ライフサイエンスコーパス: binge

1 tomography (PET), before and after a cocaine binge.

2 The first alcohol binge activates mTORC1 in NAc D1+ neurons and increases

3 on translocation within both regions reduced binge alcohol consumption in a manner requiring intact g

4 ATEMENT We examined the relationship between binge alcohol drinking and spike timing-dependent plasti

5 th the NAc and CeA is a major contributor to binge alcohol drinking and to the genetic propensity to

6 ration after a history of repeated cycles of binge alcohol drinking and withdrawal.

7 ptor (Y1R) activation in the BNST suppressed binge alcohol drinking by enhancing inhibitory synaptic

8 Binge alcohol drinking elevated p(Ser729)-PKCepsilon lev

9 Specifically, a mouse paradigm that mimics binge alcohol drinking in humans produced a robust reduc

10 Binge alcohol drinking is a tremendous public health pro

11 role of dopamine in mediating the effects of binge alcohol drinking on synaptic plasticity of NAc MSN

12 sed drinking in the dark (DID) as a model of binge alcohol drinking to assess its effects on spike ti

13 Binge alcohol drinking, a behavior characterized by rapi

14 (STDP), the manner by which STDP responds to binge alcohol drinking, and its sensitivity to dopamine

15 These results indicate that chronic-plus-binge alcohol exposure inhibits the granulopoietic respo

16 To study the effect of chronic-plus-binge alcohol exposure on the granulopoietic response, a

17 st of neutrophils isolated from chronic plus binge alcohol fed mice or from human blood, and decrease

18 CBD on liver injury induced by chronic plus binge alcohol feeding in mice.

19 Chronic-plus-binge alcohol induced adipose atrophy with increased aut

20 in PV-expressing interneurons in modulating binge alcohol intake and withdrawal-induced anxiety.

21 ive coping behaviors in real life, including binge alcohol intake, emotional eating, and frequency of

22 tory of a highly prevalent form of drinking, binge alcohol intake, influences enzyme priming or the f

23 -type mice were challenged with chronic-plus-binge alcohol mouse model.

24 homelessness, incarceration, substance use, binge alcohol use, depression, and not achieving a suppr

25 ate that, in male mice, a history of chronic binge alcohol-drinking elevates BNST levels of the mGlu5

26 The transition to binge and hazardous drinking occurred for 29% and 18% of

27 Binge and heavy drinking are preventable causes of morta

28 This study demonstrated that trends in binge and heavy drinking over time were not differential

29 re child-rearing, it remains unclear whether binge and heavy drinking vary by parenting status and se

30 oth with and without children are increasing binge and heavy drinking; men, regardless of parenting s

31 in system plays an important role in cocaine binges and stress-induced relapse.

32 Binge compared with nonbinge drinking (defined as report

33 cold pressor test, to induce stress, and (2) binge dosing of cocaine.

34 sitive correlation between the propensity to binge drink alcohol and constitutive p(Ser729)-PKCepsilo

35 the amygdala (CeA) in nondependent rats that binge drink alcohol and in alcohol-dependent rats.

36 e alcohol drinking in nondependent rats that binge drink alcohol and in alcohol-dependent rats.

37 e assessed in 45 adolescents, who went on to binge-drink (but were alcohol-naive at baseline), and 68

38 We further assessed 32 young binge drinkers and 36 abstinent subjects with alcohol us

39 The pathways associated with both binge drinkers and AD are also analyzed.

40 that subthalamic connectivity differentiates binge drinkers and individuals with alcohol use disorder

41 s (IPA) shows that high levels of ethanol in binge drinkers cause a shift in the microbiome that lead

42 of binge drinking among those who were never binge drinkers, and (3) the onset of hazardous drinking

43 We further showed that binge drinkers, like those with alcohol use disorders, h

44 the age-standardized prevalence of heavy and binge drinkers.

45 ural and psychosocial markers could identify binge drinkers.

46 hey are associated with reduced frequency of binge drinking >=6 drinks (B(IVW) = -0.198, 95% CI, -0.2

47 at least a 4.0-percentage-point increase in binge drinking (95% confidence interval: 0.9, 7.0) and a

48 OR], 1.69 [95% CI, 1.17-2.44]), the onset of binge drinking (AOR, 1.38 [95% CI, 1.08-1.77]), and the

49 year), hazard ratios were increased for ever binge drinking (HR = 1.29, 95% CI: 1.15, 1.45) or blacki

50 mong those who never drank, (2) the onset of binge drinking among those who were never binge drinkers

51 By 2012, the prevalence of binge drinking among young men with children (38.5%) dec

52 Scheduled Access) to induce escalating heavy binge drinking and anxiety-like behavior in mice.

53 al relevance of PKCepsilon translocation for binge drinking and determination of potential upstream s

54 he sera of healthy individuals after alcohol binge drinking and in mice after binge or chronic alcoho

55 s study provides a foundation that shows how binge drinking and the oral microbiome dysbiosis lead to

56 in PV interneurons (PV:delta(-/-)) increased binge drinking behavior, reduced sensitivity to alcohol-

57 -reported data and measurement invariance in binge drinking cutoffs across study years.

