ライフサイエンスコーパス: appetite

1 ear death (p=0.0035 for fatigue, p=0.016 for appetite).

2 c cough, weight loss, night sweats, and poor appetite).

3 increased appetite, while others lose their appetite.

4 rete NTS to hypothalamus circuit controlling appetite.

5 sal, and lisdexamfetamine reduced weight and appetite.

6 de (AgRP) neurons are critical regulators of appetite.

7 en the 7 UK liver transplant centers in risk appetite.

8 mediates psychotropic effects and regulates appetite.

9 de in the circuit that contributes to sodium appetite.

10 symptoms such as lethargy, itch, or loss of appetite.

11 ncluding early morning awakening and loss of appetite.

12 ted having fatigue, dizziness, and decreased appetite.

13 sulin secretion, carbohydrate metabolism and appetite.

14 role in energy homeostasis and regulation of appetite.

15 coexpressed Y1 and Y5 receptors to suppress appetite.

16 lity and secretion, glucose homeostasis, and appetite.

17 ality in unstressed animals without altering appetite.

18 peptides are essential for the regulation of appetite.

19 TS(HSD2) neurons) were shown to drive sodium appetite.

20 included drowsiness, fatigue, and decreased appetite.

21 ion without a change in physical activity or appetite.

22 supplementation is associated with increased appetite.

23 atine phosphokinase elevation, and decreased appetite.

24 stinct brain regions that induce or suppress appetite.

25 sed patients with increased versus decreased appetites.

26 38, 95% CI 1.07-1.78; p=0.013) and decreased appetite (1.42, 1.11-1.82; p=0.0058) were reported as sy

27 sex (1.41, 1.1-1.81; p=0.0072) and decreased appetite (1.56, 1.19-2.06; p=0.0015).

28 the following beverages cause a decrease in appetite: 1) a nonalkalized cocoa mixture; 2) epicatechi

29 (162 [33%]), asthenia (141 [28%]), decreased appetite (126 [25%]), ageusia (112 [22%]), diarrhoea (83

30 ]), fatigue (16 [25%] vs 6 [18%]), decreased appetite (15 [23%] vs 5 [15%]), and pneumonia (14 [22%]

31 fatigue (mean score 5.2, SD 2.7) and loss of appetite (2.3, SD 2.9), and both worsened significantly

32 oxicity (35%), constipation (34%), decreased appetite (32%), and dysgeusia (31%).

33 antly fatigue (63%), nausea (44%), decreased appetite (37%), thrombocytopenia (32%), and neutropenia

34 %] vs 41/184 [22%]; p<0.0001), and decreased appetite (41/86 [48%] vs 41/156 [26%]; p=0.0011).

35 mia (82.5%), constipation (50.9%), decreased appetite (45.6%), and stomatitis (45.6%).

36 (10), dysgeusia (9), alopecia (9), decreased appetite (5), and fatigue (4).

37 including nausea, 52.3% (57 of 109), loss of appetite, 50.5% (49 of 97), constipation 30.4% (21 of 69

38 70.8% (63/89); distress 63.7% (58); loss of appetite 60.4% (55); diarrhoea 59.3% (54); and cough 52.

39 patients in the placebo group) and decreased appetite (65 [49%] and 45 [34%]).

40 igue (13.1%), diarrhea (9.8%), and decreased appetite (8.2%).

41 uded fever (90.4%), fatigue (88.3%), loss of appetite (87.0%), headache (77.9%), joint pain (73.7%),

42 w that Furin deletion in osteoblasts reduced appetite, a function not modulated by OCN, thus suggesti

43 ther a population of neurons known to induce appetite ("AgRP neurons") could induce food intake to ov

44 e has been rapid, and there is now a healthy appetite among key public and private sector decision ma

45 gulation than EX, as demonstrated by greater appetite and ad libitum EI.

46 to long day (LD) photoperiods that increase appetite and adiposity, however these effects are attenu

47 y aerobic exercise alone differently affects appetite and appetite-related hormones, ad libitum feedi

48 improve our understanding of dysfunctions of appetite and behavior found in mammals, including humans

49 se level reduction and concomitantly reduced appetite and body glucose level.

50 , peripheral treatment with IMC-H7 decreased appetite and body weight and increased energy expenditur

51 onal state and that their activation reduces appetite and body weight in mice.

