ライフサイエンスコーパス: eating behavior

1 sm, and may control leptin levels and affect eating behavior.

2 nt is rapid and includes dramatic changes in eating behavior.

3 tissues independent of mechanisms regulating eating behavior.

4 cesses (liking and wanting) in driving human eating behavior.

5 ight influence the development of compulsive eating behavior.

6 ody mass index, age, sex, comorbidities, and eating behavior.

7 a hindered ability to make changes in their eating behavior.

8 d (GL) are derived do not reflect real-world eating behavior.

9 ined the neural correlates of addictive-like eating behavior.

10 he polymorphism, influence reward coding and eating behavior.

11 rentiated rats with the most compulsive-like eating behavior.

12 ptors and these forms of naturally occurring eating behavior.

13 mental effects of social influences on their eating behavior.

14 uniquely relevant and influential to youths' eating behavior.

15 ical factor linking reduced energy stores to eating behavior.

16 ith this mutation normalized body weight and eating behavior.

17 associated with measurable effects on child eating behavior.

18 tial for an innate compensation mechanism of eating behavior.

19 contribute to the perpetuation of compulsive eating behavior.

20 We investigated the genetic underpinnings of eating behavior.

21 shell sites elicited appetitive increases in eating behavior.

22 rphine at locations that caused increases in eating behavior.

23 f genetic and environmental factors in human eating behavior.

24 ivity are accompanied by specific changes in eating behavior.

25 educed 2 h food intake, 8-OH-DPAT stimulated eating behavior.

26 ors may affect different stimuli that impact eating behavior.

27 , eating disorders, and other pathologies of eating behavior.

28 ncluding depression, anxiety, and disordered eating behavior.

29 ns and more realistic paradigms for studying eating behavior.

30 task and employed a rat model of binge-like eating behavior.

31 ken into account in the promotion of healthy eating behavior.

32 tributes to metabolic control by suppressing eating behavior.

33 tionship between perceived food scarcity and eating behavior.

34 goal-directed behaviors and had no impact on eating behavior.

35 ic, neuroendocrine, and visual modulation of eating behavior.

36 XFP3 blockade within the PVN prevented binge-eating behavior.

37 te risk score and adiposity was moderated by eating behaviors.

38 ay be a viable strategy to promote healthier eating behaviors.

39 ility, continue to mold food preferences and eating behaviors.

40 ful eating are protective against disordered eating behaviors.

41 ing to probe the underlying basis of altered eating behaviors.

42 ing a key regulator of reward-based, hedonic eating behaviors.

43 did not translate into unequivocally better eating behaviors.

44 es increased physical activity and healthful eating behaviors.

45 ing for sociodemographics, health status and eating behaviors.

46 1000 d and adiposity at 6 y is moderated by eating behaviors.

47 olites associated with healthy and unhealthy eating behaviors.

48 oving glycemic control and suppressing binge eating behaviors.

49 dy, the microbial community itself, or human eating behaviors.

50 fast life-history strategy, and dysregulated-eating behaviors.

51 d the prefrontal cortex result in compulsive eating behaviors.

52 changes across groups and their relations to eating behaviors.

53 ress) and consummatory (going to the feeder, eating) behaviors.

54 They self-reported their height and weight, eating behaviors (15 items), diet quality, and self-meas

55 ounding dieting, body weight, or problematic eating behaviors (27 of 84 [32.1%]); improper laxative,

56 Eating behavior affects weight and thus the development

57 Although the data on eating behavior after bariatric surgery are substantial,

58 he study was to obtain objective measures of eating behavior among patients with AN before and immedi

59 latively few objective laboratory studies of eating behavior among persons with eating disorders.

