ライフサイエンスコーパス: saccharin

1 cose) or did not predict increased calories (saccharin).

2 tex and striatum, which were unresponsive to saccharin.

3 gonist were able to acquire CTAs to familiar saccharin.

4 increase in sucrose and chow intake but not saccharin.

5 -induced conditioned taste aversion (CTA) to saccharin.

6 s people more sensitive to the bitterness of saccharin.

7 o the bitterness of an artificial sweetener, saccharin.

8 antly associated with preferences for 1.6 mm saccharin.

9 and also preferred the noncaloric sweetener saccharin.

10 nduced larger increases in FLI than familiar saccharin.

11 rague-Dawley rats were given 5 min access to saccharin.

12 ent of a conditioned taste aversion (CTA) to saccharin.

13 y 2 times higher than the average loading of saccharin.

14 t off-target CAs (Ki > 50000 nM) compared to saccharin.

15 tes a so far unknown isomer that we call iso-saccharin.

16 this effect was replicated by D-fructose or saccharin.

17 en ethanol (EtOH) (10% v/v), and a palatable saccharin (0.0125% g/v) solution.

18 ver for EtOH (10% v/v) and another lever for saccharin (0.05% or 0.75% g/v), then dose-response and t

19 o, or 5min after, a single pairing of sodium saccharin (0.125%, 10-min access) and LiCl or NaCl (0.15

20 Conditioned place preference (CPP) and saccharin (0.2% w/v) self-administration were also inves

21 Saccharin (0.2% w/v) was subsequently added to the ethan

22 ed by acesulfame (1.22 g/d/1000 people), and saccharin (1.07 g/d/1000 people).

23 f taste compounds (cycloheximide, 10 microm; saccharin, 2 mm; denatonium, 1 mm; SC45647, 100 microm).

24 g/g dw, followed by acesulfame (92 ng/g) and saccharin (49 ng/g).

25 eness to a surrogate nipple providing water, saccharin, 5% ethanol, or 10% ethanol was tested in newb

26 solution compared with a placebo containing saccharin (60.4 +/- 3.7 and 61.6 +/- 3.8 min, respective

27 Significant removal of aspartame (68.2%) and saccharin (90.3%) was found in WWTPs; however, sucralose

28 However, saccharin, a cyclic secondary sulfonamide, has unusually

29 tocol of daily ingestion of a 3% solution of saccharin, a noncaloric sweetener, induced synaptic GluA

30 e results showed that rats avoided intake of saccharin after saccharin-cocaine pairings and that grea

31 ral-lesions displayed a CTA by rejecting the saccharin, although increases in c-FLI on the side of th

32 nstead given a low value reward (e.g., 0.15% saccharin), an effect termed successive negative contras

33 procedures and the same taste stimuli (0.15% saccharin and 1.0 M sucrose), the authors tested the hyp

34 Approximately, 1180 g of saccharin and 291 g of acesulfame were transformed in or

35 Intake of saccharin and 5% ethanol was high in newborns, far excee

36 small molecule artificial sweeteners such as saccharin and acesulfame K, and proteins such as monelli

37 ctivation of hTAS2R31 (formerly hTAS2R44) by saccharin and acesulfame K, two common artificial sweete

38 precursor cells with artificial sweeteners, saccharin and acesulfame potassium, enhanced adipogenesi

39 The structures of the conjugate bases of saccharin and iso-saccharin were also computed theoretic

40 pared with STDRLO, STDRHI mice consumed more saccharin and less quinine, exhibited greater ethanol-in

41 stered before (but not after) the pairing of saccharin and LiCl resulted in a significantly stronger

42 Rats conditioned with saccharin and LiCl showed a decreased preference for sac

43 s assessed using self-administration of 0.2% saccharin and locomotor activity tests.

44 f OA, because rats given OA and a pairing of saccharin and NaCl did not acquire a CTA.

45 ir intake of food and water, and of sucrose, saccharin and quinine solutions, was normal.

46 Most known applications of saccharin and saccharyl derivatives and their potential

47 They were then given brief access to 0.15% saccharin and soon thereafter injected with either cocai

48 er: aspartame (50.4%) > acesulfame (10.9%) > saccharin and sucralose (0.8%).

