ライフサイエンスコーパス: food intake

1 = 1.97, 95%CI: 1.28-3.04) and recent reduced food intake.

2 Subsequently, we measured ad libitum food intake.

3 terventions aimed at advancing the timing of food intake.

4 on activity and, in turn, hedonic aspects of food intake.

5 n receptors (LepRs) in NTS neurons increases food intake.

6 se and water to bypass the cephalic phase of food intake.

7 mic progenitors but have opposing effects on food intake.

8 neural circuit from VMH to PVT that inhibits food intake.

9 althy FF commercials predicted greater total food intake.

10 ecreased energy expenditure without changing food intake.

11 onic pathways distinctly interact to control food intake.

12 played increased body weight, adiposity, and food intake.

13 genetic liability to a morning preference on food intake.

14 us activate hD2R cells and can also decrease food intake.

15 ithout wheel access and showed no changes in food intake.

16 in body temperature, energy expenditure and food intake.

17 insulin secretion, nutrient assimilation and food intake.

18 oopiomelanocortin (Pomc) gene expression and food intake.

19 tfeeding status, physical activity, and fast food intake.

20 than wild type littermates owing to reduced food intake.

21 HCD or METH intake, and prior to measures of food intake.

22 the lateral hypothalamus (LH) also decreases food intake.

23 hormone responses to visual food stimuli and food intake.

24 ed glucagon-like peptide 1 (GLP-1) supresses food intake.

25 include reductions in adipose lipolysis and food intake.

26 intestinal metabolism, spermatogenesis, and food intake.

27 y play a negative role in energy balance and food intake.

28 nt, such as light exposure and the timing of food intake.

29 ate the independent effects of OSE and ER on food intake.

30 ndirect influence of heat stress via reduced food intake.

31 iors, along with the quality and quantity of food intake.

32 of genetic variation in the control of binge food intake.

33 and are sufficient and necessary to control food intake.

34 the dorsomedial hypothalamus (DMH) regulate food intake.

35 rols brain activity and behaviors, including food intake.

36 energy expenditure, despite reduced overall food intake.

37 s relative to others stimulates appetite and food intake.

38 in systems functionally interact to regulate food intake.

39 how eating behavior factors influence total food intake.

40 he hypothalamus to signal hunger and promote food intake.

41 ntestinal activity, systemic metabolism, and food intake.

42 ow leptin acts in the NTS neurons to inhibit food intake.

43 Longer oral processing decreases food intake.

44 stinal motility and secretion, appetite, and food intake.

45 yos and larvae showed reduced locomotion and food intake.

46 n contributes to leptin-induced reduction of food intake.

47 yogenesis, gastrointestinal homeostasis, and food intake.

48 rs that are essential for energy balance and food intake.

49 leptin might act on these neurons to reduce food intake.

50 healthier FF commercials predicted healthier food intake.

51 hypothalamic circuitries regulates mammalian food intake.

52 d unhealthier food intake, but not healthier food intake.

53 = 0.47) and glycemic (r = 0.77) responses to food intake.

54 without compromising lean mass or affecting food intake.

55 olfactory perception is strongly involved in food intake.

56 ed the role of dyadic verbal interactions on food intake.

57 eeking behavior without affecting ad libitum food intake.

58 to understanding how food advertising drives food intake.

59 t feeding behaviors accompanied by decreased food intake.

60 yles(3,4), as behaviour accounts for overall food intake(5).

61 Reproduction induces increased food intake across females of many animal species(1-4),

62 Despite robust changes in food intake, activation or inhibition of AgRP neurons di

63 Body weight, food intake, adiposity index, fasting insulin, triglycer

64 PPG-ablated mice increased food intake after a prolonged fast and after a liquid di

65 la predicted increased subsequent ad libitum food intake after distraction (r = 0.36).

66 oncaloric fluid intake, but did not decrease food intake after fasting or salt intake following salt

67 test how central olfactory mechanisms alter food intake after sleep deprivation.

68 ) of female mice control the daily timing of food intake, along with the circadian regulation of loco

69 erform a genomewide association on 85 single food intake and 85 principal component-derived dietary p

70 KD and CTRL rats displayed similar home cage food intake and a similar hypophagic response to systemi

71 erived hormone Lipocalin-2 (LCN2) suppresses food intake and acts as a satiety signal.

72 cutaneous, and oral administration increased food intake and body weight and preserved fat mass and l

73 mc expression are significantly reduced, and food intake and body weight are increased.

74 There were no significant differences in food intake and body weight between all groups.

75 Our findings indicate that MANF influences food intake and body weight by modulating hypothalamic i

76 alamic leptin action, resulting in increased food intake and body weight gain.