60 disorder content and engaging in disordered eating behaviors, an examination of the accuracy of and

61 The eating behavior and activity levels of 19 weight-gaining

62 re, we present evidence to relate compulsive eating behavior and addiction and to characterize their

63 mol microinjections (75 ng) caused increased eating behavior and also caused positive conditioned pla

64 results show that OSU6162 reduces binge-like eating behavior and attenuates the impact of cues on see

65 Opportunistic eating behavior and BMI were both positively associated

66 y abnormal patterns of weight regulation and eating behavior and by disturbances in attitudes and per

67 utrients to the brain, initiating changes in eating behavior and energy expenditure, to maintain ener

68 t that PD is associated with disturbances in eating behavior and energy intake.

69 bstrates in the VP that mediate increases in eating behavior and enhancements in taste hedonic "likin

70 generated DAMGO-induced robust increases in eating behavior and food intake.

71 This study compared eating behavior and hormones among adolescents in a bari

72 in the support of self-regulatory aspects of eating behavior and inhibitory control.

73 difficult but critical for the evaluation of eating behavior and intervention effects.

74 Eating behavior and measurement errors (MEs) of dietary

75 no adverse effects of aspiration therapy on eating behavior and no evidence of compensation for aspi

76 th BDNF or NT4/5 can transiently reverse the eating behavior and obesity.

77 sorders are characterized by disturbances in eating behavior and occur worldwide, with a lifetime pre

78 ies for understanding how the brain controls eating behavior and opens alternative routes for the tre

79 policy development with the aim of improving eating behavior and preventing obesity.

80 Body weight and measures of eating behavior and psychological state were obtained at

81 uman leptin (metreleptin) rapidly normalized eating behavior and resulted in weight loss.

82 activation are implicated in addictive-like eating behavior and substance dependence: elevated activ

83 ivating these neurons to suppress binge-like eating behavior and suggest ERalpha and/or SK current in

84 Significant familial effects on eating behavior and suggestive genetic linkage were foun

85 ion, we tested for interactions between each eating behavior and the BMI-GRS on BMI.The association b

86 Eating behavior and thus dietary intake affect the devel

87 Neuropeptide Y (NPY) is known to stimulate eating behavior and to be related to behavioral patterns

88 y heart disease (CHD), CHD risk factors, and eating behavior and to examine whether the associations

89 determining whether they were predictive of eating behavior and weight change.

90 w the effects of palatability and variety on eating behavior and weight.

91 an intention to lose weight reported better eating behaviors and a more active lifestyle than did pa

92 their CVD risk status, benefit from healthy eating behaviors and appropriate physical activity.

93 (CVD), can gain health benefits from healthy eating behaviors and appropriate physical activity.

94 ammatory marker or adipokine concentrations, eating behaviors and changes in waist circumference duri

95 rgery and that these changes would influence eating behaviors and contribute to the positive outcomes

96 he utility of programs to modify problematic eating behaviors and eating patterns should be addressed

97 eliminary findings suggest that pathological eating behaviors and frank eating disorders are surprisi

98 explore the dynamic interplay between their eating behaviors and gut microbiota, modeling the social

99 Also, individual eating behaviors and nutritional satisfaction are linked

100 itive period for the development of habitual eating behaviors and obesity risk, with potential mediat

101 the nucleus accumbens [NAcc]) and unhealthy eating behaviors and outcomes; however, the mechanisms u

102 A questionnaire assessed eating behaviors and parental feeding practices at 18 an

103 ticipants completed questionnaires to assess eating behaviors and substance use at preoperative basel

104 Eating behaviors and weight change have been linked to t

105 that parental feeding determines children's eating behaviors and weight gain, but feeding practices

106 (inhibitory control and approach) on girls' eating behaviors and weight outcomes at 5 and 7 y.

107 ecent literature examining eating disorders, eating behavior, and body image in middle-aged and elder

108 ary focus on anorexia nervosa (AN) and binge-eating behavior, and encourages further study of all con

109 e and fat fuel interactions appear to affect eating behavior, and may play a role in the overconsumpt

110 of neural pathways controlling body weight, eating behavior, and peripheral metabolism.