52 the blood with a monoclonal antibody reduced appetite and body weight in obese mice, in addition to i

53 , an intermingled population that suppresses appetite and body weight.

54 opioid receptors in the long-term control of appetite and body weight.

55 altered feeding behavior, including reduced appetite and changes in taste/food preferences, is now r

56 outcomes include change in body composition, appetite and dietary adherence, glycemic and insulinemic

57 eating behavior were also measured using the Appetite and Eating Habits Questionnaire (APEHQ) and the

58 ogenous intestinal cannabinoid that controls appetite and energy balance by engagement of the enteric

59 rosin causes a syndrome characterized by low appetite and extreme leanness; this is phenocopied by mi

60 Serial ratings of appetite and food appeal were obtained.

61 resentations are important in the control of appetite and food intake.

62 conomic status relative to others stimulates appetite and food intake.

63 expressing VTA neurons in the modulation of appetite and food-motivated behavior.

64 at central and peripheral levels to mediate appetite and glucose metabolism.

65 are necessary for full expression of sodium appetite and have distinct downstream targets that are a

66 pressed patients with increased or decreased appetite and healthy control subjects while viewing phot

67 ake during meal ingestion, and the return of appetite and hunger after fasting.

68 hance dietary diversity, such as an improved appetite and increased body size, need elucidation.

69 f IMC-H7 into the third ventricle suppressed appetite and increased energy expenditure.

70 cute sleep loss is associated with increased appetite and insulin insensitivity, while chronically sl

71 ts, 24-h SER transiently elevated subjective appetite and marginally increased energy intake, but hor

72 iron play an important role in regulation of appetite and metabolism through CREB-dependent modulatio

73 iture (EE) and physical activity, decreasing appetite and modulating sympathetic nervous system (SNS)

74 e PBN (PBel) as being sufficient to suppress appetite and necessary for the anorexigenic effects of a

75 usions about the effects of DF properties on appetite and preclude the development of reliable, predi

76 Early life may be a "critical period" when appetite and regulation of energy balance are programmed

77 assessed at lunch and dinner with subjective appetite and resting metabolism assessed throughout.

78 hysiological hyperarousal, while diminishing appetite and sleep.

79 e low levels of leptin, leading to increased appetite and suppressed fertility.

80 t 11betaHSD2-positive neurons integrate salt appetite and the blood pressure response to dietary sodi

81 cts on the hypothalamus receptors to control appetite and thermogenesis.

82 Appetite and weight changes are common but variable diag

83 ctivated during energy deficit and increases appetite and weight-gain.

84 typical features, characterized by increased appetite and/or weight (A/W) during an active episode.

85 Y secretion, suppressed aspects of VAS-rated appetite, and decreased ad libitum EI at a subsequent me

86 n part, to modulations in energy metabolism, appetite, and energy intake.

87 of the brain related to glucose homeostasis, appetite, and food reward, despite lower plasma insulin

88 m a buffet meal (180-210 min; energy intake, appetite, and gastric emptying in the men have been publ

89 rations, carbohydrate metabolism, subjective appetite, and gut hormones in healthy women.

90 eriences of out-of-control eating, increased appetite, and increased fat storage arouse greater fears

91 bute to human neurological diseases of mood, appetite, and movement.

92 were fatigue, alopecia, diarrhoea, decreased appetite, and nausea.

93 d with glucose may be a weaker suppressor of appetite, and neuroimaging research shows that food cues

94 pain and inflammation, regulate motility and appetite, and produce anticancer, anxiolytic, and neurop

95 the circuit by which NTS(HSD2) neurons drive appetite, and uncover an interaction between the NTS(HSD

96 on between energy intake, physical activity, appetite, and weight gain during a 1-y follow-up period

97 , NTS(HSD2) neurons are necessary for sodium appetite, and with concurrent ATII signaling their activ

98 ngs of depressed participants with increased appetites, and its functional connectivity to reward cir

99 s in obesity, our findings show that reduced appetite- and taste-processing area morphometry is assoc

100 e with regard to meal-related gut control of appetite, arcuate nucleus-based hypothalamic circuits li

101 Depression-related increases in appetite are associated with hyperactivation of putative

102 ferences substantially affect differences in appetites as well as aptitudes suggest a genetic way of

103 25-30 g protein/meal provide improvements in appetite, body weight management, cardiometabolic risk f

104 ural circuits strongly and acutely influence appetite but with notably different characteristics.

