ライフサイエンスコーパス: eating behavior

1 tissues independent of mechanisms regulating eating behavior.

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

3 ight influence the development of compulsive eating behavior.

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

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

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

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

8 he polymorphism, influence reward coding and eating behavior.

9 ptors and these forms of naturally occurring eating behavior.

10 mental effects of social influences on their eating behavior.

11 uniquely relevant and influential to youths' eating behavior.

12 ical factor linking reduced energy stores to eating behavior.

13 ith this mutation normalized body weight and eating behavior.

14 associated with measurable effects on child eating behavior.

15 tial for an innate compensation mechanism of eating behavior.

16 We investigated the genetic underpinnings of eating behavior.

17 shell sites elicited appetitive increases in eating behavior.

18 rphine at locations that caused increases in eating behavior.

19 f genetic and environmental factors in human eating behavior.

20 ivity are accompanied by specific changes in eating behavior.

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

22 ors may affect different stimuli that impact eating behavior.

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

24 tributes to metabolic control by suppressing eating behavior.

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

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

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

28 tionship between perceived food scarcity and eating behavior.

29 ful eating are protective against disordered eating behaviors.

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

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

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

33 did not translate into unequivocally better eating behaviors.

34 d the prefrontal cortex result in compulsive eating behaviors.

35 es increased physical activity and healthful eating behaviors.

36 changes across groups and their relations to eating behaviors.

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

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

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

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

41 Eating behavior affects weight and thus the development

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

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

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

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

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

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

48 Opportunistic eating behavior and BMI were both positively associated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 Eating behavior and thus dietary intake affect the devel

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

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

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

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

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

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

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

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

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

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

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

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

78 Eating behaviors and weight change have been linked to t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 Abnormal eating behaviors are common in patients with frontotempo

95 Abnormal eating behaviors are prominent in patients with bvFTD an

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

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

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

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

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

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

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

103 1; 2001-2003) was associated with disordered eating behaviors at time 2 (2004-2006), as well as weigh

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 The eating behaviors-emotional eating, uncontrolled eating,

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

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

129 Eating behaviors examined included the following: report

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

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

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

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

134 Disordered eating behaviors have also been associated with PTSD and

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

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

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

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

139 Evidence suggests altered eating behavior in obesity.

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

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

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

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

144 2,5-anhydro-D-mannitol (2,5-AM), stimulates eating behavior in rats.

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

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

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

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

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

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

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

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

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

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

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

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

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

158 Compulsive eating behavior is a transdiagnostic construct that is c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 Unhealthy eating behaviors often develop in the setting of inadequ

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

200 Associations between eating behavior scores and physical characteristics were

201 Eating behavior scores were associated with obesity and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

218 Eating behavior was examined in some rats, whereas hypot

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

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

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

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

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

224 Eating behaviors were assessed by using the validated Ch

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

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

227 Pretreatment eating behaviors were unrelated to subsequent weight cha

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

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

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

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

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

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

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