ライフサイエンスコーパス: appetite

1 rt, Pomc and Npy (neuropeptides that control appetite).

2 stive drives (i.e., hunger, thirst, and salt appetite).

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

4 at impinges upon multiple circuits to govern appetite.

5 t of MGL in the gut-brain axis regulation of appetite.

6 well established that cannabis use promotes appetite.

7 process by which eating and drinking reduce appetite.

8 lipid metabolic disorder, and regulation of appetite.

9 ss prodynorphin, and for satiation of sodium appetite.

10 late food absorption, insulin secretion, and appetite.

11 ver, chills, abdominal bloating, and loss of appetite.

12 e-related hormones or subjective feelings of appetite.

13 s fall, triggering compensatory increases in appetite.

14 s-acyl-ghrelin (DAG), potentially decreasing appetite.

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

16 nucleus (LPBN(Htr2c) neurons) inhibit sodium appetite.

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

18 sulin secretion, carbohydrate metabolism and appetite.

19 ality in unstressed animals without altering appetite.

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

21 atine phosphokinase elevation, and decreased appetite.

22 stinct brain regions that induce or suppress appetite.

23 ssed by LPBN neurons is to disinhibit sodium appetite.

24 ver, chills, abdominal bloating, and loss of appetite.

25 associated with increased weight regain and appetite.

26 equired for the full manifestation of sodium appetite.

27 sufficient for Ap to alter the fly's protein appetite.

28 mass, while inhibiting gastric emptying and appetite.

29 OVLT neurons stimulated thirst but not salt appetite.

30 bolic stabilization evidenced by recovery of appetite.

31 headache (21.5%), nausea (10.7%), decreased appetite (10.7%), nasopharyngitis (9.0%), dry mouth (7.3

32 ), dry mouth (12.8% and 8.0%), and increased appetite (10.9% and 12.3%).

33 pecia (47%), weight loss (47%) and decreased appetite (19%).

34 in (20 [27%]; two [3%] grade >=3), decreased appetite (20 [27%]; one [1%] grade >=3), and vomiting (1

35 ral sodium detection rapidly quenches sodium appetite(3,4), suggesting that taste signals have a cent

36 ory tract infection, insomnia, and decreased appetite (37.5% each).

37 ), alopecia (49%), any rash (48%), decreased appetite (44%), and dysgeusia (40%).

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

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

40 [44%]), conjunctivitis (63 [43%]), decreased appetite (53 [36%]), constipation (52 [35%]), diarrhoea

41 s included nausea/vomiting (97%) and lack of appetite (54%).

42 Sleep difficulties (87.1%, n = 108), lack of appetite (58.1%, n = 72), and lack of pleasure in life (

43 e headache (10.1%), nausea (7.9%), decreased appetite (7.6%), anxiety (7.0%), and nasopharyngitis (5.

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

45 oss (WL) is usually accompanied by increased appetite, a response that seems to be absent when ketoge

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

47 e symptoms such as vomiting, nausea, loss of appetite and abdominal growth are mistaken with pregnanc

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

49 l and lateral hypothalamic nuclei regulating appetite and autonomic function.

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

51 proglucagon (PPG) neurons in regulating both appetite and behavioral and autonomic responses to acute

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

53 SCFAs, which are associated with measures of appetite and cardiometabolic health.

54 Appetite and compensatory health beliefs were measured b

55 rthralgia, paresthesia, sleep disorder, poor appetite and concentration difficulties.

56 Osteoblast-secreted LCN2 suppresses appetite and decreases fat mass while improving glucose

57 ts were reported in five patients (decreased appetite and diarrhoea in one patient with urothelial ca

58 lates life-sustaining functions ranging from appetite and digestion to heart rate and breathing.

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

60 anocortin signaling and therefore stimulates appetite and enhances anabolism, indicating that TCMCB07

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

62 rom the environment can powerfully stimulate appetite and food consumption in the absence of hunger.

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

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

65 one-receptor pair INSL5-RXFP4 that regulates appetite and glucose homeostasis, which likely relates t

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

67 odulates the impact of WL-induced changes in appetite and if ketosis alters these responses.

