ライフサイエンスコーパス: hyperphagia

1 adipokine levels, and increased food intake (hyperphagia).

2 expenditure occurred even in the absence of hyperphagia.

3 ncreased fat content in tissues, produced by hyperphagia.

4 reportedly causes leanness in the setting of hyperphagia.

5 ophy and hepatic steatosis in the absence of hyperphagia.

6 stress, and is dependent on the concomitant hyperphagia.

7 of the POMC gene leads to severe obesity and hyperphagia.

8 lso blocked intra-Acb shell muscimol-induced hyperphagia.

9 induced by 24 hr fasting or suckling-induced hyperphagia.

10 25% to 50% than from increased adiposity or hyperphagia.

11 lop central obesity, insulin resistance, and hyperphagia.

12 dents and in humans has been associated with hyperphagia.

13 tion to atypical features of hypersomnia and hyperphagia.

14 ersed vegetative symptoms of hypersomnia and hyperphagia.

15 rs did not respond in a manner indicative of hyperphagia.

16 osition in young adult mutants despite their hyperphagia.

17 s of age without increases in their level of hyperphagia.

18 ood deprivation with markedly reduced reflex hyperphagia.

19 CRH signaling, could contribute to diabetic hyperphagia.

20 to PVN pathway may contribute to the related hyperphagia.

21 , indicating that obesity was not induced by hyperphagia.

22 pected correction from hyperglucagonemia and hyperphagia.

23 it obesity, decreased energy expenditure and hyperphagia.

24 s are hypothesized to contribute to diabetic hyperphagia.

25 (1-2 h) duration of action upon 2DG-induced hyperphagia.

26 e arcuate nucleus that promotes compensatory hyperphagia.

27 in the PVN may underlie the diabetes-induced hyperphagia.

28 also pair fed with lean controls to prevent hyperphagia.

29 isability, and susceptibility to obesity and hyperphagia.

30 was profound increase in body weight without hyperphagia.

31 sed body weight gain, energy expenditure and hyperphagia.

32 LEPRb was sufficient to cause HFD-dependent hyperphagia.

33 adulthood, increased energy expenditure and hyperphagia.

34 weaning (nocturnal) feeding and NPY-mediated hyperphagia.

35 nocturnal) feeding and mediating NPY-induced hyperphagia.

36 ceptors is required for vHP ghrelin-mediated hyperphagia.

37 postweaning feeding and blunted NPY-induced hyperphagia.

38 y in LMO4-deficient PVH neurons accounts for hyperphagia.

39 rwise lacking MC4Rs is sufficient to abolish hyperphagia.

40 esity and reduced energy expenditure without hyperphagia.

41 to decreased nutrient-induced satiation and hyperphagia.

42 compounds reduced binge-like palatable food hyperphagia.

43 HFD did not result in significantly greater hyperphagia [150 +/- 7 g (ghrelin+HFD) vs. 136 +/- 4 g (

44 ylin dose-dependently reversed DAMGO-induced hyperphagia; 3 ng of amylin reduced DAMGO-mediated feedi

45 cal and behavioral dysregulations, including hyperphagia, a condition that can lead to life-threateni

46 presents a single-gene model of obesity with hyperphagia, abnormal fat distribution and altered hypot

47 evelop enhanced intermale aggressiveness and hyperphagia accompanied by significant weight gain in ea

48 europeptides, and no impairment of reflexive hyperphagia after fasting.

49 Postdieting hyperphagia along with altered hypothalamic neuro-archit

50 ), but significant reductions in 2DG-induced hyperphagia, an AS ODN probe directed against the DOR-1

51 y analysis showed that Cc1(-/-) mice develop hyperphagia and a significant reduction in physical acti

52 receptor-null mutant (MC4R-/-) mice exhibit hyperphagia and accelerated weight gain compared to wild

53 in the central nervous system (CNS) mediate hyperphagia and adiposity induced by acyl ghrelin (AG).

54 dysregulated signaling leading to programmed hyperphagia and adult obesity.

55 Also, fasting-induced hyperphagia and after acute or chronic pharmacological t

56 Furthermore, mg/mg induced hyperphagia and an increase in basal metabolic rate in t

57 Hence, mu-opioid-induced hyperphagia and carbohydrate intake can be elicited with

58 The obesity is associated with hyperphagia and decreased activity.

59 sity that stems from the combined effects of hyperphagia and decreased energy expenditure.

