ライフサイエンスコーパス: food intake

1 rols brain activity and behaviors, including food intake.

2 at are important for sleep-wake behavior and food intake.

3 stimulation of PVT glutamate neurons reduced food intake.

4 ys including processes linked to obesity and food intake.

5 body weight, at least in part, by decreasing food intake.

6 iet that mimicked each individual's habitual food intake.

7 PVN), which is involved in the regulation of food intake.

8 n children with illnesses that limited their food intake.

9 s relative to others stimulates appetite and food intake.

10 gulation of energy expenditure, satiety, and food intake.

11 in systems functionally interact to regulate food intake.

12 eficient mice have increased body weight and food intake.

13 e concentrations of which can be affected by food intake.

14 ere seen in reward circuits or on ad libitum food intake.

15 ng new insights into how the brain regulates food intake.

16 eases the biological body weight via reduced food intake.

17 l effect of glucose on insulin secretion and food intake.

18 xic chambers without alterations to maternal food intake.

19 us circadian clock, independent of light, is food intake.

20 her serotonin-dependent behaviours including food intake.

21 how eating behavior factors influence total food intake.

22 cal phenotypes that can inhibit or stimulate food intake.

23 rivals by raising their own growth rate and food intake.

24 he hypothalamus to signal hunger and promote food intake.

25 with functions that oscillate in response to food intake.

26 inhibition of septal vGAT neurons increased food intake.

27 seeking in mice after SDe without affecting food intake.

28 own, however, as is its ability to stimulate food intake.

29 es deficits in motor function, learning, and food intake.

30 are important in the control of appetite and food intake.

31 ponses to intravenous alcohol challenge, and food intake.

32 on fails to evoke any significant changes in food intake.

33 Ca(2+) signaling pathway in ARC glia reduces food intake.

34 leads to a robust and sustained increase in food intake.

35 can prime future food approach behaviors and food intake.

36 PVT GLP-1R signaling increased meal size and food intake.

37 Hunger is a powerful drive that stimulates food intake.

38 f changes in hepatic de novo lipogenesis and food intake.

39 ith neural circuits of motivation to control food intake.

40 Both drugs reduced food intake.

41 ose homeostasis independently of obesity and food intake.

42 ory activity in the LH can induce changes in food intake.

43 n addition, osteoblast-derived LCN2 inhibits food intake.

44 ctive duration of eating, and 3) the maximal food intake.

45 and consistent factor influencing children's food intake.

46 in brain regions involved in the control of food intake.

47 cells evokes food approach without affecting food intake.

48 ustatory stimulation, satiation, and maximal food intake.

49 s that GLP-1R signaling in the LDTg controls food intake.

50 t and is accomplished by more than increased food intake.

51 ol of glucose homeostasis and suppression of food intake.

52 atabolism, which are prevented by increasing food intake.

53 d lose weight despite the absence of reduced food intake.

54 1 and FGF21 but is independent of changes in food intake.

55 ted by high fat diet and driven by increased food intake.

56 energy expenditure, despite reduced overall food intake.

57 e not associated with reduced body weight or food intake.

58 rease, whereas DRN(VGLUT3) neurons suppress, food intake.

59 synchronizers, such as physical activity or food intake.

60 ide Y (NPY), which regulates both stress and food-intake.

61 y be useful for helping people control their food intakes.

62 At TNZ, leptin reduced food intake (-11.0 +/- 0.5 g cumulative deficit) and bod

63 cture mobile phone application to record all food intake across 7 consecutive days during a participa

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

65 th the effective eating duration and maximum food intake (adjusted R(2) = 0.06 and 0.11).

66 The timing of food intake affects various aspects of the circadian clo

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

68 However, food intake also impacts multiple biochemical processes

69 cachexia, which are associated with reduced food intake, altered body composition, and decreased fun

70 the hypothesis that temporal desynchrony of food intake alters innate immune responses.

71 NeuromedinU is a potent regulator of food intake and activity in mammals.

72 al risk factors such as amount or content of food intake and activity level, plays an important role

73 Tmem18 in the PVN of wild-type mice reduced food intake and also increased energy expenditure.

74 es of NTS SRC-1 in mediating E2's actions on food intake and apoA-IV gene expression and suggest that

75 th exendin-(9-39) dose-dependently increases food intake and attenuates the hypophagic effects of gas

76 we have examined the effects of brain TTR on food intake and body weight and have further determined

77 ese neurons in obese (ob/ob) mice suppresses food intake and body weight and normalizes locomotor act

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

79 ion, increases glucose tolerance and reduces food intake and body weight gain in healthy, obese and d

80 Subchronic administration of 11 reduced food intake and body weight gain without causing CNS-rel

81 r abrogates the ability of GDF15 to decrease food intake and body weight in mice.