68 taste signals have a central role in sodium appetite and its satiation.

69 hat are necessary and sufficient to suppress appetite and maintain physiological satiation.

70 This review discusses how GDF15 regulates appetite and metabolism, the role it plays in resistance

71 hormone with pleiotropic functions affecting appetite and mood.

72 targets for potential treatment of excessive appetite and overeating.

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

74 es possess a state-dependent sterol-specific appetite and redressed their sterol deficit by feeding o

75 We further discuss how distinct appetite and satiation systems for each factor may contr

76 Htr2c) neurons act as a brake against sodium appetite and that their alleviation is required for the

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

78 ing increased (N = 23) or decreased (N = 31) appetite and weight in their current depressive episode

79 Reduced appetite and weight loss are common after esophagectomy

80 during weight loss on subsequent changes in appetite and weight outcomes at 26 wk in individuals eng

81 nterventions associated with improvements in appetite and/or body weight include progesterone analogs

82 hen it is decided to trial a drug to improve appetite and/or improve weight gain, currently available

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

84 ng pathway that controls both the phagocyte 'appetite' and its anti-inflammatory response.

85 ther OBG viscosity affects gastric emptying, appetite, and ad libitum food intake is unknown.

86 Ghrelin also acts on inflammation, appetite, and adipogenesis and therefore has been consid

87 oted a nonproductive cough, fatigue, loss of appetite, and an unintentional weight loss of 9 kg over

88 monoclonal antibodies reduce blood glucose, appetite, and body weight, validating asprosin as a ther

89 rthralgia, paresthesia, sleep disorder, poor appetite, and concentration difficulties.

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

91 neutropenia, fatigue, hypokalemia, decreased appetite, and decreased white blood cell count.

92 of gastrointestinal motility and secretion, appetite, and food intake.

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

94 indexes, energy intake, energy expenditure, appetite, and glucose tolerance were measured at baselin

95 Gastric emptying, subjective appetite, and glucose, insulin, ghrelin, and peptide tyr

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

97 ted to anger, self-confidence, irritability, appetite, and interest in leisure activities had the low

98 ning personal economic decisions: incentive, appetite, and learning.

99 fection, diarrhea, pneumonia, shock, lack of appetite, and lower WHZ are independent predictors of in

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

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

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

103 ache, nausea, vomiting, muscle pain, lack of appetite, and rash.

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

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

106 Appetite, appetite-related hormones, BChE activity, and

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

108 ry 2 wk with energy intake, expenditure, and appetite assessed every 4 wk.

109 conclusion, smoking may cause suppression of appetite but smokers tend to have other unhealthy habits

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

111 Specifically, it stimulates appetite by activating orexigenic AgRP neurons and inhib

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

113 ich changes in body composition (by DXA) and appetite (by visual analog scale appetite perceptions in

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

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

116 ulated water-specific and non-specific fluid appetite caused by the two distinct dipsogenic stimuli.

117 ver, how cannabis interacts with the brain's appetite center, the hypothalamus, to stimulate feeding

118 pression subtypes for which the direction of appetite change may be an easily measured behavioral mar

119 Insomnia, fatigue and appetite changes had lower centrality values.

120 Emerging evidence suggests that individual appetite circuits for major nutrients-water, sodium, and

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

122 ignals that differentially quench individual appetite circuits.

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

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

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

126 t loss, both at the level of the homeostatic appetite control system and energy expenditure, are in f

127 3 receptors (MC3R) have a contextual role in appetite control that is amplified with hypocaloric cond

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

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

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

131 to reverse this defective servomechanism for appetite control.

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

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

134 Hunger or appetite decreased for 4 weeks after embolization and in

135 y in the fenfluramine groups) were decreased appetite, diarrhoea, fatigue, lethargy, somnolence, and

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

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

138 of these neurons specifically drives sodium appetite, even during euvolemic conditions.

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

140 epressed participants experiencing increased appetite exhibited marked immunometabolic dysregulation,

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

142 t hormones may be a novel target to increase appetite, food intake, and body weight among patients af

143 This survey reflects an appetite for a specialist service for paediatric glaucom

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

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

146 en known for decades to harbor an insatiable appetite for iron, only recently has the chemistry emerg

147 The insatiable human appetite for wildlife products drives species to extinct

148 sm because of its involvement in controlling appetite, fuel distribution, and utilization.