105 X-A in endocannabinoid-mediated promotion of appetite by combining OX-induced alertness with food see

106 hypothalamus to include hedonic controls of appetite by cortical and subcortical brain areas process

107 amount of activity in neurons that suppress appetite can cause malnutrition and a severe reduction i

108 al amount of activity in neurons that induce appetite can cause obesity, whereas an abnormal amount o

109 ers Glut-4 and Glut-12, and the regulator of appetite Cartpt) and to LAC responsiveness (leptin recep

110 Anxiety, appetite changes, delusions, and repetitive motor activi

111 vidual differences in the depression-related appetite changes.

112 summarize some of the key characteristics of appetite circuits that are emerging from recent work and

113 ncreased dysphagia, gagging, cough, and poor appetite compared to their counterparts in the EoE-IH gr

114 would increase gastric distension and reduce appetite compared with a control drink.

115 abdominal pain, swollen stomach, and loss of appetite, compared with people infected with assemblage

116 the effects of prebiotic supplementation on appetite control and energy intake in children with over

117 e glycemic load (GL) of the diet may benefit appetite control but its utility is complicated by psych

118 netics and optogenetic techniques to dissect appetite control circuits originating from ventral hippo

119 a result, normal production and secretion of appetite control hormones, PYY, alpha-MSH, and CART, are

120 s, and the specific contribution of these to appetite control is not well characterized.The influence

121 3 receptors (MC3R) have a contextual role in appetite control that is amplified with hypocaloric cond

122 ecific neural circuitry and pharmacology for appetite control within the DRN.

123 nges in directly studying CCK1Rs relevant to appetite control, our goal was to develop and apply a me

124 e network involved in glucose metabolism and appetite control, suggesting a possible role for L. rham

125 g appetite, thereby forming three pillars of appetite control.

126 to reverse this defective servomechanism for appetite control.

127 tailed analyses of the mechanisms underlying appetite-control systems.

128 MBH) in association with decreased number of appetite-curbing pro-opiomelanocortin (POMC) neurons; wh

129 d 652 children with genotype, adiposity, and appetite data.

130 ty to food stimuli than both those reporting appetite decreases and healthy control subjects.

131 5%), rash (five; 42%), and chills, decreased appetite, diarrhoea, and nausea (four each; 33%).

132 Provincial Pediatric EnTeric Infection TEam (APPETITE) did a study in three outpatient cohorts in Cal

133 arget for the treatment of anorexia or other appetite disorders.

134 elated adverse events such as asthenia, poor appetite, dizziness, nausea, and vomiting occurred signi

135 dentified that some older patients with good appetites do not receive sufficient nourishment because

136 Loss of appetite during sickness is a common and often debilitat

137 stipation (seven [27%] vs none), and loss of appetite (eight [31%] vs two [8%]).

138 Leptin, a host-derived adipokine linking appetite, energy balance and immune function, is require

139 binoid signaling, which is known to regulate appetite, energy balance, and metabolic processes throug

140 to test the hypothesis that Gpr17 regulates appetite, energy expenditure, and metabolism.

141 neurobehavioural outcomes such as increased appetite, enhanced sensitivity to food stimuli, and, ult

142 lin is an oral ghrelin-receptor agonist with appetite-enhancing and anabolic activity.

143 nd identify a biological factor required for appetite evoked by alcohol.

144 gions, depressed participants with increased appetites exhibited greater hemodynamic activity to food

145 mptoms, including dyspnea, constipation, low appetite, fatigue, depression, and anxiety.

146 rowth hormone, as well as the stimulation of appetite, food intake and maintenance of energy homeosta

147 room with fever, sore throat, cough and poor appetite for 2 weeks.

148 Sodium-depleted animals develop an appetite for aversive concentrations of sodium.

149 h their partner, beliefs about the partner's appetite for equity, beliefs about the partner's model o

150 ecifically regulates glucose intake and that appetite for glucose is an important driver of overall f

151 lic logic of the proliferating cancer cells' appetite for glutamine-which goes far beyond satisfying

152 (MC4R) gene, contributing to the insatiable appetite found in some populations of cavefish.