60 that helps defend against infection, exhibit hyperphagia and develop hallmark features of metabolic s

61 sociated virus short hairpin RNA resulted in hyperphagia and exacerbated body weight gain in rats mai

62 NTS PPG knockdown caused hyperphagia and exacerbated high-fat diet (HFD)-induced

63 VMH-lesioned rats exhibiting hyperphagia and excessive weight gain in a time-related

64 These results demonstrate that hyperphagia and excessive weight gain in VMH-lesioned ra

65 BDNF infusion into the brain suppressed the hyperphagia and excessive weight gain observed on higher

66 rkB at a quarter of the normal amount showed hyperphagia and excessive weight gain on higher-fat diet

67 al hypothalamus (VMH) of rats induce instant hyperphagia and excessive weight gain.

68 ucose metabolism of gold thioglucose-induced hyperphagia and high-fat diet.

69 e of the participation of this phenomenon in hyperphagia and hormonal dysregulation in obesity.

70 bances, and behavioral disturbances, such as hyperphagia and hypersexuality.

71 somnia, whereas atypical patients experience hyperphagia and hypersomnia.

72 Loss of MC4R is known to induce hyperphagia and hypometabolism in mice.

73 anocortin-3/4 receptor agonist abrogated the hyperphagia and hypothalamic immunohistochemistry showed

74 ced obesity when they were group housed with hyperphagia and impaired sympathetic activity.

75 wth, hyperinsulinaemia, glucose intolerance, hyperphagia and increased adiposity in mice heterozygous

76 ng term changes in diet, possibly leading to hyperphagia and increased body weight.

77 body weight, while Mc4r KO and DKO exhibited hyperphagia and increased body weight.

78 or protein was accompanied by rapid onset of hyperphagia and increased fat mass.

79 Agouti Related Peptide (AgRP) also produces hyperphagia and increased the preference for a high fat

80 nsing could contribute to the rapid onset of hyperphagia and insulin resistance in this model.

81 a novel therapeutic paradigm to prevent both hyperphagia and intestinal tumorigenesis in obesity.

82 ruption of the Ankrd26 gene in mice leads to hyperphagia and leptin-resistant obesity.

83 a complex obesity phenotype comprising both hyperphagia and lowered metabolism.

84 gand-receptor encounters, produces mice with hyperphagia and maturity-onset obesity resembling mice w

85 tly, chronic central infusions of MCH induce hyperphagia and mild obesity in wild-type mice, but not

86 nd failure to thrive in infancy, followed by hyperphagia and obesity among other symptoms.

87 uka Long-Evans Tokushima Fatty rats reversed hyperphagia and obesity and reduced DMH NPY levels.

88 axis is not the initiating event leading to hyperphagia and obesity associated with cilia dysfunctio

89 potonia, hypogonadism, small hands and feet, hyperphagia and obesity in adulthood.

90 tal model that reproduces olanzapine-induced hyperphagia and obesity in female C57BL/6 mice.

91 ggesting a role for NO in the development of hyperphagia and obesity in rats fed a palatable diet.

92 logic treatments have been available for the hyperphagia and obesity that characterize the condition.

93 Hyperphagia and obesity were observed in a subgroup of p

94 agents that suppress appetite and developed hyperphagia and obesity when they were fed a high-fat/hi

95 mice and people exhibit early onset profound hyperphagia and obesity, diabetes, and infertility.

96 during specific physiological conditions of hyperphagia and obesity, however, the role of DMH-NPY ne

97 c factor), a gene previously associated with hyperphagia and obesity, is downregulated in the Rai1(+/

98 ; loss of leptin signaling results in marked hyperphagia and obesity.

99 Animals treated with MCH develop hyperphagia and obesity.

100 al nucleus of the hypothalamus, resulting in hyperphagia and obesity.

101 ere independent of the partial correction of hyperphagia and obesity.

102 logous Lepob/Lepob mice, effectively reduces hyperphagia and obesity.

103 l afferent signalling is sufficient to drive hyperphagia and obesity.