82 DDs)-mediated synaptic silencing ablates the food intake and body weight reduction following vCA1 GLP

83 nsable element of normal food reinforcement, food intake and body weight regulation.

84 a regulator of leptin signalling that adapts food intake and body weight to our dietary environment.

85 Although food intake and body weight were reduced compared with n

86 However, there were almost no changes in food intake and body weight when wortmannin injection (i

87 e hypothalamus play a key role in regulating food intake and body weight, by releasing three differen

88 B334867 caused anorectic effects by reducing food intake and body weight, our results unravel a previ

89 trated MC3R deficiency caused a reduction of food intake and body weight, whereas at the same time ex

90 that EX-4 treatment significantly decreased food intake and body weight.

91 ic nervous system, independent of changes in food intake and body weight.

92 ance of NTS astrocytic GLP-1R activation for food intake and body weight.

93 ighlight their additional role in modulating food intake and body weight.

94 tion of TTR in normal growing rats decreased food intake and body weight.

95 E2's anorectic action, leading to increased food intake and body weight.

96 ctivation also induced a robust reduction in food intake and body weight.

97 ective pan-JNK (JNK1/2/3) inhibitor, reduced food intake and body weight.

98 the brain circuits by which leptin regulates food intake and cardiovascular function are differential

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

100 hemerin on a 12 h:12 h photoperiod inhibited food intake and decreased body weight with associated ch

101 anisms are not fully understood, but reduced food intake and effects on gastrointestinal hormones are

102 dramatic loss of body weight due to reduced food intake and elevated energy expenditure; they also m

103 olved in the hypothalamic control exerted on food intake and energy expenditure by the leptin-melanoc

104 g that variations in the genes that regulate food intake and energy expenditure may contribute to obe

105 RKD(DeltaNkx2.1cre) mice exhibited increased food intake and energy expenditure with no net effect on

106 onents of the neuronal circuits that control food intake and energy homeostasis.

107 inly secreted from the stomach and regulates food intake and energy homeostasis.

108 hypothalamus has a vital role in controlling food intake and energy homeostasis; its activity is modu

109 ive, dose-response relationship between fast food intake and exposure to phthalates (p-trend < 0.0001

110 l nuclei and other brain regions involved in food intake and food reward.

111 s of downstream cells to produce a change in food intake and glucose homeostasis and that these effec

112 Body composition, food intake and glucose homeostasis were measured throug

113 mediating the effects of endogenous GLP-1 on food intake and glycemia and may promote the further dev

114 Global HDAC5 KO mice have increased food intake and greater diet-induced obesity when fed hi

115 fatty acids (FAs) act centrally to decrease food intake and hepatic glucose production and alter hyp

116 ody weight as a result of both reduced daily food intake and increased caloric expenditure, driven by

117 not of the saturated FA palmitate, decreased food intake and increased locomotor activity.

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

119 e detection was studied in vivo by measuring food intake and insulin secretion in response to increas

120 he functions of CARTp, such as regulation of food intake and interactions with the social control net

121 These effects were independent of food intake and involved specific efferent autonomic pat

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

123 lved in central nervous system regulation of food intake and leptin signalling.

124 is involved in MC4R-mediated suppression of food intake and linear growth, which are believed to be

125 emptying, reduce body weight by reduction of food intake and lower circulating lipoproteins, inflamma

126 ity in the mediobasal hypothalamus increases food intake and modulates pathways implicated in leptin

127 -1R signaling is required for the control of food intake and motivation to feed, and provide a new st

128 ic proopiomelanocortin, leading to increased food intake and obesity accompanied with hyperinsulinemi

129 pment of systemic insulin resistance but not food intake and obesity.

130 Food intake and other constituents were recorded every d

131 ets to assess changes in energy expenditure, food intake and other metabolic endpoints.

132 -receptor (MC4R)-expressing neurons modulate food intake and preference in rodents but their role in

133 is likely implicated in emotional aspects of food intake and provide new insights into the developmen

134 lease peptide products that potently inhibit food intake and reduce body weight.

