ライフサイエンスコーパス: hyperphagia

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

2 cation of gut hormone levels, dysbiosis, and hyperphagia.

3 rwise lacking MC4Rs is sufficient to abolish hyperphagia.

4 to decreased nutrient-induced satiation and hyperphagia.

5 compounds reduced binge-like palatable food hyperphagia.

6 ncreased fat content in tissues, produced by hyperphagia.

7 reportedly causes leanness in the setting of hyperphagia.

8 ophy and hepatic steatosis in the absence of hyperphagia.

9 this response is required for the associated hyperphagia.

10 ich may imply changes in food preference and hyperphagia.

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

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

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

14 25% to 50% than from increased adiposity or hyperphagia.

15 lop central obesity, insulin resistance, and hyperphagia.

16 dents and in humans has been associated with hyperphagia.

17 tion to atypical features of hypersomnia and hyperphagia.

18 ersed vegetative symptoms of hypersomnia and hyperphagia.

19 osition in young adult mutants despite their hyperphagia.

20 gs approved for the treatment of obesity and hyperphagia.

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

22 ood deprivation with markedly reduced reflex hyperphagia.

23 CRH signaling, could contribute to diabetic hyperphagia.

24 to PVN pathway may contribute to the related hyperphagia.

25 , indicating that obesity was not induced by hyperphagia.

26 it obesity, decreased energy expenditure and hyperphagia.

27 Bbs1 gene in POMC neurons is associated with hyperphagia.

28 s are hypothesized to contribute to diabetic hyperphagia.

29 (1-2 h) duration of action upon 2DG-induced hyperphagia.

30 e arcuate nucleus that promotes compensatory hyperphagia.

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

32 also pair fed with lean controls to prevent hyperphagia.

33 esity and reduced energy expenditure without hyperphagia.

34 expenditure occurred even in the absence of hyperphagia.

35 stress, and is dependent on the concomitant hyperphagia.

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

37 pected correction from hyperglucagonemia and hyperphagia.

38 isability, and susceptibility to obesity and hyperphagia.

39 sed body weight gain, energy expenditure and hyperphagia.

40 LEPRb was sufficient to cause HFD-dependent hyperphagia.

41 d upon palatable food consumption to promote hyperphagia.

42 adulthood, increased energy expenditure and hyperphagia.

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

44 nocturnal) feeding and mediating NPY-induced hyperphagia.

45 ceptors is required for vHP ghrelin-mediated hyperphagia.

46 postweaning feeding and blunted NPY-induced hyperphagia.

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

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

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

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

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

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

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

54 Postdieting hyperphagia along with altered hypothalamic neuro-archit

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

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

57 emia, and insulin resistance associated with hyperphagia and accelerated postweaning weight gain indu

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

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

60 dysregulated signaling leading to programmed hyperphagia and adult obesity.

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

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

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

64 The obesity is associated with hyperphagia and decreased activity.

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

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

67 cortins, the absence of which induces marked hyperphagia and early-onset obesity.

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

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

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

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

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

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

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

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

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

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

78 somnia, whereas atypical patients experience hyperphagia and hypersomnia.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 -lineage neural cells, promoted diet-induced hyperphagia and obesity in both male and female mice, an

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

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

100 YNG is associated with a lower prevalence of hyperphagia and obesity than PWS.

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

102 Hyperphagia and obesity were observed in a subgroup of p

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

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

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

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

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

108 projecting to either VMH or LPBN results in hyperphagia and obesity.

109 Animals treated with MCH develop hyperphagia and obesity.

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

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

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

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

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

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

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

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

118 Calorie-rich diets induce hyperphagia and promote obesity, although the underlying

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

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

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

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

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

124 of enteric neurons reduces both reproductive hyperphagia and reproductive fitness.

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

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

127 Deletion carriers exhibited hyperphagia and severe insulin resistance disproportiona

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

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

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

131 ce, as mutations in its gene (NTRK2) lead to hyperphagia and severe obesity.

132 coded byPomc, and Pomc mutations may lead to hyperphagia and severe obesity.

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

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

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

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

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

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

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

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

141 were specifically associated with AP-induced hyperphagia and weight gain in mice.

142 treatment abrogates olanzapine (OLZ)-induced hyperphagia and weight gain in mice.

143 abolomic profiles associated with AP-induced hyperphagia and weight gain provide candidate biomarkers

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

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

146 and hypothalamus associated with OLZ-induced hyperphagia and weight gain.

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

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

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

150 is even worse, leading to leptin resistance, hyperphagia, and decreased EE.

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

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

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

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

155 4-R deletion or mutation results in obesity, hyperphagia, and insulin resistance.

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

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

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

159 orsens their glucose homeostasis, adiposity, hyperphagia, and POMC neuronal projections, all of which

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

177 Hyperphagia continued in maturity, with overeating great

178 Prevention of hyperphagia decreased deaths attributable to ESRD (males

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

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

181 The hyperphagia derived from the paraventricular nucleus (PV

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

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

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

185 Hyperphagia elicited by intra-Acb shell muscimol was not

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

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

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

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

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

191 Hyperphagia has therefore been termed passive overconsum

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

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

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

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

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

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

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

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

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

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

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

203 ther proteinopathies, such as cancer, marked hyperphagia, impaired immune function, and inflammation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 Hyperphagia, obesity, or metabolic syndrome could have p

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

253 neonatal hypotonia, developmental delay and hyperphagia/obesity.

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

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

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

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

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

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

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

261 ivo, activation of tanycytes triggered acute hyperphagia only in the fed state during the inactive ph

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

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

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

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

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

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

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

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

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

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

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

273 rk2 deletion in the DMH of adult mice led to hyperphagia, reduced energy expenditure, and obesity.

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

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

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

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

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

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

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

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

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

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

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

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

286 2DG-induced hyperphagia was significantly reduced by AS ODNs directe

287 2-Deoxy-D-glucose (500 mg/kg, i.p.)-induced hyperphagia was significantly reduced by high (50 microg

288 ical mechanisms underlying this cold-induced hyperphagia, we asked whether agouti-related peptide (Ag

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

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

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

292 g altered energy intake/expenditure balance (hyperphagia, weight gain, hypersomnia, fatigue, and lead

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

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

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

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

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

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

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

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