49 d, sucrose, and ethanol), those that do not (saccharin and water), and those lacking biological relev

50 responsive to natural rewards (in this case saccharin), and the stronger preference for saccharin se

51 he number of meals initiated for water, 0.1% saccharin, and 1.0 M sucrose solutions, but meal size wa

52 The total mass loading of sucralose, saccharin, and acesulfame in the WWTP that served a smal

53 n and LiCl showed a decreased preference for saccharin, and OA administered before (but not after) th

54 (NPY) on licking microstructure for sucrose, saccharin, and water solutions were evaluated.

55 Using saccharin as a taste stimulus in a taste preference para

56 The same effects occurred with saccharin as the reinforcer in olfactory conditioning.

57 strong conditioning occurred with sucrose or saccharin as the US.

58 es, and environmental emission of sucralose, saccharin, aspartame, and acesulfame were determined bas

59 Second, firing evoked by cues signalling saccharin availability shifted from a pattern of primari

60 ophobia, retarded acquisition of conditioned saccharin avoidance and apparently attenuated the magnit

61 A series of novel, saccharin-based antagonists have been identified for the

62 tes, as is the case of the recently proposed saccharin-based ionic liquids.

63 The ingestion of saccharin before the OGTT did not alter any of the measu

64 Preexposure to a nipple providing ethanol or saccharin (but not a nipple alone or fluids alone) incre

65 sioned rats displayed a CTA by rejecting the saccharin, but increases in c-FLI were evident only on t

66 t P1 and P2, pups exhibited a preference for saccharin, but not for 5% ethanol.

67 and testing occur in a novel environment, CS saccharin causes an increase in c-Fos expression, and wh

68 TAS2R agonists such as saccharin, chloroquine and denatonium evoked increased i

69 that rats avoided intake of saccharin after saccharin-cocaine pairings and that greater avoidance of

70 voided intake of the saccharin cue following saccharin-cocaine pairings; however, the rats in the yok

71 ed yogurt dietary supplements sweetened with saccharin compared with those fed glucose-sweetened diet

72 Rats decrease intake of a saccharin conditioned stimulus (CS) when followed by: (1

73 uppress intake of a normally preferred 0.15% saccharin conditioned stimulus (CS) when it is paired wi

74 Rats suppress intake of a saccharin conditioned stimulus (CS) when it is paired wi

75 Rats suppress intake of a saccharin conditioned stimulus (CS) when paired with a d

76 ley rats were given 20-min access to a 0.15% saccharin conditioned stimulus (CS).

77 ue-Dawley rats acquired a strong aversion to saccharin (conditioned stimulus; CS) and then underwent

78 sulin sensitivity index independent of prior saccharin consumption (P < 0.025).

79 ovelty, morphine had little influence on the saccharin consumption of IC-lesioned rats.

80 d taste aversion learning induced by pairing saccharin consumption with LiCl injection, by making the

81 ce consumed less ethanol but were similar in saccharin consumption, sensitivity to ethanol-induced CP

82 One compound also reduced sucrose and saccharin consumption, while the other was selective for

83 he wide variety of interfering UV spectra in saccharin-containing beverage matrices, the same method

84 data suggest that rats suppress intake of a saccharin CS in anticipation of the availability of a pr

85 ructural analysis of licking) for a standard saccharin CS paired with the following: lithium chloride

86 se animals actually suppressed intake of the saccharin CS.

87 ulus, did not reduce the palatability of the saccharin CS.

88 In turn, a single exposure to the saccharin cue also blunted the unconditioned dopamine re

89 In Experiment 3, avoidance of the saccharin cue and the propensity to self-administer coca

90 aFosB in the striatum were given access to a saccharin cue and then injected with saline, 10 mg/kg co

91 d value of drug, but the reward value of the saccharin cue as well.

92 othesis suggests that rats avoid intake of a saccharin cue following pairings with a drug of abuse be

93 Both cocaine groups avoided intake of the saccharin cue following saccharin-cocaine pairings; howe

94 ted controls, all rats reduced intake of the saccharin cue following saccharin-DAMGO pairings.