111 nisms by which ghrelin mediates reward-based eating behavior, and those studies suggesting an obligat

112 e associations between occupational burnout, eating behavior, and weight among working women.

113 aggerated depressive-like behaviors, changed eating behaviors, and altered metabolism in response to

114 ly adolescence, which can lead to disordered eating behaviors, and future cardiometabolic health is,

115 s important for both homeostatic and hedonic eating behaviors, and its orexigenic actions occur mainl

116 to 18 mo of age on food and nutrient intake, eating behaviors, and parental feeding practices in 18-

117 It is known that the mouse-genome, eating-behavior, and exercise-status promotes higher tax

118 Key factors driving eating behavior are hunger and satiety, which are contro

119 lf-respect caused by chronic work stress) on eating behavior are lacking.

120 indings indicate that the effects of BDNF on eating behavior are neural substrate-dependent and that

121 otes obesity, but the controls of children's eating behavior are poorly understood.

122 Sex differences in eating behavior are well documented, but it is not known

123 Abnormal eating behaviors are common in patients with frontotempo

124 Abnormal eating behaviors are prominent in patients with bvFTD an

125 Potentially modifiable mechanisms, including eating behaviors, are of particular interest to public h

126 eostatic central nervous networks regulating eating behavior as well as decreased hunger feelings and

127 outcomes included energy self-regulation and eating behaviors assessed with questionnaires at 6, 12,

128 mes a day; however, compensatory dietary and eating behaviors associated with snacking in free-living

129 , the GABAA antagonist bicuculline increased eating behavior at all VP sites, yet completely failed t

130 which is a time with special significance to eating behavior at the next meal.

131 of neonatal and maternal characteristics on eating behaviors at 2 y of age.

132 tational age is not associated with impaired eating behaviors at the age of 2 y.

133 1; 2001-2003) was associated with disordered eating behaviors at time 2 (2004-2006), as well as weigh

134 gained popularity in contributing to healthy eating behavior because of their antioxidant properties

135 on of bitter tastes has been associated with eating behavior, body composition, and cardiovascular di

136 sitive/negative valence (positive appetitive eating behavior but negative place avoidance and negativ

137 l accumbens shell in rats elicits appetitive eating behavior, but in the caudal shell instead elicits

138 Qualitative aspects of diet influence eating behavior, but the physiologic mechanisms for thes

139 titive direction by amplifying generation of eating behavior by middle to caudal NAc disruptions, wit

140 or reducing maladaptive, palatability-driven eating behavior by reducing the motivational properties

141 The disturbed eating behavior can be restored by substitution with the

142 Dysregulation of eating behavior can lead to obesity, which affects 10% o

143 rts might therefore benefit from focusing on eating behavior change, particularly in genetically susc

144 Furthermore, eating behaviors changed with increasing time since surg

145 y outcomes examined included meal- and snack-eating behaviors, clock time of eating episodes, and int

146 ammatory marker or adipokine concentrations, eating behaviors, comorbid psychiatric disorders or life

147 Genetic effects, some mediated by eating behavior, contribute importantly to the potential

148 amined the association of SES with disturbed eating behavior (DEB) and related factors in Korean adol

149 Binge eating and other forms of disordered eating behavior (DEB) are associated with failed inhibit

150 Because the influence of metabolism on eating behavior depends on where and in what way metabol

151 nts with AN show a persistent disturbance in eating behavior, despite the restoration of body weight

152 d with sham tDCS) has an immediate effect on eating behavior during ad libitum food intake, resulting

153 To describe their children's eating behavior during the first 3 mo of life while they

154 o how and what children learn about food and eating behavior during these first years is limited.