77 lastrol administration substantially reduces food intake and body weight in MC4R-null comparable to D

78 as well as causing significant reductions in food intake and body weight in mice.

79 The effects of oxytocin on food intake and body weight reduction have been demonstr

80 vels during adulthood.SIGNIFICANCE STATEMENT Food intake and body weight regulation depend on hypotha

81 utide, the two peptides synergized to reduce food intake and body weight relative to each monotherapy

82 that these two metabolic receptors modulate food intake and body weight via reciprocal functional in

83 leptin concentration lead to alterations in food intake and body weight, but the regulatory mechanis

84 e metabolic side effects including increased food intake and body weight, but the underlying mechanis

85 Chronic intranasal leptin decreased food intake and body weight, whereas intraperitoneal lep

86 etic activation of LS(Nts) neurons decreases food intake and body weight, without altering locomotion

87 peptide Pro-opiomelanocortin (Pomc) regulate food intake and body weight.

88 ignaling in AgRP neurons initially increased food intake and caused dramatic weight gain, in agreemen

89 tal depletion of GLP-1R in the PVN increases food intake and causes obesity.

90 and this acute activation promotes increased food intake and decreased energy expenditure.

91 Combining biomarkers of food intake and dietary intake data is a high priority.

92 We examined food intake and digestion in three mixed-sex groups of a

93 dy aimed to examine the relationship between food intake and dyadic verbal interactions.

94 Food intake and energy expenditure were not altered in M

95 cting as anorectic neurons in CNS control of food intake and energy homeostasis.

96 Leptin is a hormone that critically impacts food intake and energy homeostasis.

97 efine our understanding of the physiology of food intake and energy metabolism.

98 When activated, these cells inhibit food intake and facilitate weight loss.

99 em, regulates multiple behaviours, including food intake and food reward.

100 secretion could open up new ways to control food intake and glucose metabolism.

101 cts principally in the hindbrain to decrease food intake and has recently been shown to act as a neur

102 ontrol of feeding thwarts attempts to reduce food intake and how this might be overcome.

103 abolished alpha-klotho's ability to suppress food intake and improve glucose clearance.

104 GLP1 administered centrally reduces food intake and increases anxiety-like behavior and plas

105 r reveal that vCA1 GLP-1R activation reduces food intake and inhibits impulsive operant responding fo

106 enterocytes-interstitial cells-by promoting food intake and insulin/IGF signalling.

107 ucagon-like peptide-1) or increase (ghrelin) food intake and learned food reward-driven responding, t

108 r 15 (GDF15), which has been shown to reduce food intake and lower body weight through a brain-stem-r

109 rly for type 2 diabetic patients, to control food intake and maintain glucose homeostasis.This trial

110 es with well-established roles in regulating food intake and metabolism.

111 requent luminal distortions occurring during food intake and movement.

112 y in POMC cells is associated with increased food intake and obesity.

113 the MC3R agonist, MTII, decreases home-cage food intake and operant responding for sucrose pellets.

114 tracted eating" is associated with increased food intake and overweight.

115 physiologically relevant for the control of food intake and pica (i.e., behavioral measure of malais

116 hormone secretagogue 1a (GHSR1a), to promote food intake and prevent hypoglycemia.

117 considered as a promising strategy to reduce food intake and promote weight management.

118 ty-induced glucose intolerance by decreasing food intake and promoting adaptive beta-cell proliferati

119 ls, D2R-OE(NAc) mice of both sexes increased food intake and ran more than controls.

120 ed in various functions including attention, food intake and response to stress.

121 ed intestinal metabolic state in controlling food intake and sperm production through gut-derived cit

122 likely influences the chronic regulation of food intake and the binge-like consumption of a palatabl

123 ) receptor agonist, has been shown to reduce food intake and to increase proopiomelanocortin (POMC) g

124 ulates glucose-stimulated insulin secretion, food intake and/or energy expenditure in animal models a

125 may be a novel target to increase appetite, food intake, and body weight among patients after ES.

126 ons or their projections to the PVT inhibits food intake, and chemical genetic inactivation of PVT ne

127 ry tract (NTS) contributes to the control of food intake, and injections of leptin into the NTS reduc

128 of crop enlargement, resulting in increased food intake, and preventing the post-mating remodelling

129 TA circuit in mice increases body weight and food intake, and reduces depression-like behaviors and a

130 ntrols growth hormone and insulin secretion, food intake, and reward-seeking behaviors.

131 st 25% of their initial body weight, reduced food intake, and substantially increased wheel running.