104 neurons impairs Pomc expression, leading to hyperphagia and obesity.

105 lean, and resistant to high-fat diet-induced hyperphagia and obesity.

106 hed BDNF signaling in mice results in severe hyperphagia and obesity.

107 racteristic behavioural features, especially hyperphagia and polydipsia, and a normal body-mass index

108 s of catch-up growth that are independent of hyperphagia and precede the development of overt adipocy

109 Cc2-/- mice develop obesity from hyperphagia and reduced energy expenditure, indicating i

110 /- mice exhibited obesity that resulted from hyperphagia and reduced energy expenditure.

111 sis, and Mc4r(-/-) mice are obese because of hyperphagia and reduced energy expenditure.

112 al ablation of the PVH causes obesity due to hyperphagia and reduced energy expenditure.

113 ass in Cc1(-/-) mice is mainly attributed to hyperphagia and reduced spontaneous physical activity.

114 s; a major deterrent to smoking cessation is hyperphagia and resultant weight gain.

115 We sequenced LEPR in 300 subjects with hyperphagia and severe early-onset obesity, including 90

116 Deletion carriers exhibited hyperphagia and severe insulin resistance disproportiona

117 eversible genetic mouse model of early-onset hyperphagia and severe obesity by selectively blocking t

118 the differential diagnosis in any child with hyperphagia and severe obesity in the absence of develop

119 We report a 19-year-old male with hyperphagia and severe obesity, mild learning difficulti

120 d their absence from mice or humans leads to hyperphagia and severe obesity.

121 stered (CF) mice demonstrated juvenile onset hyperphagia and significantly higher body weight (from w

122 Y2C in mice disrupts satiation, resulting in hyperphagia and subsequent obesity and metabolic syndrom

123 lower leptin levels contributes to diabetic hyperphagia and that this effect is not due to altered l

124 ownstream substrate for vHP ghrelin-mediated hyperphagia and that vHP ghrelin activated neurons commu

125 Thus, their hyperglycemia, hyperphagia and urine output declined significantly.

126 mice were resistant to rosiglitazone-induced hyperphagia and weight gain and, relative to rosiglitazo

127 expenditure is elevated during fasting, and hyperphagia and weight gain are blunted during refeeding

128 Furthermore, olanzapine-induced hyperphagia and weight gain were blunted in mice lacking

129 ist lorcaserin suppressed olanzapine-induced hyperphagia and weight gain.

130 LP-1 signaling during obesity may exacerbate hyperphagia and weight gain.

131 n blunts, but does not completely block, the hyperphagia and weight regain caused by acute leptin def

132 lanocortin signaling, even in the absence of hyperphagia, and are consistent with feeding-independent

133 ring infancy and reduced energy expenditure, hyperphagia, and developmental delays later in life.

134 partially corrected the increased fat mass, hyperphagia, and glucose intolerance while restoring fer

135 ion can correct or improve hyperinsulinemia, hyperphagia, and hyperlipidemia associated with these mo

136 e POMC transgene partially reversed obesity, hyperphagia, and hypothermia and effectively normalized

137 4-R deletion or mutation results in obesity, hyperphagia, and insulin resistance.

138 eficiencies as adolescents and hypogonadism, hyperphagia, and obesity as adults.

139 a mutation rescued the elevated body weight, hyperphagia, and obesity of A(y) mice.

140 acterized after infancy by hyperghrelinemia, hyperphagia, and obesity.

141 key mediator for postweaning feeding and NPY hyperphagia, and the PVH as one major downstream site th

142 at POMC neurons promotes 2-AG biosynthesis, hyperphagia, and weight gain by blunting alpha-MSH produ

143 irrespective of the foods provided, but the hyperphagia appears driven by variety and/or novelty, ra

144 sumed) argues that mechanisms in addition to hyperphagia are instrumental in causing weight gain.

145 erely reduced fat mass, despite compensatory hyperphagia, as a result of constitutive activation of t

146 onist (CL316,243) prevented obesity, but not hyperphagia associated with high fat feeding (body weigh

147 Y in positive energy balance, such as during hyperphagia associated with the development of obesity.

148 f growth and energy homeostasis universal to hyperphagia-associated childhood-onset obesity.

149 reased adipose mass, and is a consequence of hyperphagia-associated hyperinsulinaemia.