155 neurotransmission may contribute to improved eating behavior (e.g. reduced hunger and improved satiet

156 importance of assessing behaviors related to eating behavior, eating problems, weight control practic

157 enty-five postoperative behaviors related to eating behavior, eating problems, weight control practic

158 Individual patterns of food preferences and eating behaviors emerge and differ depending on the food

159 The eating behaviors-emotional eating, uncontrolled eating,

160 pleted validated questionnaires on appetite, eating behaviors, energy consumption, and dietary macron

161 e within-person differences in self-reported eating behaviors, energy intake, and other dietary chara

162 Eating behaviors examined included the following: report

163 lations, and can be applied to determine how eating behavior factors influence total food intake.

164 demonstration that muscimol elicits positive eating behavior from rostral shell versus negative defen

165 cohort, we investigated associations between eating behaviors, genetic predispositions for high body

166 These findings suggest that eating behavior has an important role in the prevention

167 fluence of parents versus friends on youths' eating behavior has not been directly compared, and litt

168 Disordered eating behaviors have also been associated with PTSD and

169 ucleus accumbens shell produces increases in eating behavior (i.e. 'wanting' for food).

170 nvolving ADRB3 and PPARG variants influences eating behavior in children.

171 We identified compulsive-like eating behavior in female rats through progressive ratio

172 VN) is necessary for the expression of binge-eating behavior in female rats.

173 ion in GVA signaling may underpin changes in eating behavior in HFD-induced obesity.

174 tastes predicts similar food preferences and eating behavior in later life and is associated with chi

175 ocesses that distinguish normal and abnormal eating behavior in men and women.

176 Evidence suggests altered eating behavior in obesity.

177 lacement substantially suppresses binge-like eating behavior in ovariectomized female mice.

178 Differing neural networks control eating behavior in patients with bvFTD and semantic deme

179 our understanding of structures that control eating behavior in patients with FTD and healthy individ

180 nhibitor of fatty acid oxidation, stimulates eating behavior in rats.

181 2,5-anhydro-D-mannitol (2,5-AM), stimulates eating behavior in rats.

182 determinant of CHD, related risk factors, or eating behavior in the British Women's Heart and Health

183 rvational learning affect the development of eating behavior in the context of the current food envir

184 DAMGO similarly stimulated eating behavior in the posterior and central VP and supp

185 Despite the importance of eating behavior in the presentation of AN, there have be

186 ompleted a validated questionnaire to assess eating behaviors in 4 domains: refusal/picky eating, ora

187 e frequency of recent self-reported abnormal eating behaviors in bulimic subjects.

188 ly regulate fat metabolism without affecting eating behaviors in Caenorhabditis elegans, and identifi

189 contributes to decreased reward and negative eating behaviors in obesity.

190 aracteristics associated with overweight and eating behaviors in preschool children.

191 t differences in food and nutrient intake or eating behaviors in the groups receiving the FAB interve

192 The role of potentially modifiable eating behaviors in this association is unclear.

193 appetitive (food-seeking) and consummatory (eating) behaviors in vGat-ires-cre mice, while inhibitio

194 tions were observed between gut microbes and eating behaviors, including eating frequency, early ener

195 n obligatory role for ghrelin in the changed eating behaviors induced by stress.

196 tin-responsive pathways in the regulation of eating behavior, intermediary metabolism, and the onset

197 Compulsive eating behavior is a transdiagnostic construct that is c

198 e extent to which participants believe their eating behavior is being measured may affect energy inta

199 e to which participants are aware that their eating behavior is being measured.

200 ropionate on the human brain or reward-based eating behavior is currently unavailable.

201 Compulsive eating behavior is hypothesized to be driven in part by

202 ation of increased food reward and increased eating behavior is related but dissociable.

203 Yet the full extent of the lions' man-eating behavior is unknown; estimates range widely from

204 ion of the links between PTSD and obesogenic eating behaviors is necessary to clarify this pathway an

205 esity is often induced by changes in diet or eating behavior, it remains unclear whether obesity, die

206 which, in turn, may contribute to unhealthy eating behaviors later in life.

207 biome disruptions that can promote unhealthy eating behaviors, leading to increased risk for obesity.