153 he effects of whey protein on energy intake, appetite, gastric emptying, and gut hormones in healthy

154 re was no effect of sex on gastric emptying, appetite, gastrointestinal symptoms, glucose, or gut hor

155 t the mutated allele contributes to elevated appetite, growth, and starvation resistance.

156 This did not relate to appetite hormone levels with early (6 hr) rises in plasm

157 popituitarism, colitis, diarrhoea, decreased appetite, hyponatremia, and pneumonitis (each in two [1%

158 fector systems involved in the regulation of appetite, immune responses, and gastrointestinal motilit

159 tabolic regulatory effects, which suppresses appetite in a MC4R-dependent manner, and show that the c

160 BKO) mice, measuring blood pressure and salt appetite in adults.

161 ported that dark chocolate acutely decreased appetite in human subjects, but the authors did not asse

162 xonazine, which significantly reduced sodium appetite in mice.

163 eptor (MOR) signaling strongly drives sodium appetite in sodium-depleted mice, whereas a role for kap

164 t known whether the VP is necessary for salt appetite in terms of seeking out salt or consuming salt

165 %), confusional state in two (4%), decreased appetite in two (4%), haemoptysis in two (4%), hypercalc

166 Salt appetite, in which animals can immediately seek out salt

167 line VP activity.SIGNIFICANCE STATEMENT Salt appetite, in which rats will immediately seek out a once

168 Objective measures of appetite included energy intake at an ad libitum breakfa

169 y subjects and those with depression-related appetite increases.

170 counterpart of marijuana's psychotropic and appetite-inducing component Delta(9)-tetrahydrocannabino

171 To maintain energy homeostasis, orexigenic (appetite-inducing) and anorexigenic (appetite suppressin

172 de Y, NPY; agouti-related protein, AGRP) and appetite-inhibiting (cocaine and amphetamine-regulated t

173 pendent manner, and show that the control of appetite is an endocrine function of bone.

174 The neural control of appetite is important for understanding motivated behavi

175 One of the key gut hormones that controls appetite is peptide tyrosine-tyrosine 3-36 (PYY3-36) who

176 Pain (4.4 of 10), fatigue (4.7 of 10), and appetite loss (4.0 of 10) were moderate after surgery.

177 In contrast, depressed subjects experiencing appetite loss exhibited hypoactivation within a region o

178 c reward circuitry, while depression-related appetite loss is associated with hypoactivation of insul

179 , social functioning, fatigue, dyspnoea, and appetite loss on the EORTC QLQ-C30 and pain and sensory

180 inally increased energy intake, but hormonal appetite markers did not respond in a manner indicative

181 rgy metabolism and body-composition metrics, appetite, markers of glycemic control, and gut microbiot

182 logical and physiological systems regulating appetite may also be sensitive to subjective feelings of

183 Previous studies suggest that appetite may be dysregulated at low levels of activity,

184 ference in age at diet-diary completion, and appetite measurement, higher FR was associated with more

185 in the gut stimulate the release of several appetite modulators acting at central and peripheral lev

186 and motor (efferent) vagus in regulation of appetite, mood, and the immune system, as well as the pa

187 er therapy: nausea (n = 109; 84.5%), loss of appetite (n = 97; 75.2%), pain (n = 96; 74.4%), anxiety

188 ents were somnolence (n=41 [25%]), decreased appetite (n=31 [19%]), diarrhoea (n=31 [19%]), fatigue (

189 rse events reported were insomnia, decreased appetite, nausea, and dry mouth.

190 ded dysgeusia (13 [28%] patients), decreased appetite (nine [19%]), and alopecia (seven [15%]).

191 ts and was proposed to contribute to loss of appetite observed during sickness.

192 led energy depletions can differently affect appetite parameters and olfaction.

193 eptide YY, insulin, glucagon, blood glucose, appetite perceptions, and gastrointestinal symptoms were

194 ak grip strength, slowed walking speed, poor appetite, physical inactivity, and exhaustion.

195 rie deficiency the circulating levels of the appetite-promoting hormone, acyl-ghrelin, rise sharply.