95 Fischer rats exhibit greater avoidance of a saccharin cue following saccharin-morphine pairings.

96 hibit greater cocaine-induced avoidance of a saccharin cue relative to Fischer 344 rats; while reward

97 Rats suppress intake of a saccharin cue when paired with a drug of abuse such as m

98 Rats avoid intake of a saccharin cue when paired with a drug of abuse.

99 D-glucose, D-fructose, saccharin, D-mannitol, and water were infused for 3 hour

100 educed intake of the saccharin cue following saccharin-DAMGO pairings.

101 on of intraorally infused water, sucrose, or saccharin, demonstrating that ingestion analgesia does n

102 Artificially sweetened (saccharin) drink reproduces the stress dampening, wherea

103 caused rats to significantly suppress their saccharin drinking (relative to controls) - indicating a

104 eet-tasting molecules as diverse as sucrose, saccharin, dulcin, and acesulfame-K.

105 minister ethanol (10-15%, w/v) in 0.2% (w/v) saccharin during daily 30 min sessions and were surgical

106 However, when switched from sucrose to saccharin during the postshift trials these rats display

107 t 1, water-deprived rats had 5-min access to saccharin followed by active or yoked intravenous delive

108 ischer rats were given 5 min access to 0.15% saccharin followed by an icv injection of either DAMGO (

109 g of intraoral infusion of 5-ml 0.15% sodium-saccharin followed by injection with LiCl (0.15 M, 20 ml

110 g of intraoral infusion of 5 ml 0.15% sodium-saccharin followed by injection with LiCl (0.15 M, 20 ml

111 al nicotine administration (100 mug/ml in 2% saccharin for 14 days), with special emphasis on amyloid

112 nstrate that the affinity and selectivity of saccharin for CA IX can be further modulated when linked

113 er pairing intake of a palatable glucose and saccharin (G+S) solution with magnetic field exposure.

114 h a fixed amount of a yogurt diet mixed with saccharin gained more weight and showed impaired caloric

115 m ascorbate, like other sodium salts such as saccharin, glutamate, and bicarbonate, produces urinary

116 reference for water flavored with sucrose or saccharin in a two-bottle free-choice drinking paradigm.

117 Suppression of lipolysis by saccharin in adipocytes was also independent of T1R2 and

118 nduced CTA strongly decreased motivation for saccharin in an operant task to obtain the tastant.

119 mmonly used methods to identify and quantify saccharin in non-alcoholic beverages.

120 The presence of saccharin in non-diet beverages - a fraud commonly used

121 immunoreactivity than the familiar taste of saccharin in the basolateral region of the amygdala, cen

122 esulfame potassium approximately sucralose > saccharin, in parallel with their ability to increase in

123 of neohesperidin dihydrochalcone (NHDC) and saccharin] included in piglets' feed reduces incidence o

124 Novel saccharin induced larger increases in FLI than familiar

125 charin with lithium or wheel-running reduced saccharin intake as well as lick cluster size, initial l

126 that greater morphine-induced suppression of saccharin intake by the Fischer rats is not likely media

127 infusions of 6% carbohydrate did not affect saccharin intake during the first ingestive bout, but la

128 thium chloride (LiCl)-induced suppression of saccharin intake in Sprague-Dawley rats.

129 Saccharin intake was either not altered by RO19-4603 or

130 A/2J mice, exhibit attenuated suppression of saccharin intake when it is paired with cocaine.

131 l rats, morphine caused a rapid reduction in saccharin intake when the taste was novel but not when i

132 Pairing saccharin with amphetamine reduced saccharin intake without reducing the size of licking cl

133 th attenuated cocaine-induced suppression of saccharin intake.

134 core reduces methamphetamine SA, as well as saccharin intake.

135 cimol was demonstrated for water, saline, or saccharin intake.

136 Ac of mice did not alter water, quinine, and saccharin intake.

137 onditionally preferred taste stimulus (e.g., saccharin) is reduced by contingent administration of a

138 unpaired' controls received a non-contingent saccharin-LiCl presentation.

139 unpaired' controls received a non-contingent saccharin-LiCl presentation.

140 tly reduced EtOH-maintained responding, with saccharin-maintained responding being reduced only with

141 The saccharin-maintained responding was reduced only with th

142 daily prior access to a palatable glucose + saccharin mixture.