58 g men (ages 18-29) with children, among whom binge drinking declined.

59 with an increased frequency of drinking and binge drinking episodes in adolescents.

60 oncerning for adult morbidity and mortality: binge drinking has increased among both sexes, and heavy

61 s 30-44 without children (from 21% reporting binge drinking in 2006 to 42% in 2018); the exception wa

62 The influence of ERs on binge drinking in female mice suggests that treatments f

63 Our data show that acute alcohol binge drinking in healthy volunteers results in increase

64 The prevalence of binge drinking in the United States is rising.

65 ses than those traditionally associated with binge drinking in young adults.

66 Binge drinking increased for both sexes in nearly all ag

67 Binge drinking is associated with disease and death, and

68 Binge drinking is short-term drinking that achieves bloo

69 Binge drinking may be an early indicator of vulnerabilit

70 Binge drinking may reduce telomere length.

71 D hippocampus and following a rat adolescent binge drinking model.

72 ion of the plasma exosomal CYP2E1 level in a binge drinking murine model.

73 R modulator, LM11A-31, significantly reduced binge drinking of alcohol.

74 4-hour, 2-bottle choice drinking in the dark binge drinking or limited access 2-bottle choice.

75 For binge drinking outcomes only, we saw evidence of interac

76 l neurons projecting to the brainstem before binge drinking predicted the ultimate emergence of compu

77 pproaches within the context of two distinct binge drinking procedures, drinking in the dark and sche

78 Two fMRI-based models predicted binge drinking status better than chance, corresponding

79 crobiome in relation to alcohol misuse- from binge drinking to addiction.

80 Binge drinking unmasked individual differences, revealin

81 for alcohol consumption (units per week and binge drinking) from Scottish Health Surveys done in 199

82 Even in the absence of binge drinking, alcohol consumption during pregnancy can

83 t concentrations seen in blood alcohol after binge drinking, and diminished ALDH1a1 leads to enhanced

84 ing after adjustment for weekly consumption, binge drinking, BMI, and smoking.

85 % CI: 0.3, 12.2; p = 0.041), and past-30-day binge drinking, by 3.5 percentage points (95% CI: -0.1,

86 We examined national trends in binge drinking, defined as 5 or more drinks in a single

87 Binge drinking, defined as reaching a blood alcohol leve

88 Despite widespread increases in binge drinking, heavy drinking declined or remained stab

89 inhibit TLR4 or MCP-1 expression nor reduce binge drinking, identifying a neuronal TLR4/MCP-1 signal

90 le diseases); health risks (tobacco smoking, binge drinking, overweight, and anaemia); and social det

91 nalysis method to establish the link between binge drinking, the oral microbiome and AD.

92 the amygdala to examine both idiopathic and binge drinking-induced changes in constitutive PKCepsilo

93 vioral maladaptations during withdrawal from binge drinking.

94 nd blocked the expression of withdrawal from binge drinking.

95 sodes of excessive alcohol drinking known as binge drinking.

96 t against severe intoxication in response to binge drinking.

97 inhibited target gene expression and blunted binge drinking.

98 on targets, which plays an important role in binge drinking.

99 n have been implicated in sex differences in binge drinking.

100 We found that the first binge-drinking alcohol session produced enduring enhance

101 Both future binge-drinking and familial alcoholism were associated w

102 characterized plasma exosomal contents in a binge-drinking animal model and their effect on ALC/APAP

103 ng drinking limit guidelines in adults or on binge-drinking episodes or social consequences of alcoho

104 development of compulsive drinking across a binge-drinking experience in male mice.

105 Familial alcoholism and adolescent binge-drinking have both been associated with altered wh

106 ibutes to excessive alcohol consumption in a binge-drinking model.

107 he effects of familial alcoholism and future binge-drinking on white matter microstructural developme

108 white matter regions identified where future binge-drinking or familial alcoholism were significantly

109 While several binge-drinking-related effects persisted throughout adol

110 f response to alcohol, would predict rate of binging during an individual alcohol consumption session

111 Identifying genetic variants that regulate binge eating (BE) is critical for understanding the fact

112 Obese subjects with binge eating also have impaired discrimination of subjec

113 uses evolved protective mechanisms including binge eating and increased metabolic efficiency and fat

114 4.5)], eating continuously [1.6% (0.1-3.1)], binge eating and loss-of-control eating [8.0% (5.1-11.0)

115 Secondary endpoints related to binge eating and medical parameters, safety, and treatme

116 Binge eating and other forms of disordered eating behavi

117 ore, results suggested that higher levels of binge eating and overeating in males at age 13 y likely

118 Furthermore, higher levels of binge eating and overeating may cause higher BMI in late

119 MI at age 7 y likely causes higher levels of binge eating and overeating, weight and shape concerns,

120 major significant genetic factor underlying binge eating and provide a behavioral paradigm for futur

121 sdexamfetamine, SGAs, and topiramate reduced binge eating and related psychopathology, and lisdexamfe

122 Self-reported binge eating and/or purging were used to indicate presen

123 r improving glycemic control and suppressing binge eating behaviors.