196 (dual-energy X-ray absorptiometry), fasting appetite ratings (visual analog scales), eating behavior

197 eal) and daily (24-h) EI and between fasting appetite ratings and certain eating behavior traits with

198 In addition, we investigated appetite ratings and concentrations of appetite-regulati

199 ndings suggest that combined measurements of appetite ratings and RMR could be used to estimate EI in

200 ht influence longer-term food intake-related appetite ratings in individuals with obesity.In a random

201 n MRI scanner where abdominal scans and oral appetite ratings on a 100-point scale were obtained ever

202 ted the effects of well-characterized DFs on appetite ratings or energy intake were identified from a

203 Subjective appetite ratings were assessed while fasting, after the

204 Appetite ratings were assessed with the use of visual an

205 c resonance imaging (MRI), and self-reported appetite ratings were collected and quantified by the ar

206 tide-1 (GLP-1) concentrations and subjective appetite ratings were determined.

207 Subjective appetite ratings were obtained from visual analog scales

208 were measured before and after cycling, and appetite ratings were recorded twice daily.

209 ough glucose to the duodenum also suppressed appetite ratings, eating behavior was not altered.

210 h overweight and obesity improved subjective appetite ratings.

211 PFC]) and increased perfusion in homeostatic appetite regions of the brain (hypothalamus).

212 stic connection between dietary iron and the appetite-regulating hormone leptin.

213 gated appetite ratings and concentrations of appetite-regulating hormones.

214 own to owe part of its regulatory effects on appetite-regulating hypothalamic neuropeptides to the el

215 that VDR colocalized with and activated key appetite-regulating neurons in the arcuate, namely proop

216 mechanisms by which RYGBP may affect central appetite-regulating pathways.

217 ietary change has the potential to help with appetite regulation in children with obesity.

218 Peripheral mechanisms in appetite regulation include the motor functions of the s

219 elin and Y2 receptors play a central role in appetite regulation inducing opposite effects.

220 IET represented a greater acute challenge to appetite regulation than EX, as demonstrated by greater

221 ferent G proteins and identify a pathway for appetite regulation that could be selectively targeted b

222 eview is to cover the major underpinnings of appetite regulation, describe recent advances resulting

223 ts cellular ultrastructure, gene expression, appetite regulation, hormone production, vigilance, and

224 We determined the effect of 24-h SER on appetite regulation, metabolism, and energy intake.

225 as set the stage for a deep understanding of appetite regulation.

226 esize these findings into an updated view of appetite regulation.

227 long-standing "synergy hypothesis" of sodium appetite regulation.

228 can induce substantial weight loss, but the appetite regulatory responses to SER are unknown and may

229 rcise alone differently affects appetite and appetite-related hormones, ad libitum feeding, food rewa

230 aterial of interest was efficacious for >/=1 appetite-related outcome.

231 fermentability, or molecular weight (MW)] on appetite-related outcomes was assessed in healthy humans

232 tested the effect of dietary fibers (DFs) on appetite-related outcomes, with inconsistent results.

233 We assessed the appetite response to low-glycemic index (LGI) and high-g

234 The postprandial appetite response was determined for 180 min postmeal.

235 the duodenum and ileum differentially alters appetite response, food intake, and secretion of satiety

236 to control the postexercise energy balance, appetite responses after meals differing in GI are of pa

237 portunity to evaluate the influence of GI on appetite responses independently of insulinemia, which c

238 Hunger/appetite scores decreased in the first 2 weeks after the

239 stigate diet-induced-thermogenesis (DIT) and appetite sensation.

240 y expenditure (243 kJ/d) and an anorexigenic appetite-sensation profile.Protein supplementation does

241 Appetite sensations were assessed by using visual analog

242 Finally, appetite sensations were similar between conditions at a

243 anges comprise sleep loss-induced changes in appetite-signaling hormones (e.g., higher levels of the

244 and calorie intake usually suppresses brain appetite signals.

245 mistry and in situ hybridization to localize appetite-stimulating (neuropeptide Y, NPY; agouti-relate

246 coupling of hypothalamic responses involving appetite-stimulating fasting-responsive hypothalamic neu

247 Thus, larger appetite-stimulating neurons (NPY, AGRP) likely promote

248 a GABA-dependent manner, which then leads to appetite stimulation and a drive to accumulate adiposity

249 nd vomiting associated with chemotherapy and appetite stimulation in wasting illnesses.