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

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

151 epressed participants experiencing decreased appetite had higher cortisol levels than subjects in the

152 While leptin's role in the regulation of appetite has been extensively studied in hypothalamic ne

153 hanisms underlying the stimulation of sodium appetite have received much attention recently, mechanis

154 rted reduced fullness, consistent with their appetite hormone changes.

155 played typical baseline levels of peripheral appetite hormones during a negative energy balance.CONCL

156 (HR: 3.67; 95% CI: 2.24, 6.03), and lack of appetite (HR: 2.16; 95% CI: 1.48, 3.16) were associated

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

158 ed with abdominal pain, dyspepsia or loss of appetite in 54 (53.465%) subjects.

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

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

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

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

163 nts), diarrhoea (in 65 [52%]), and decreased appetite (in 48 [38%]); and the most common grade 3-4 ad

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

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

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

167 hous ulcer, arthralgia, arthritis, increased appetite, increased weight, restlessness, tendon disorde

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

169 gical processes like anxiety, blood glucose, appetite, inflammation and blood pressure.

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

171 Sodium appetite is a powerful form of motivation that can drive

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

173 Appetite is driven by nutritional state, environmental c

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

175 However, in normal conditions, sodium appetite is suppressed to prevent homeostatic deviations

176 understanding salt taste, which informs salt appetite, is important from a fundamental sensory perspe

177 ), and whole-body (eg, physical activity and appetite) levels.

178 he stimulation of growth hormone release and appetite, little is known of the effects of its unacylat

179 [-4.53 to -1.50] vs -5.2 [-7.45 to -2.98]), appetite loss (-5.8 [-7.28 to -4.36] vs -7.0 [-9.17 to -

180 2.13 to 2.93), fatigue (2.2, -0.38 to 4.78), appetite loss (1.2, -1.27 to 3.67), physical functioning

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

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

183 , back pain/aches/discomfort, early satiety, appetite loss, and having less strength.

184 hanges in energy expenditure and homeostatic appetite markers seen in reduced-obese individuals are a

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

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

187 crosses the blood-brain barrier to stimulate appetite-modulating neurons in the arcuate nucleus of th

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

189 6; 47%), nausea (n = 13; 38%), and decreased appetite (n = 12; 35%).

190 ]), constipation (n = 56 [39.4%]), decreased appetite (n = 48 [33.8%]), and diarrhea (n = 47 [33.1%])

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

192 e describe the temporal relationship between appetite neuron activity and consumption behaviors.

193 The function of central appetite neurons is instructing animals to ingest specif

194 on of sodium rapidly suppresses these sodium-appetite neurons.

195 and sends rapid inhibitory signals to sodium-appetite neurons.

196 Vitamin D repletion stimulated appetite, normalized weight gain, and improved fat and l

197 lipid administration strongly suppressed the appetites of MGL-KO and CB(1)/MGL double-KO mice, but no

198 onal analysis showed that effects of general appetite on zWFL were mediated by FRR (indirect effect =

199 (one [2%]), diarrhoea (one [2%]), decreased appetite (one [2%]), dehydration (one [2%]), hyperkalaem

200 ays where macronutrients might act on either appetite or adipogenesis to cause weight gain.

201 Loss of appetite or anorexia associated with inflammation impair

202 r perception could be a tool for controlling appetite or food choices.

203 driven by changes in satiety, motor fatigue, appetite or perseveration.

204 1.03-2.33), adverse events due to decreased appetite (OR 3.56, 95% CI: 1.94-6.53), diarrhoea (OR 2.6

205 l changes, suggesting involvement of hedonic appetite pathways in males.

206 Associations between %FFML and change in appetite perceptions during weight loss were inconsisten

207 by DXA) and appetite (by visual analog scale appetite perceptions in response to a fixed test meal) w

208 cagon-like peptide-1 (GLP-1) concentrations, appetite perceptions, and gastrointestinal symptoms at 1

209 ) weight outcomes at 26 wk and 2) changes in appetite perceptions.