150 d adiposity and the progressive worsening of hyperphagia-associated hyperinsulinaemia.

151 antagonist exendin (9-39) caused significant hyperphagia at 2 h posttreatment, suggesting that endoge

152 of the obese animals were neither caused by hyperphagia because they were pair-fed with the control

153 ains; however, SWR/J mice exhibited a marked hyperphagia (calorie intake 60% higher than C57Bl/6J) to

154 Here we show that hyperphagia can be driven by mu-opioid receptor stimulat

155 In addition, 2-deoxy-D-glucose (2DG)-induced hyperphagia, central Angiotensin II (ANG-II) induced hyp

156 iation between the Cys23Ser polymorphism and hyperphagia (chi2 = 6.7, df = 2, P = 0.03) (P = 0.3 afte

157 Mutation carriers exhibited hyperphagia, childhood-onset obesity, disproportionate i

158 cluding increased weight gain and adiposity, hyperphagia, cold intolerance, and insulin resistance.

159 in energy intake (8-18%) required to prevent hyperphagia compared with the 35-40% in most other studi

160 Hyperphagia continued in maturity, with overeating great

161 Prevention of hyperphagia decreased deaths attributable to ESRD (males

162 or of functional leptin receptors results in hyperphagia, decreased energy expenditure, and obesity.

163 es profound obesity of early onset caused by hyperphagia, defective nonshivering thermogenesis, and p

164 eir core body temperature and not because of hyperphagia, defining a new role for CREB1 in the PVN.

165 The hyperphagia derived from the paraventricular nucleus (PV

166 diabetes, hyperlipidemia, and, surprisingly, hyperphagia despite hyperleptinemia.

167 energy expenditure and later accompanied by hyperphagia despite increased levels of circulating lept

168 ar (i.c.v.) injection of NPB in mice induces hyperphagia during the first 2 h, followed by hypophagia

169 Hyperphagia elicited by intra-Acb shell muscimol was not

170 rinking water of Pomc mice recapitulated the hyperphagia, excess weight gain and fat accumulation, an

171 This deficit contributes to the hyperphagia exhibited by BDNF mutant mice because select

172 s (Streptopelia risoria) and may promote the hyperphagia exhibited by parent doves when provisioning

173 t, MTII, inhibited feeding in four models of hyperphagia: fasted C57BL/6J, ob/ob, and A(Y) mice, and

174 We show that hyperphagia following germline loss of MC4R in male mice

175 ice displayed diminished weight gain despite hyperphagia, had diminished serum concentrations of both

176 Hyperphagia has therefore been termed passive overconsum

177 The syndrome, which produces measurable hyperphagia, has focused attention on the role of MC4R i

178 aspects of the A-ZIP/F-1 phenotype including hyperphagia, hepatic steatosis, and somatomegaly were ei

179 Chronic ICV Ex9 also caused hyperphagia; however, increased fat accumulation and glu

180 show that 2C null mice predictably developed hyperphagia, hyperactivity, and obesity and showed atten

181 Induction of diabetes caused hyperphagia, hyperglycemia, and decreases in heart rate

182 urity onset obesity syndrome associated with hyperphagia, hyperinsulinemia, and hyperglycemia.

183 In common forms of obesity, hyperphagia, hyperinsulinemia, and hyperleptinemia coexi

184 ypic metabolic disorders, including obesity, hyperphagia, hyperinsulinemia, and hyperleptinemia, simi

185 of primary and/or secondary effects such as hyperphagia, hypermetabolism, disturbed glucose homeosta

186 C4R) expressed in neurons, and this leads to hyperphagia, hypoactivity, and increased fat mass.

187 tin (POMC) have extreme early-onset obesity, hyperphagia, hypopigmentation, and hypocortisolism, resu

188 d depressive-related behavior, hyperhedonia, hyperphagia, impaired learning and memory and exaggerate

189 or metabolic syndrome and marked by obesity, hyperphagia, impaired tolerance to glucose, and reduced

190 The mechanism of hyperphagia in Cc2-/- mice is not clear, but appears to

191 sexes; modulates stress coping; and induces hyperphagia in males.