132 How these factors contribute to food intake, and the underlying physiological mechanisms

133 -based combination therapies produce greater food intake- and body weight-suppressive effects compare

134 regulated neither in course of aging nor by food intake; and (e) central NPY levels are augmented in

135 genic effects on apoA-IV gene expression and food intake are impaired.

136 and daily rhythms of sleep-wake behaviour or food intake as a result of genetic, environmental or beh

137 poq-deficient mice show increased rest phase food intake associated with disrupted transcript rhythms

138 d weight relative to wild-type and increased food intake at 20 months of age, much later than previou

139 a breakfast meal on the primary endpoint of food intake at a subsequent meal.

140 imulation study demonstrated that the use of food intake biomarkers may be feasible and beneficial in

141 with its multifaceted beneficial effects on food intake, body weight and blood glucose levels.

142 ody weight) showed no significant changes in food intake, body weight gain and relative weight of vit

143 rug arabinofuranosyl cytidine (AraC) blunted food intake, body weight gain, and adiposity.

144 ated analog of the NT peptide (P-NT) reduces food intake, body weight, and adiposity in diet-induced

145 ty rats, a model of T2D, and monitored daily food intake, body weight, and blood glucose levels over

146 Acyl-ghrelin administration increases food intake, body weight, and blood glucose.

147 the neuronal basis for the effects of MCH on food intake, body weight, and glucose metabolism and hig

148 In male mice, nPM exposure increased food intake, body weight, fat mass, adiposity, and whole

149 ects have normal-range hormonal profiles and food intake but exhibit resistance to weight gain despit

150 ocks the effect of cold exposure to increase food intake but has no effect on energy expenditure.

151 staurants is unlikely to encourage healthier food intake, but interventions that reduce the ability o

152 n worms quantify either foraging behavior or food intake, but not both.

153 predicted greater total food and unhealthier food intake, but not healthier food intake.

154 ations, gastrointestinal peptide release and food intake, but the degree to which it does remains unc

155 mediobasal hypothalamus is known to suppress food intake, but the role of the eIF2alpha phosphatases

156 r reproduction is mainly derived from direct food intake, but there is limited somatic reserve remobi

157 T(2C)Rs) attenuates cocaine and high caloric food intake, but whether a 5-HT(2C)R agonist can reduce

158 tment of lean monkeys with rh-LCN2 decreases food intake by 21%, without overt side effects.

159 Reducing food intake by 40% to slow growth reduced podocyte hyper

160 uggest that leptin acts in the NTS to reduce food intake by increasing NMDAR-mediated currents, thus

161 Leptin influences food intake by informing the brain about the status of b

162 These findings suggest that the ECS drives food intake by interfering with anticipatory, cephalic p

163 evious studies showed that optimal timing of food intake can improve metabolic health.

164 n and metabolically normal despite increased food intake, comparable activity, and equivalent fecal f

165 ojections to the VTA bidirectionally control food intake, consistent with a permissive role in feedin

166 o homeostasis were PPG neurons necessary for food intake control.

167 s and light exposition; (c) 7-day-diaries of food intake; (d) anthropometry and metabolic parameters;

168 o correct measurement error in self-reported food intake data.

169 In metabolic cages, food intake decreased by 3 kcal/kg per hour in Ad-GcR(-/

170 ative utterances (independent variables) and food intake (dependent variable) were coded from the vid

171 Oral food intake did not differ between the 2 groups.

172 erences in food intake, shows how aspects of food intake differ across subpopulations, and can be app

173 binge eating disorder, avoidant-restrictive food intake disorder, pica, and rumination disorder.

174 mping syndrome (73% relative reduction), and food intake disturbance (50% relative reduction).

175 en fed a high-fat diet (HFD) and had reduced food intake during refeeding after an unfed period but w

176 that short-term leptin administration alters food intake during refeeding after fasting, whereas long

177 Food intake during wake stimulates biosynthesis followed

178 Human exposure pathways include food intake, dust ingestion, and use of personal care pr

179 The central clock regulates food intake, energy expenditure and whole-body insulin s

180 he host scales immune responses according to food intake, featuring FXR as a T cell-intrinsic sensor.

181 Concurrently, fat mass, food intake (FI), and ucp1 expression in brown adipose t

182 of DCPP-ene attenuate reduction of overnight food intake following intra-NTS leptin injection.

183 al and nonexperimental approaches to examine food intake/food choice as a function of the number of c

184 auses long-term amelioration of body weight, food intake, glucose homeostasis, and pro-opiomelanocort

185 g hormone (MCH) is an important regulator of food intake, glucose metabolism, and adiposity.

186 ostnatal trauma recapitulates the effects on food intake, glucose response to insulin and risk-taking

187 of NAc projections to the VTA in the control food intake has been largely unexplored.