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

211 tive feelings about herself, poor sleep, low appetite, poor concentration, and lack of energy.

212 General appetite positively correlated with FRR and zWFL, but ne

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

214 Subjective appetite, PYY, and ghrelin responses after 2gOBG, 4gOBG,

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

216 d with lower compensation reported increased appetite ratings and beliefs that healthy behaviors can

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

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

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

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

221 Appetite ratings were assessed with the use of visual an

222 Subjective appetite ratings were obtained from visual analog scales

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

224 h overweight and obesity improved subjective appetite ratings.

225 One logical strategy targets the appetite-regulating actions of gut hormones such as incr

226 th disrupted transcript rhythms of clock and appetite-regulating genes in the MBH.

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

228 ptake after cold stimulation, are related to appetite regulation in young adults.

229 However, the link between BAT and appetite regulation needs to be more rigorously examined

230 the neural mechanisms of chemosensory-based appetite regulation remain poorly understood.

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

232 a key role in the human reward system and in appetite regulation, suggesting that altered dopamine ac

233 brain regions traditionally associated with appetite regulation.

234 This review focuses on two aspects of appetite regulation.

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

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

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

238 lly relevant paradigm for the exploration of appetite regulation.

239 tted to our hospital for high fever, lack of appetite related to nausea and vomiting, headache and si

240 ration of beta-hydroxybutyrate (beta-HB) and appetite-related hormones (active ghrelin, active glucag

241 ficant sex x time interactions for any other appetite-related hormones or subjective feelings of appe

242 Appetite, appetite-related hormones, BChE activity, and energy int

243 dulate the changes in the secretion of other appetite-related hormones, or subjective feelings of app

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

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

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

247 Appetite-related sensations (i.e., hunger and fullness)

248 consumption had any significant influence on appetite-related sensations after breakfast or after mea

249 Appetite-related sensations and metabolic hormones were

250 nalized cold exposure with energy intake and appetite-related sensations in young healthy humans.

251 ion recently, mechanisms that inhibit sodium appetite remain largely obscure.

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

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

254 -related hormones, or subjective feelings of appetite, seen with WL, regardless of the ketotic state.

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

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

257 may influence satiety through differences in appetite sensations, gastrointestinal peptide release an

258 and calorie intake usually suppresses brain appetite signals.

259 for driving a behavior that resembles Na(+) appetite.SIGNIFICANCE STATEMENT This is the first invest

260 and behaviorally sated rats, validating the appetite stimulating properties of cannabis.

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

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

263 promote weight loss by reducing ghrelin, an appetite-stimulating hormone secreted from the gastric f

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

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

266 It remains unknown if sex modulates the appetite suppressant effect of ketosis.

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

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

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

270 The main neural substrate mediating the appetite-suppressing activity of TrkB, however, remains

271 pression following administration of various appetite-suppressing compounds.

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

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

274 these neurons produce aversive and sustained appetite-suppressing signals, which discourages the init

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

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

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

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

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

280 tolerated in severely obese adults, inducing appetite suppression and weight loss for up to 12 months

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

282 the excitatory basal forebrain in regulating appetite suppression through food avoidance mechanisms,

283 Appetite suppression was reversed by vagotomy, suggestin

284 serotonin 2C receptor agonist that promotes appetite suppression, led to sustained weight loss witho

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

286 ved and excluding all children with negative appetite test.

287 The loss of appetite that typically accompanies infection or mere ex

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

289 ty incidence involves mechanisms that affect appetite, thermogenesis and metabolism, and the outcomes

290 quality of life (IWQOL-Lite), and hunger or appetite using a visual assessment scale.

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

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

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

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

295 Fatigue, nausea, and decreased appetite were common and were typically grade 1 or 2 (gr

296 nin and insulin), and subjective feelings of appetite were measured at baseline, week 9 in ketosis, a

297 h to explain why some individuals lose their appetite when they become depressed, while others eat mo

298 d energy intake and concomitant increases in appetite, which can be treated with dietary or pharmacol

299 individuals with PWS who may seek to control appetite with the new obesity treatment 5-HT2CR agonist

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