250 between acetylcholine and nicotine, a known appetite suppressant.

251 atic drive to eat on feeding behavior during appetite suppressing conditions are unknown.

252 AgRP neurons induces feeding to overcome the appetite suppressing effects of amylin, CCK, and LiCl, b

253 igenic (appetite-inducing) and anorexigenic (appetite suppressing) brain systems functionally interac

254 pression following administration of various appetite-suppressing compounds.

255 re additional factor(s) to exert the maximal appetite-suppressing effect.

256 l component that induces inflammation, exert appetite-suppressing effects and activate PBN CGRP neuro

257 neural activity in a separate population of appetite-suppressing neurons, providing new insights int

258 nd necessary for the anorexigenic effects of appetite-suppressing substances including lithium chlori

259 nd activates an MC4R-dependent anorexigenic (appetite-suppressing) pathway.

260 ) neurons as key mediators of cancer-induced appetite suppression and associated behavioral changes.

261 AgRP neurons could overcome various forms of appetite suppression and decrease neural activity in a s

262 s small patient cohort, it appears to induce appetite suppression and may induce weight loss.

263 ncrease feeding during noninflammatory-based appetite suppression and to decrease activity in anorexi

264 These data suggest that the appetite suppression in WT mice after parabiosis to db m

265 Appetite suppression induced by foams could largely be e

266 We previously described a neural circuit for appetite suppression involving calcitonin gene-related p

267 We found that cholinergic circuits modulate appetite suppression on downstream targets in the hypoth

268 urons") could induce food intake to overcome appetite-suppression following administration of various

269 All treatments elicited appetite-suppressive effects.

270 n-deficient individuals experience a loss of appetite that can be restored with iron supplementation.

271 l animals have evolved an instinctive sodium appetite that is commensurate with sodium deficiency.

272 oric restriction results in rapid changes in appetite that result in compensatory eating, which may i

273 role for central opioid signaling in sodium appetite, the endogenous influence of specific opioid re

274 With respect to appetite, the thick 100-kcal shake led to higher fullnes

275 parate but interlinked processes influencing appetite, thereby forming three pillars of appetite cont

276 h motivation, fear, anxiety, depression, and appetite; therefore, we assess the potential role for gh

277 e stomach-derived hormone ghrelin stimulates appetite through interactions with neurons in the arcuat

278 l novel neurobiological circuitry regulating appetite through which ghrelin signaling in hippocampal

279 socaloric controls, aerated foods can reduce appetite throughout an entire dieting day.

280 it, increase glucose tolerance, and suppress appetite; thus, FFA2 has therapeutic potential for type

281 Cross-sectional studies suggest appetite traits as a candidate mechanism.

282 with lower genetic risk at age 6 years, but appetite traits did not mediate genetic associations wit

283 childhood samples are needed to test whether appetite traits explain how genetic risks accelerate gro

284 However, middle childhood appetite traits may not be a promising target for such i

285 gitudinal studies are needed to test whether appetite traits mediate genetic influences on children's

286 risk had higher levels of alleged obesogenic appetite traits than peers with lower genetic risk at ag

287 Appetite traits were measured at age 6 years with the Ch

288 Importantly, NTS(HSD2) neurons stimulate appetite via projections to the vlBNST, which is also th

289 At regular intervals over 180 min, appetite (visual analog scales), gastric emptying (3-dim

290 Our primary measure of appetite was ad libitum pizza intake 150 min after bever

291 Appetite was assessed with the use of the Child Eating B

292 Appetite was evaluated with a visual analog scale (VAS).

293 Subjective appetite was greater during ER on the morning of day 2 (

294 Salt appetite was inhibited by spironolactone.

295 a marked alveolitis, accompanied by loss of appetite, weight loss, and heavy breathing.

296 ot realize their presence, and their role in appetite, weight, and health is controversial.

297 n only the highly discriminatory symptoms of appetite/weight were used to define subtypes.

298 decreased (typical) and increased (atypical) appetite/weight.

299 ome depressed individuals manifest increased appetite, while others lose their appetite.

300 ran Africa to improve nutritional status and appetite without evidence for their effectiveness or int