135 lease peptide products that potently inhibit food intake and reduce body weight.

136 in regions critically involved in regulating food intake and resolving affective conflict, respective

137 sis that PVT GLP-1R signaling contributes to food intake and reward inhibition.

138 ts, BChE treated mice had modest postdieting food intake and showed normal glucose homeostasis.

139 ional cues, and hypothalamic MANF influences food intake and systemic energy homeostasis.

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

141 d-type mice, tamoxifen significantly reduced food intake and totally prevented adiposity, insulin res

142 ociated with lower weight status and limited food intake and variety in childhood.

143 ctating at 30 degrees C had lower asymptotic food intake and weaned lighter litters than those at 21

144 f SR3306 (7 days) prevented the increases in food intake and weight gain in lean mice upon high-fat d

145 s in brain activation to oxytocin effects on food intake and weight.

146 MC4R agonists function to lower food intake and weight.

147 l nervous system factor in the regulation of food intake and weight.

148 ition of CNS aPKC activity acutely increases food intake and worsens glucose tolerance in chow-fed ro

149 t hyperactivity disorder (ADHD) may increase food intake and, consequently, weight gain.

150 s of recombinant human GDF15 on body-weight, food-intake and glucose parameters.

151 ur and endogenous circadian time, content of food intake, and body composition.We enrolled 110 partic

152 Energy homeostasis, food intake, and body weight are regulated by specific b

153 Body weight, food intake, and disease activity index (DAI) were asses

154 a in adipocytes does not affect body weight, food intake, and energy expenditure but results in an ex

155 -induced increases in energy expenditure and food intake, and exacerbated LP-induced weight loss.

156 eight, body composition, energy expenditure, food intake, and insulin/glucose tolerance were measured

157 itonin dose-dependently reduces body weight, food intake, and motivated feeding behaviors.

158 eum differentially alters appetite response, food intake, and secretion of satiety-related gastrointe

159 ing protein 1 (UCP1), energy expenditure and food intake, and these effects require the metabolic hor

160 While activation of GCG+ neurons did reduce food intake, and variably decreased hepatic glucose prod

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

162 individual's menu approximated her habitual food intake as estimated from her 4-d food record and ad

163 te, were examined for their association with food intake at baseline and with MetS at endpoint.

164 timulation of mouse ARC TH neurons increased food intake; attenuating transmitter release reduced bod

165 n multiple circuits in the brain to regulate food intake, autonomic outflow, and endocrine function t

166 synaptic, and molecular) explanation of how food intake behavior and body weight are regulated by en

167 ae results in reduced larval path length and food intake behavior, while conversely showing an increa

168 to maintain energy homeostasis and regulate food intake behavior.

169 Food intake, body weight and glucose handling were asses

170 d with salidroside showed slightly decreased food intake, body weight and hepatic triglyceride conten

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

172 Remarkably, although food intake, body weight, and systemic insulin sensitivi

173 We established the impact of intervention on food intake, body weight, and visceral adipose tissue (V

174 a high-fat diet, these mice exhibited normal food intake but elevated energy expenditure, yielding re

175 15 degrees C, leptin infusion did not alter food intake but increased MAP and HR (8 +/- 1 mmHg and 3

176 associated with strong circadian changes in food intake, but the contributing mechanisms have yet to

177 mouse the hypothesis that IL-18 can decrease food intake by acting on neurons of the bed nucleus of t

178 t of TEI from fat in fast food); and c) fast food intake by food group (dairy, eggs, grains, meat, an

179 intracellular proteins (O-GlcNAc), regulates food intake by modulating excitatory synaptic function i

180 lations were found between the clock hour of food intake, caloric amount, meal macronutrient composit

181 a variety of biological functions including: food intake, cardiovascular regulation, cognition, seizu

182 hase with an LED for 8 wk and 8 wk of normal food intake combined with 2 LED products/d, followed by

183 tering erythromycin significantly stimulated food intake compared with placebo (53% +/- 13% compared

184 a novel function for PVT GLP-1R signaling in food intake control and suggest a role for the PVT-to-NA

185 The contribution of these brain regions to food intake control, however, is poorly understood.

186 ay represent cellular correlates of impaired food intake control.