208 Compensatory eating behaviors likely diminish, and in some cases nega

209 importance of the hippocampus in modulating eating behaviors linked to emotional eating and lack of

210 works involved in mediating these changes in eating behavior may enable treatment of these features i

211 ution and air-displacement plethysmography), eating behavior (measured by using a 3-factor eating que

212 est to public health.Here we explore whether eating behaviors mediate or modify genetic susceptibilit

213 MI and sum of skinfolds (SSF), and candidate eating behavior moderators were portion size, eating rat

214 ed to emotion, eating related to reward, non-eating behavior motivated by reward or sensitivity to pu

215 titute a neural substrate for the compulsive eating behavior observed in bulimia nervosa.

216 ognizes that it can influence and modify the eating behavior of Americans.

217 ror neurons that cause people to imitate the eating behavior of others without awareness; and limited

218 The dysfunctional eating behavior of VAChTcKO mice was alleviated by donep

219 s syndrome, the obsessions of OCD, the binge eating behaviors of bulimia, and the self-starvation of

220 mice was sufficient to phenocopy maladaptive eating behaviors of VAChTcKO mice.

221 Unhealthy eating behaviors often develop in the setting of inadequ

222 The mediating effect of each eating behavior on the association between the BMI-GRS a

223 overall dietary patterns that reflect actual eating behaviors on mortality caused by cardiovascular o

224 Relatively little is known about changes in eating behavior or hormonal responses to food after bari

225 l heterozygous mice exhibit abnormalities in eating behavior or locomotor activity.

226 se alterations are secondary to pathological eating behavior or traits that could contribute to the p

227 a are available on the normal development of eating behavior, or resilience and risk factors for eati

228 e primary impairments, the result of altered eating behavior, or side effects of psychotropic medicat

229 h), average (7-8 h), and long (>/=9 h) with eating behavior outcomes.

230 Both diseases are a result of maladaptive eating behaviors (overeating or undereating) and are ass

231 ntified 4 moderately heritable (h2 = 36-48%) eating behavior patterns labeled "snacking," "infrequent

232 Eating behavior patterns share a common genetic liabilit

233 to test mediation models between the PRSBMI, eating behavior patterns, and obesity measures.

234 sed principal component analyses to identify eating behavior patterns, twin modeling to decompose cor

235 in energy and nutrient intake as well as in eating behavior phenotypes and selected eating disorders

236 ibition, and hunger and 1-y changes in these eating behaviors predict short- and long-term weight cha

237 l motor problems, oral hypersensitivity, and eating behavior problems.

238 essed eating behavior using the Three-Factor Eating Behavior Questionnaire 18 and burnout using the B

239 Short UPPS-P scale (impulsive traits), Dutch Eating Behavior Questionnaire and Depression, Anxiety an

240 etite was assessed with the use of the Child Eating Behavior Questionnaire when the children were 16

241 ed with a standard psychometric scale (Child Eating Behavior Questionnaire).

242 on the food/nonfood reinforcement task, Baby Eating Behavior Questionnaire, and anthropometrics and d

243 fruit) and the FF scale from the Children's Eating Behavior Questionnaire.

244 measured at age 6 years with the Children's Eating Behavior Questionnaire.

245 the twins completed 4 subscales of the Baby Eating Behavior Questionnaire: "enjoyment of food," "foo

246 ed by using the Diet Habit Survey, a 40-item eating-behavior questionnaire.

247 Children's Eating Behavior Questionnaires were also completed by ca

248 r studied, with subthreshold loss-of-control eating behaviors receiving increased empirical examinati

249 eptide, galanin (GAL), is known to stimulate eating behavior, reduce energy expenditure and affect th

250 rties of dietary fat to reward valuation and eating behavior remain unclear.

251 sms to ensure survival by governing adaptive eating behaviors, remains mysterious.

