, glycerol, tartaric acid and glucose/fructose on the refractive index in model aqueous soluti

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

246 ar weight fractions which contained glucose, fructose, organic acids and amino acids.

247 ariectomy (OVX) and aged + ovariectomy + 10% fructose (OVF) in drinking water (n = 8-16/group) to ind

248 The fructose-phosphate metabolites, F-1-P and F-6-P, could m

249 ets rich in fat and added sugars (especially fructose) play an important role in the pathogenesis of

250 ses (LSs) synthesize levan, a beta2-6-linked fructose polymer, by successively transferring the fruct

251 Notably, the reaction of the ketose d-fructose proceeds with complete stereoselectivity to yie

252 cascade reactions of lactose conversion into fructose, producing a lactose-fructose syrup (LFS).

253 is stimulation is associated with endogenous fructose production and fat accumulation.

254 s stimulation was associated with endogenous fructose production and triglyceride accumulation.

255 eedback mechanism that stimulates endogenous fructose production by stimulating aldose reductase in t

256 Fructose reaching the lower intestine can modify the com

257 high-fat load alone or a high-fat load with fructose, respectively, but was not affected when glucos

258 abolites when cells were grown on glucose or fructose, respectively.

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

260 assessments were performed before and after fructose restriction.

261 nd assigned into 4 groups that fed standard, fructose-rich, high fat-, and western-diet for 8 weeks a

262 ke disease in mice by feeding a diet rich in fructose, saturated fat, and cholesterol and found that

263 single-pass yields of 58 % are observed at a fructose selectivity of 94 %, and continuous operation f

264 R up-regulation, and consequent elevation in fructose, sorbitol and/or uric acid, are important facto

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

266 ith progressive reductions in the percent of fructose-stimulated peak fractional DNL (R(2) = -0.749,

267 Fructose substitution in some subgroups resulted in sign

268 yses revealed that the uptake of the labeled fructose subunit into the capsule is <10% that of glucos

269 s developed where, sugar solutions (glucose, fructose, sucrose) were used to pre-treat Robusta coffee

270 nce from other sugars (for example, maltose, fructose, sucrose, lactose, and galactose) was observed.

271 ess and adiposity in mice fed a high fat and fructose supplemented western diet (WD).

272 Interestingly, a continuous process for High Fructose Syrup (HFS) production was established with the

273 onversion into fructose, producing a lactose-fructose syrup (LFS).

274 t was successfully used in the production of fructose syrup from lactose in a single reaction vessel.

275 ion, can break down sucrose into glucose and fructose that can be readily metabolized by C. albicans,

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

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

278 Ketohexokinase (KHK) converts fructose to fructose-1-phosphate (F1P) in the first step

279 However, the route from dietary fructose to hepatic acetyl-CoA and lipids remains unknow

280 f the Bronsted acid-catalyzed dehydration of fructose to hydroxymethylfurfural (HMF) show that the us

281 ically, in the representative dehydration of fructose to produce 5-hydroxymethylfurfural, dramatic ac

282 ed from a preferred carbohydrate (glucose or fructose) to lactose, initiation of growth can take seve

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

284 Furthermore the aroma of the fructose treated Robusta was more stable than Arabica ov

285 Intestinal fructose uptake is not regulated by the same transport s

286 This finding suggests that fructose uptake mainly results in intracellular fructose

287 Within the tumors, fructose was converted to fructose-1-phosphate, leading

288 Glucose/fructose was found to have the greatest effect on the re

289 The estimate for blood fructose was in the same direction.

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

291 t diet (HFMCD) or a Western diet with liquid fructose (WDF) to induce steatohepatitis; control mice w

292 ree sucrose, lactose, galactose, glucose and fructose were determined in yoghurts, milk and honey usi

293 Replacing fructose with an equivalent energy amount of glucose red

294 In conclusion, combined ingestion of fructose with glucose may be preferred over the ingestio

295 were beneficially affected by replacement of fructose with glucose.

296 inear from 0.1 to 15 g L(-1) for glucose and fructose with limits of detection of 0.012 g L(-1) and 0

297 gh the selective complexation of glucose and fructose with phenyl boronic acid (PBAc) followed by eth

298 0.23 mmol/L; 95% CI: -0.38, -0.07 mmol/L) or fructose with starch (MD: -0.22 mmol/L; 95% CI: -0.39, -

299 gs indicate that substitution of sucrose and fructose with starch yielded lower LDL cholesterol.

300 ngly little is known about the metabolism of fructose within other organs, specifically subcutaneous