187 Translating food intake data into phytochemical outcomes is a crucia

188 r TDS food and used these, along with NHANES food intake data, to develop 4 estimates of each partici

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

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

191 ese results show that EX-4 likely suppresses food intake due to its ability to enhance insulin signal

192 xigenic PBN CGRP neurons, thereby increasing food intake during homeostatic need.SIGNIFICANCE STATEME

193 omc1a neurons may act as a signal to inhibit food intake during mouth brooding.

194 nd LR decreased body and fat mass, increased food intake, elevated lipid cycling in WAT and improved

195 The Melanocortin-4 receptor (MC4R) regulates food intake, energy balance, and somatic growth in both

196 GDF15 regulates food intake, energy expenditure and body weight in respo

197 regnancy, and body weight, body composition, food intake, energy expenditure, total cage activity, an

198 mediation of gut-derived GLP-1's effects on food intake, energy homeostasis, and glycemic control.

199 sed ghrelin action, MENX rats show increased food intake, enhanced body fat mass, and elevated plasma

200 both studies including survival, bodyweight, food intake, fasting glucose levels and age-related morb

201 PVT GLP-1R agonism reduced food intake, food-motivation, and food-seeking, while bl

202 ) significantly reduced c-fos activation and food intake for at least 6 h.

203 in both the periphery and the CNS to change food intake, glucose homeostasis, and metabolic rate whi

204 that olanzapine treatment acutely increased food intake, impaired glucose tolerance, and altered phy

205 Oral administration of 69 to rats reduced food intake in an ad libitum feeding model, which could

206 reek did not alter body weight, fat mass, or food intake in either group, but did transiently improve

207 Obesity is primarily due to food intake in excess of the body's energetic requiremen

208 producing neurons reduces metabolic rate and food intake in fed and fasted states and suppresses gluc

209 Furthermore, Oamb appears to suppress sugar food intake in fed larvae in an acute manner, and neuron

210 centrations, hunger and satiety ratings, and food intake in healthy volunteers.Lingual bitter taste s

211 stimulation generated 35% of normal 24-hour food intake in just 10 minutes.

212 exhibit circadian variations inversely with food intake in lean mice.

213 (LH) that contribute to neural regulation of food intake in mice.

214 riority results in inadequate and unbalanced food intake in patients and huge amounts of wasted food.

215 this links to the control of body weight and food intake in photoperiodic F344 rats.

216 Animals regulate their food intake in response to the available level of food.

217 blunted muscle protein synthetic response to food intake in the elderly but may be effective only in

218 critical regulator of energy homeostasis and food intake in the hypothalamus.

219 ons of GDF15 with respect to body weight and food intake in vivo in mice.

220 ocortin 4 receptors (MC4Rs) leads to reduced food intake, increased energy expenditure, increased ins

221 ers within the PVN is sufficient to suppress food intake independent of glutamate release.

222 , and adipsin to influence processes such as food intake, insulin sensitivity, and insulin secretion.

223 ustatory stimulation, satiation, and maximal food intake into account.

224 Food intake is a complex behavior that can occur or ceas

225 Atypical food intake is a primary cause of obesity and other eati

226 Thus, the likelihood for reduced food intake is easily estimated through access to patien

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

228 Food intake is essential for maintaining homeostasis, wh

229 an MC4R agonist delivered to PVN to inhibit food intake is lost in mice lacking G(q/11)alpha in the

230 poor patient outcome, but ensuring adequate food intake is not a priority in clinical routine worldw

231 Appropriate circadian control of food intake is vital for maintaining metabolic health.

232 naling in the CNS has been linked to reduced food intake, lower body weight, improved glucose homeost

233 tion on gluconeogenesis were lost, while the food intake-lowering effects remained, resulting in redu

234 sures from supplements combined with typical food intake may have unintended health consequences, alt

235 ating, suggesting an alteration in circadian food intake mechanisms.

236 rmacological activities such as reduction of food intake mediated by the antagonism of the CB1Rs and

237 Food intake, muscle and bone mass and adiposity were unc

238 from the septum to the hypothalamus control food intake negatively.

239 LH-21 did not affect food intake nor body weight but it improved glucose hand

240 ons, can abolish food approach behaviors and food intake observed days after 24-h access to SHF.