252 mined the association of sleep duration with eating behaviors reported by adult Americans to understa

253 Body weight was measured; further, eating behaviors (restraint, disinhibition), dietary int

254 -GI meal in prespecified regions involved in eating behavior, reward, and craving.

255 Associations between eating behavior scores and physical characteristics were

256 Eating behavior scores were associated with obesity and

257 should be treated first and that burnout and eating behavior should be evaluated in obesity treatment

258 halamic RLN3/RXFP3 signaling regulates binge-eating behavior.SIGNIFICANCE STATEMENT Binge-eating diso

259 However, little is known about downstream eating behaviors subsequent to skipping breakfast in fre

260 VES: Shift work has been linked to unhealthy eating behaviors such as imbalanced diet, or increased e

261 evels of DE were assessed with the Minnesota Eating Behavior Survey.

262 ssed with the total score from the Minnesota Eating Behavior Survey.

263 A mechanism for the control of eating behavior that is sensitive to a stimulus generate

264 rweight individuals also display patterns of eating behavior that resemble the ways in which addicted

265 that genetic risk for obesity may influence eating behaviors that contribute to weight and could be

266 d fast-food outlets and individual unhealthy eating behaviors that jointly affect weight gain; howeve

267 n short-duration sleepers were suggestive of eating behaviors that may increase energy intake, but 24

268 ychiatric disorder characterized by abnormal eating behaviors that results in weight loss and has ser

269 Behavioral variables included eating behavior [Three-Factor Eating Questionnaire (TFEQ

270 ing and energy restriction and may influence eating behaviors through brain hedonic reward-cognitive

271 practices were prospectively linked to these eating behaviors too (e.g., Bstandardized = 0.033; 95% C

272 ing appetite ratings (visual analog scales), eating behavior traits (Three-Factor Eating Questionnair

273 y was partially mediated by the "appetitive" eating behavior traits (uncontrolled and emotional eatin

274 between fasting appetite ratings and certain eating behavior traits with daily EI.

275 We assessed eating behavior using the Three-Factor Eating Behavior Q

276 n important role in attenuating reward-based eating behavior via striatal pathways, independent of ch

277 Alzheimer disease) were recruited, and their eating behavior was compared with that of 25 healthy con

278 Eating behavior was determined using the Three Factor Ea

279 Eating behavior was examined in some rats, whereas hypot

280 The abnormal eating behavior was found in the 2 groups (bvFTD and SD)

281 e duodenum also suppressed appetite ratings, eating behavior was not altered.

282 void the confounding effects of pathological eating behavior, we studied 30 women after long-term rec

283 Changes in eating behavior were also measured using the Appetite an

284 Energy balance and eating behavior were also normal, even after exposure to

285 Three quantifiable components of eating behavior were measured: restraint, disinhibition,

286 Developmental milestones and eating behavior were the most important predictors.

287 Eating behaviors were assessed by using the validated Ch

288 Regions of interest (ROI) relevant to eating behaviors were delineated.

289 rsations that were focused only on healthful eating behaviors were less likely to diet and use unheal

290 Disordered eating behaviors were present in 27.8% of the cohort (84

291 Pretreatment eating behaviors were unrelated to subsequent weight cha

292 hat small doses of leptin that do not effect eating behavior when delivered to the ventricle or the d

293 at translates taste stimulation to motivated eating behavior when hungry may facilitate food avoidanc

294 ith increased risk for adolescent disordered eating behaviors, whereas conversations focused on healt

295 rly learning influences food preferences and eating behavior, which, in turn, shape differences in di

296 It is unclear whether objective measures of eating behavior will prove useful in evaluating the impa

297 diabetes and, additionally, show a disturbed eating behavior with reduced satiety.

298 the association of psychological measures of eating behavior with the accuracy of rEI assessed by 7-d

299 o determine the association of 3 measures of eating behavior with weight gain and body mass index (BM

300 tions, ate faster, and consumed more energy (eating behavior x risk score interactions: P < 0.05).