143 on transfer (ET) between the triplet excited saccharin moiety and sulfur atom.

144 The results showed that a single saccharin-morphine pairing led to a marked reduction in

145 all rats were exposed to the same number of saccharin-morphine pairings, only half of these animals

146 eater avoidance of a saccharin cue following saccharin-morphine pairings.

147 rences in intake suppression following seven saccharin-morphine pairings.

148 rent types of stimuli were used: taste (0.5% saccharin), olfactory (0.1% amyl acetate), and trigemina

149 These subjects consumed a higher percent saccharin on test day and their CTAs extinguished more r

150 s demonstrated greater nipple attachment for saccharin or 5% ethanol than for water.

151 ng showed that this did not generalize to Na-saccharin or galactose.

152 In Experiment 1, saccharin or salt were either mixed in distilled water,

153 n and preference, with no similar effects on saccharin or sucrose consumption.

154 lution of either 300 parts per million (ppm) saccharin or water with or without the addition of 500 p

155 hat HR rats display a greater preference for saccharin over cocaine compared with ST and HA whereas t

156 ats were then tested on their preference for saccharin over cocaine in a discrete-trial choice proced

157 e, most rats prefer natural rewards, such as saccharin, over cocaine.

158 ingestion of water, chocolate, sucrose, and saccharin, pain-related behaviors are suppressed.

159 ppressed CS intake and caused a reduction in saccharin palatability.

160 both anions may be relevant in systems where saccharin participates, as is the case of the recently p

161 trains showed the strongest association with saccharin preference at three sites: nucleotide (nt) -79

162 ggest that the polymorphisms associated with saccharin preference do not act by blocking gene express

163 ify Tas1r3 sequence variants associated with saccharin preference in a large number of inbred mouse s

164 f recent studies suggest that the mouse Sac (saccharin preference) locus is identical to the Tas1r3 (

165 m six inbred mouse strains with high and low saccharin preference, including the strains in which the

166 amphetamine hypersensitivity, and increased saccharin preference.

167 strains with different Tas1r3 haplotypes and saccharin preferences.

168 ver, those subjects which were preexposed to saccharin prior to CS/US pairing displayed significantly

169 ts showed normal responsivity to sucrose and saccharin prior to the reward downshift.

170 oning and testing occur in the home cage, CS saccharin produces a decrease in c-Fos expression relati

171 No effects were seen on saccharin responding except with the highest dose level

172 g a dose-dependent increase in the slope for saccharin responding.

173 tal area did not significantly alter EtOH or saccharin responding.

174 ng of the accumbens dopamine response to the saccharin reward cue.

175 uired to find the sweet tastes of sucrose or saccharin rewarding.

176 2 knockdown reduces methamphetamine, but not saccharin, SA on a progressive ratio schedule of reinfor

177 A was formed through 3 pairings of 0.3% oral saccharin (SAC) and 81 mg/kg i.p. lithium chloride (LiCl

178 ed a strong CTA [via 3 pairings of 0.3% oral saccharin (SAC; the CS) and 81mg/kg i.p. lithium chlorid

179 itly unpaired (EU) conditioned stimulus (CS; saccharin, SAC) and unconditioned stimulus (US; lithium

180 rats reached 90% reacceptance of a tastant (saccharin: SAC) that had previously been associated with

181 stration at doses that neither affected 0.2% saccharin self-administration nor locomotor activity.

182 Conversely, saccharin self-administration was not affected by NOP de

183 TP-10 also reduced saccharin self-administration, suggesting a general role

184 saccharin), and the stronger preference for saccharin serves to militate against drug.

185 current presentation of EtOH (10% v/v) and a saccharin solution (0.05% w/v).

186 lf of all subjects were preexposed to a 0.2% saccharin solution (CS) for 4 consecutive days prior to

187 ly higher during consumption of the devalued saccharin solution after CTA induction.

188 mulation, rats were again presented with the saccharin solution as we tested for SR of the CTA.