241 ata indicate that 1,25D3-mediated changes in food intake occur through action within the arcuate nucl

242 Parental restrictive feeding (i.e., limiting food intake of children) has been linked to childhood ov

243 Here, we simultaneously measured sleep and food intake of individual flies and found a transient ri

244 Estimated food intake of omega-3 fatty acids were obtained from fo

245 t were most strongly associated with reduced food intake on nutritionDay were reduced intake during t

246 BMRs, implying that habitual differences in food intake or activity counterbalance variations in BMR

247 nditure in the KCP mutants with no effect on food intake or activity.

248 riven by diurnal cycles of rest-activity and food intake or are able to persist in vitro in a cell-au

249 r, few studies have examined the relation of food intake or dietary patterns with PAD.We examined the

250 d not have an immediate effect on ad libitum food intake or thereby weight change, relative to sham t

251 supplementation to WD significantly reduced food intake (p < 0.001), fasting plasma triglyceride (p

252 dietary recall data, we quantified: a) fast food intake [percent of total energy intake (TEI) from f

253 compared with controls, in particular during food intake periods.

254 ll intestine to promote satiety and suppress food intake provides a new target for weight loss.

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

256 wn of autophagic proteins, or suppression by food intake), recombinant AAV-mediated transgene express

257 prone to HFD-induced obesity, with increased food intake, reduced energy expenditure, and impaired gl

258 controlled T1D was associated with decreased food intake, reduced plasma glucagon and corticosterone

259 , and whether it might influence longer-term food intake-related appetite ratings in individuals with

260 egression analysis showed that the timing of food intake relative to melatonin onset was significantl

261 Nettle et al. describe increasing food intake (relative to energy expenditure) in response

262 effect on eating behavior during ad libitum food intake, resulting in weight change, and whether it

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

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

265 Food intake studies have provided estimates for TFA conc

266 Moreover, erythromycin stimulated food intake, suggesting a physiologic role of motilin as

267 e in sucrose seeking and consumption but not food intake, suggesting a selective enhancement of motiv

268 overlap to some degree with those regulating food intake, these findings suggest that activation of c

269 reproglucagon neurons that were activated by food intake; these GLP-1 fibers formed close appositions

270 Direct activation of LDTg GLP-1R suppresses food intake through a reduction in average meal size and

271 d by using the percentage of contribution of food intake to overall protein intake.

272 nduce appetite ("AgRP neurons") could induce food intake to overcome appetite-suppression following a

273 ustatory stimulation, satiation, and maximal food intake using 3 key parameters: 1) the initial eatin

274 erythrocyte and plasma scores directly from food intake using regression models.

275 key brain regions involved in the control of food intake (ventral tegmental area, striatum, hypothala

276 ed nucleus of the stria terminalis to reduce food intake via the IL-18 receptor.

277 Ad libitum food intake was assessed through the use of a vending ma

278 Food intake was assessed with the use of three 24-h food

279 by the standardized mean difference (SMD) in food intake was calculated between unhealthy food advert

280 Differential methylation after food intake was detected in 13% of the analyzed probes (

281 Timing of food intake was estimated with a validated questionnaire

282 On each occasion, food intake was evaluated from 4- or 7-d dietary records

283 the effect of erythromycin administration on food intake was examined in 15 healthy volunteers (40% m

284 The frequency of medical food intake was higher with GMP-MFs than with AA-MFs.

285 ircuitry for "hedonic suppression." Finally, food intake was increased by stimulations at several pre

286 nternet) was experimentally manipulated, and food intake was measured.

287 Food intake was monitored with a 7-d dietary record to c

288 The SD to LD transition (increased food intake) was mimicked by 2 weeks of ICV infusion of

289 atypical protein kinase C (aPKC) constrains food intake, weight gain, and glucose intolerance in bot

290 Body weight and food intake were monitored daily.

291 Hunger and snack food intake were reduced only after a longer period of a

292 In birds, CART inhibits food intake, whereas neuropeptide Y (NPY), a well-known

293 ed peptide (AgRP) neurons potently stimulate food intake, whereas proopiomelanocortin (POMC) neurons

294 Sweet perception promotes food intake, whereas that of bitterness is inhibitory.

295 robust suppression of energy expenditure and food intake, which lowers body temperature and body weig

296 e nucleus (ARC) reversibly induces increased food intake while disruption of Ca(2+) signaling pathway

297 P) neurons play an important role in driving food intake, while proopiomelanocortin (POMC) neurons in

298 integrates taste and hunger cues to balance food intake with metabolic needs.

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

300 Dietary restriction (DR), a reduction in food intake without malnutrition, increases most aspects