192 We next prevented hyperphagia in MC4RKO mice through restricting calorie i

193 creating a feed-forward loop contributing to hyperphagia in obesity.

194 FP(26) injection causes slight and transient hyperphagia in rats without changing any other energy ba

195 owing refeeding in association with relative hyperphagia in Snord116p-/m+ mice.

196 Remarkably, however, mg/mg did not reduce hyperphagia in the AY/a mouse.

197 esting that decreased apoE may contribute to hyperphagia in these obese animals.

198 tered NPYergic-leptin signaling may underlie hyperphagia in VMH-lesioned rats.

199 he POMC transgene attenuated fasting-induced hyperphagia in wild-type mice.

200 to inhibit food intake in several models of hyperphagia including neuropeptide Y (NPY)-induced eatin

201 Preventing hyperphagia increased maximum life span in both males (1

202 presses CB(1) cannabinoid receptor-dependent hyperphagia (increased appetite) in fasting animals by r

203 bioactive ghrelin, which was associated with hyperphagia, increased energy expenditure, glucose intol

204 stinal and hypothalamic satiation signaling, hyperphagia, increased weight gain and adiposity, and en

205 ms identifying the atypical subtype, such as hyperphagia, increased weight, and leaden paralysis.

206 We suggest that the hyperphagia induced by pCPA is mediated by increased NPY

207 Finally, the hyperphagia induced by STZ injection was completely reve

208 significantly and markedly reduced (81-93%) hyperphagia induced by the anti-metabolic glucose analog

209 educed melanocortin signaling contributes to hyperphagia induced by uncontrolled diabetes, male Sprag

210 ed with numerous neuropathologies, including hyperphagia-induced obesity, hypogonadism, and learning

211 feeding behavior and BBS is associated with hyperphagia-induced obesity, our results suggest that al

212 taining PVH activity is important to prevent hyperphagia-induced obesity.

213 ocortin obesity syndrome consistently yields hyperphagia irrespective of the foods provided, but the

214 but did not abolish obesity, indicating that hyperphagia is a major but not sole determinant of the p

215 The hypothesis that benzodiazepine-induced hyperphagia is due to a specific enhancement of the pala

216 ased body fat content still results when the hyperphagia is prevented.

217 Marked hyperphagia is restricted to bvFTD, present in all patie

218 AgRP, but the increase in food intake (i.e. hyperphagia) is not.

219 sorder include mood reactivity, hypersomnia, hyperphagia, leaden paralysis, and rejection sensitivity

220 at least 2 additional symptoms: hypersomnia, hyperphagia, leaden paralysis, or lifetime sensitivity t

221 ociated with feeding and induce compensatory hyperphagia, leading to obesity.

222 Chronic hyperphagia leads to a 'middle-aged'-onset obesity assoc

223 In ZDF rats, hyperphagia leads to hyperinsulinemia, which up-regulate

224 Pair feeding experiments showed that hyperphagia led to peripheral insulin resistance.

225 ic effects of high-fat diets, independent of hyperphagia, may also be contributing to the obesity ind

226 mice fed a normal diet and without apparent hyperphagia, mimicking basic characteristics of human me

227 However, this deficiency caused neither hyperphagia nor obesity in mice fed on either a standard

228 a complex genetic disorder characterized by hyperphagia, obesity and hypogonadotrophic hypogonadism,

229 ortin-4-receptor (MC4R) signalling result in hyperphagia, obesity and increased growth.

230 he melanocortin 4 receptor (MC4R) results in hyperphagia, obesity and increased growth.

231 ulin secretion, increased ghrelin secretion, hyperphagia, obesity and related sequelae.

232 AV-mediated RNA interference ameliorated the hyperphagia, obesity, and diabetes of Otsuka Long-Evans

233 DNF mutant VMH significantly mitigates their hyperphagia, obesity, and liver steatosis and normalizes

234 including hyperlipidemia, leptin resistance, hyperphagia, obesity, hyperglycemia, insulin resistance,

235 on chromosome 15q11-13 in an individual with hyperphagia, obesity, hypogonadism and other features as

236 conditional postnatal Sim1(-/-) mice exhibit hyperphagia, obesity, increased linear growth and suscep

237 Hyperphagia, obesity, or metabolic syndrome could have p

238 ssion, cell-cycle re-entry, apoptosis, and a hyperphagia-obesity-diabetes syndrome.