189 -like state, and loss of taste preference in saccharin solution consumption test which pointed to the

190 l infusions of a cocaine-predictive flavored saccharin solution elicited aversive orofacial responses

191 Results revealed that the taste of the novel saccharin solution evoked more Fos immunoreactivity than

192 -like behaviors were assessed by sweet-taste Saccharin solution preference (SSP) and forced swimming

193 red 1.0 M sucrose solution or the same 0.15% saccharin solution.

194 did control subjects that only received the saccharin solution.

195 trient diets as well as saline, sucrose, and saccharin solutions.

196 d food (15% sucrose), and non-nutrient (0.2% saccharin) solutions following intraperitoneal (i.p.) ad

197 ocity values for aqueous solutions of sodium saccharin (SS) has been measured as a function of concen

198 Surprisingly, neither saccharin-stimulated adipogenesis nor Thr-308 phosphoryl

199 Saccharin-stimulated Akt phosphorylation at Thr-308 occu

200 iment 2 established that a safe and familiar saccharin stimulus supports substantially weaker conditi

201 ately recognize the novelty of the postshift saccharin stimulus.

202 than does a potentially dangerous and novel saccharin stimulus.

203 e strains of mice in their responsiveness to saccharin, sucrose and other sweeteners.

204 id not cause a conditioned taste aversion to saccharin, suggesting that the anorexic effect of NAc co

205 t study examined whether a novel taste (0.5% saccharin) supports a different pattern of c-Fos express

206 tassium; AceK) as well as in animals given a saccharin-sweetened base diet (refried beans) that was c

207 creased weight gain in response to consuming saccharin-sweetened compared with glucose-sweetened supp

208 ntake, weight gain, and adiposity when given saccharin-sweetened compared with glucose-sweetened yogu

209 tional weight when subsequently exposed to a saccharin-sweetened diet.

210 g that body weight differences persist after saccharin-sweetened diets are discontinued and following

211 However, in male rats fed an HE diet, saccharin-sweetened supplements produced extra weight ga

212 were observed in the self-administration of saccharin-sweetened water.

213 ion of the bile duct (BDL) was paired with a saccharin taste developed a persistent conditioned taste

214 esponse to cue presentation, lever press and saccharin taste.

215 l, i.p.) conditioned taste aversion (CTA) to saccharin taste.

216 rials these ICX rats consistently drank more saccharin than the ICX rats maintained on saccharin thro

217 ss for an unexpected low-value reward (0.15% saccharin) than did control subjects that only received

218 nded most positively to the nipple providing saccharin, the longest time spent on an empty nipple was

219 re saccharin than the ICX rats maintained on saccharin throughout the experiment.

220 ption coefficients of ASWs ranged from 4.10 (saccharin) to 4540 L/kg (aspartame).

221 Saccharin treatment of 3T3-L1 cells and primary mesenchy

222 Here, we show that saccharin undergoes structural rearrangement when subjec

223 ly effective method to identify and quantify saccharin using HPLC with fluorescence detection (HPLC-F

224 sion could not be classically conditioned to saccharin using WRYamide as the unconditioned stimulus.

225 ehaving rats learned to dislike the taste of saccharin [via conditioned taste aversion (CTA)].

226 Photocyclization of N-(thioalkyl)-saccharin was carried out to obtain different polycyclic

227 Monomeric saccharin was isolated in low-temperature argon matrices

228 Sodium saccharin was shown to produce a low incidence of bladde

229 of the conjugate bases of saccharin and iso-saccharin were also computed theoretically.

230 sweeteners such as aspartame, cyclamate, and saccharin were not enhanced by SE-1 whereas sucrose and

231 es to NaCl, HCI, quinine-HCl, sucrose and Na saccharin were recorded simultaneously in pairs of singl

232 study are similar to those seen with sodium saccharin when administered in a two-generation bioassay

233 rienced CS/US pairing displayed aversions to saccharin when given a two bottle choice test.

234 Rodents suppress intake of saccharin when it is paired with a drug of abuse.

235 Pairing saccharin with amphetamine reduced saccharin intake with

236 By contrast, pairing saccharin with lithium or wheel-running reduced sacchari

237 ering consumption of quinine-free alcohol or saccharin with or without quinine.

238 eward value of the available solution (0.15% saccharin) with respect to the memory of the preferred s

239 Irradiation of matrix-isolated saccharin, with a narrow-band source (290 nm), generates