188 nto actionable new concepts in the timing of food intake has led to the emerging practice of time-res

189 Both homeostatic and hedonic mechanisms of food intake have been attributed to several brain region

190 How peripheral energy state affects diurnal food intake, however, is still poorly understood.

191 udy was to develop calibration equations for food intake, illustrated with an application for citrus

192 ar administration of alpha-klotho suppressed food intake, improved glucose profiles, and reduced body

193 most abundant NAT in human plasma, decreases food intake, improves glucose tolerance, and stimulates

194 search has investigated neural predictors of food intake in adolescents.

195 ed in the regulation of feeding behavior and food intake in all vertebrates.

196 nd prolonged periods of extremely restricted food intake in anorexia nervosa.

197 erable loci might affect lipids by modifying food intake in environments rich in certain nutrients, w

198 found that vapor cannabis exposure promoted food intake in free-feeding and behaviorally sated rats,

199 ed environmental context-dependent gating of food intake in intruding mice, suggesting a dynamic infl

200 nin 2 receptor (CCK-2R), strong reduction of food intake in lean pigs for up to 48 h after one subcut

201 of LEAP2 is able to inhibit ghrelin-induced food intake in mice.

202 c surgery in rodents and humans and inhibits food intake in mice.

203 chronic modulation of their activity reduces food intake in mice.

204 s peripheral glucose homeostasis and reduces food intake in preclinical models of obesity and diabete

205 including relaxin-3 (RLN3), which stimulates food intake in rats through the activation of the relaxi

206 5-HT and GLP-1 is involved in the control of food intake in rats.

207 hway is necessary for adaptive inhibition of food intake in response to external cues.

208 selection, suggesting that howlers maximize food intake in response to local aggregation of fruit th

209 retin-HCRT) and NPY, and their regulation by food intake in the short-lived vertebrate model Nothobra

210 n the orexigenic neuropeptides that regulate food intake in wild animals.

211 ss to high calorie diet (HCD), we quantified food-intake in four inbred mouse strains: C57Bl/6J (B6),

212 ections to the VTA inhibits food-seeking and food intake (in both sexes), while optogenetic inhibitio

213 cle and adipose tissue, is driven by reduced food intake, increased energy expenditure, excess catabo

214 ociated with the hedonic aspect of enhancing food intake, inhibited vGluT2 neurons.

215 obesity subsequently develops despite normal food intake, intestinal nutrient absorption and locomoto

216 utrients from endogenous stores or exogenous food intake into offspring.

217 Food intake is a complex behavior regulated by discrete

218 Regulation of food intake is a recently identified endocrine function

219 idemiologic studies have evaluated how dairy-food intake is associated with risk of early menopause.

220 lator of the neural circadian clock, time of food intake is emerging as a dominant agent that affects

221 Food intake is essential for survival, but maladaptive p

222 that malaria rhythms persist even when host food intake is evenly spread across 24 hours, suggesting

223 ion refers broadly to the condition in which food intake is inadequate to meet a child's needs for ph

224 mice how a gut neuronal signal triggered by food intake is integrated with intestinal antimicrobial

225 f homeostatic and hedonic signaling to drive food intake is less clear, therefore we aimed to identif

226 Surprisingly, we find that food intake is most sensitive to stimulation of mechanor

227 causal links between diurnal preference and food intake is now possible in Mendelian randomization (

228 Food intake is tightly regulated by a group of neurons p

229 s gastric emptying, appetite, and ad libitum food intake is unknown.

230 tin, decreases Pomc expression and increases food intake leading to high-fat diet-induced obesity.

231 ersons with dementia commonly experience low food intake leading to negative nutritional and function

232 idents with dementia commonly experience low food intake, leading to negative functional and nutritio

233 and decreases body fat mass without altering food intake, lean body mass, body temperature, or bioche

234 ellular processes, including the response to food intake, maintaining homeostasis, and the pathogenes

235 pregnancy there were no changes to maternal food intake, maternal weight gain, litter size, or gesta

236 The biochemical response to food intake must be precisely regulated.

237 ing, and other factors, total baseline dairy-food intake of >=4 servings/day versus <4 servings/week

238 pecific activity in sustaining the increased food intake of mothers during reproduction.

239 estigate the effects of circadian rhythm and food intake on several metabolite classes.

240 behaviors: foraging to find a food patch and food intake once a patch is found.

241 gmented in course of aging, and regulated by food intake only in young.

242 let function prior to significant changes in food intake or blood glucose.