239 he PVN significantly elevated at 48 h, while hyperphagia occurred sometimes after 48 h post-injection

240 intake returning to near normal and rebound hyperphagia occurring on cessation of treatment.

241 tiple systems that contribute to the chronic hyperphagia of lactation: 1) suppression of the metaboli

242 uring training the rats developed binge-like hyperphagia of palatable food and anticipatory chow hypo

243 Surprisingly, the hyperphagia of the ob/ob mouse was unaffected.

244 were given ad libitum access to the HFD, the hyperphagia of these mice led to accelerated body weight

245 resence of steatorrhea, the Clps-/- mice had hyperphagia on a high fat diet.

246 altered the magnitude of either 2DG-induced hyperphagia or ANG-II-induced hyperdipsia.

247 Interestingly, obesity is not due to hyperphagia or decreased energy expenditure, but is asso

248 -R(-/-)) mouse exhibits mild obesity without hyperphagia or hypometabolism.

249 sing hypothalamic MANF protein levels causes hyperphagia or hypophagia, respectively.

250 a functional leptin receptor do not exhibit hyperphagia or increased adiposity, and exhibit normal f

251 ovegetative symptoms (hypersomnia and either hyperphagia or weight gain).

252 ed on a daily basis), but this phenomenon of hyperphagia (or binge-feeding) is largely overlooked.

253 s not associated with altered meal patterns, hyperphagia, or excessive weight gain on a palatable die

254 ut showed markedly increased fasting-induced hyperphagia (P < 0.001).

255 Diabetes is characterized by hyperphagia, polydypsia and activation of the HPA axis.

256 observed obesity predominantly results from hyperphagia rather than a metabolic derangement.

257 e rapidly obese when fed regular chow due to hyperphagia rather than to reduced energy expenditure.

258 The hyperphagia results, at least in part, from the absence

259 The hyperglycemia and hyperphagia returned in aged Polg-Akita males after test

260 e we demonstrate that JNK3 deficiency causes hyperphagia selectively in high fat diet (HFD)-fed mice.

261 Affected subjects were characterized by hyperphagia, severe obesity, alterations in immune funct

262 congenital leptin deficiency, which includes hyperphagia, severe obesity, hypogonadism, and impaired

263 C responds to energy deficits rather than to hyperphagia stimuli related to palatability.

264 CGRP(PBN) neurons in Apc(min/+) mice permits hyperphagia that counteracts weight loss, revealing a ro

265 of SHU9119 is simply masked by the refeeding hyperphagia that follows food deprivation.

266 We expect hyperphagia to be a short-term (1-day) event that is fac

267 The importance of hyperphagia was confirmed by severe weight loss in a gro

268 Unexpectedly, hyperphagia was normalized by MSTN inhibition in muscle.

269 Hyperphagia was prevented by insulin treatment (32 +/- 2

270 2DG-induced hyperphagia was significantly reduced by AS ODNs directe

271 2-Deoxy-D-glucose (500 mg/kg, i.p.)-induced hyperphagia was significantly reduced by high (50 microg

272 C-PVN pathway precedes the onset of diabetic hyperphagia, we evaluated NPY levels in seven hypothalam

273 severe early-onset obesity and a history of hyperphagia, we found two rare sequence variants-L73P an

274 hat low leptin levels contribute to diabetic hyperphagia, we investigated the effect on food intake o

275 signaling contributes to the development of hyperphagia, weight gain, and leptin resistance during d

276 The meal patterning effects underlying this hyperphagia were also similar for the two placements (i.

277 Blood glucose and hyperphagia were reduced in double mutants independent o

278 otein (AGRP), an appetite modulator, induces hyperphagia when administered intracerebroventricularly

279 ed in obese and diabetic mice and stimulates hyperphagia when administered intracerebroventricularly

280 overt manipulation of dietary fat can induce hyperphagia, which can readily lead to spontaneous fat s

281 been proposed that a high-fat diet produces hyperphagia, which is solely responsible for the increas

282 The obesity is associated with hyperphagia with no reduction in energy expenditure and

283 soenergy-dense diets show that this high-fat hyperphagia (with diets of similar palatability) is caus