243 rotects from obesity, but it does not affect food intake or body weight under normal chow consumption

244 fed ad libitum without changing the animals' food intake or the weight of their intestines, suggestin

245 t did not affect sucrose seeking, ad libitum food intake, or body weight.

246 d in various physiological processes such as food intake, pain, inflammation, stress, and anxiety.

247 etabolically responsive neurokine, regulates food intake patterns and mouse behaviors.

248 In male mice, FAM19A1 deficiency alters food intake patterns during the light and dark cycle.

249 s a result of waking, physical activity, and food intake patterns.

250 tosis, and hyperlipidemia without changes in food intake, physical activity, and thyroid hormone leve

251 No significant differences in fluid and food intake, plasma electrolytes, intestinal/colon anato

252 Despite their opposing actions on food intake, POMC and NPY/AgRP neurons in the arcuate nu

253 f foraging locations rarely decreases colony food intake, potentially because simultaneous transmissi

254 ther, the results suggest that reductions in food intake produced by WAY163909 are associated with pa

255 alphadeltaKO mice exhibit decreased food intake, protection from weight gain on standard and

256 ng predators and their prey as well as total food intake rate.

257 vHPC ghrelin signaling counteracted the food intake-reducing effects produced by various periphe

258 Excellent efficacy in glucose control, food intake reduction, and weight loss for lead candidat

259 efficacy and safety profiles with regard to food intake reduction, weight loss, and glucose control

260 aired glucose homeostasis without changes in food intake relative to control VSG mice.

261 gs suggest that eating with others increases food intake relative to eating alone, and this is modera

262 he feeding circuit for the VMH regulation of food intake remains to be defined.

263 rons and corresponding signals that regulate food intake remains unknown.

264 The GHG emissions associated with food intake required to fuel a kilometre of walking rang

265 (PVH(TrkB)) neurons suppresses or increases food intake, respectively.

266 , in agreement with published data; however, food intake returned to baseline levels within 1 wk, and

267 othalamus, as a major site for regulation of food intake, sends only very indirect projections onto t

268 ditis elegans Our central assumption is that food intake serves a dual to gather information about th

269 Sleep deprivation has marked effects on food intake, shifting food choices toward energy-dense o

270 er quantifies interindividual differences in food intake, shows how aspects of food intake differ acr

271 n and monitoring feeding, only NEGR1 altered food intake significantly.

272 Impulsivity was associated with food intakes, snacking, and risk of EDs and could be tak

273 otor activity, energy expenditure, and daily food intake that are consistent with effects in human ca

274 han euthyroid mice, owing in part to reduced food intake, these hypothyroid mice show signs of compen

275 through a paradigm that promoted binge-like food intake through intermittent access to high calorie

276 ted in reduced body weight, fat content, and food intake to a degree similar to that seen with alteri

277 iatal Rgs4 in DIO-susceptible rats decreased food intake to levels comparable to DIO-resistant animal

278 tose, either ad libitum or restricting their food intake to match body weight to the mice on a chow d

279 based olfactory neuroimaging, and ad libitum food intake to test how central olfactory mechanisms alt

280 Taken together, restricting food intake to the active dark phase enhanced adaptation

281 ioid system regulate reward, motivation, and food intake, understanding the role of opioid signaling

282 teroidogenic factor 1 (SF1) rapidly inhibits food intake, VMH SF1 neurons project dense fibers to the

283 Food intake was controlled throughout the study.

284 Food intake was increased to a larger extent in intact a

285 P for trend = 0.02), whereas high-fat dairy-food intake was not associated with early menopause.

286 The effect on food intake was quantified in 2 ways: via ad libitum ora

287 Overall, cumulative food intake was the strongest correlate to weight loss a

288 nd after extended HCD or METH intake, and on food intake, was also tested.

289 Concomitant changes in food intake, water responses, and body weight were asses

290 ignment), while environmental conditions and food intake were controlled.

291 of food (95% CI - 26.19 (- 61.72, - 9.35) on food intake were noted.

292 portantly, no changes in body temperature or food intake were observed.

293 d 170-item food frequency questionnaire, and food intakes were categorized into food patterns based o

294 acilitation across studies that had examined food intake when participants ate alone or with stranger

295 of FGF1 appeared dependent on reductions in food intake, whereas peripheral FGF1 had acute actions o

296 dinate canonical feeding centers to regulate food intake, which could offer therapeutic targets for f

297 Injection of leptin into the NTS inhibits food intake, while knockdown of leptin receptors (LepRs)

298 Compound A reduced body weight, food intake, whole-body fat mass, and intramuscular trig

299 s circadian clocks to synchronize organismal food intake with cellular bioenergetics.

300 ts are nevertheless more effective to reduce food intake within hours of administration in overweight