124 8 weeks), lisdexamfetamine responders (</=1 binge eating day per week for 4 consecutive weeks and CG

125 Change from baseline in binge eating days/week at weeks 11-12 (primary efficacy

126 eatment differences for change from baseline binge eating days/week at weeks 11-12 significantly favo

127 g/day) was superior to placebo in decreasing binge eating days/week from baseline and improving binge

128 disorder criteria and had moderate to severe binge eating disorder (>/=3 binge-eating days per week f

129 were depression (19% [95% CI, 14%-25%]) and binge eating disorder (17% [95% CI, 13%-21%]).

130 dexamfetamine dimesylate (LDX) vs placebo in binge eating disorder (BED) was evaluated in two multice

131 anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder (BED), and purging disorder (PD).

132 ents the criterion standard for treatment of binge eating disorder (BED), most individuals do not hav

133 n phenotypes: pathological gambling (PG) and binge eating disorder (BED).

134 The Internet and Binge Eating Disorder (INTERBED) study is a prospective,

135 Our findings support a distinct subtype of binge eating disorder in obesity with similarities in ri

136 dy mass index >=18.5, met criteria for DSM-5 binge eating disorder or bulimia nervosa, had 12 months

137 Neither depression nor binge eating disorder was consistently associated with d

138 systems: anorexia nervosa, bulimia nervosa, binge eating disorder, avoidant-restrictive food intake

139 or attention deficit hyperactivity disorder, binge eating disorder, cocaine addiction, obesity, and t

140 trol disorders, including gambling disorder, binge eating disorder, compulsive sexual behaviour, and

141 rgery patients-in particular, depression and binge eating disorder.

142 binge intake of high-fat food (HFF) seen in binge eating disorder.

143 ference in the number of days with objective binge eating episodes (OBEs) during the previous 28 days

144 the anticipation of losses, obesity without binge eating had a similar pattern to other substance-us

145 We assessed binge eating in closely related C57BL/6 mouse substrains

146 Cyfip2 as a major genetic factor underlying binge eating in heterozygous knockout mice on a C57BL/6N

147 Binge eating is a highly heritable trait associated with

148 Compulsive, binge eating of highly palatable food constitutes a core

149 etrograde endocannabinoid signaling, whereas binge eating resulted in the downregulation of a gene se

150 ome to inform molecular mechanisms mediating binge eating susceptibility and establishment.

151 on a C57BL/6N background that showed reduced binge eating toward a wild-type C57BL/6J-like level.

152 ted with a smartphone app, Noom Monitor, for binge eating with or without purging.

153 (e.g., locating food) and maladaptive (e.g., binge eating) ways.

154 tions may promote hallmark bulimic behaviors-binge eating, dietary restriction, and purging.

155 (eg, more sedentary time, eating fast food, binge eating, eating continuously, not weighing oneself

156 ould yield greater reductions in symptoms of binge eating, purging, and eating disorders compared wit

157 The neuronal substrate for binge eating, which can at times lead to obesity, is not

158 eating days/week from baseline and improving binge eating-related key secondary endpoints.

159 to feed is a key contributor to obesity and binge eating.

160 tify quantitative trait loci associated with binge eating.

161 el pharmacological treatment for compulsive, binge eating.

162 loss-of-control eating [8.0% (5.1-11.0) for binge eating; 1.6 (-0.1 to 3.3) for loss of control, vs

163 We assessed the change in binge-eating (BE) behaviors measured as days per week (b

164 eus (PVN) is necessary for the expression of binge-eating behavior in female rats.

165 a primary focus on anorexia nervosa (AN) and binge-eating behavior, and encourages further study of a

166 ats, RXFP3 blockade within the PVN prevented binge-eating behavior.

167 hypothalamic RLN3/RXFP3 signaling regulates binge-eating behavior.SIGNIFICANCE STATEMENT Binge-eatin

168 reported significant reductions in objective binge-eating days (beta=-0.66, 95% CI=-1.06, -0.25; Cohe

169 derate to severe binge eating disorder (>/=3 binge-eating days per week for 14 days before open-label

170 mary outcome variable, time to relapse (>/=2 binge-eating days per week for 2 consecutive weeks and >

171 Binge-eating disorder (BED) is characterized by recurrin

172 Binge-eating disorder (BED), a public health problem ass

173 l or food, in alcohol use disorders (AUD) or binge-eating disorder (BED), suggest a disturbance in ex

174 rvosa (n = 13), bulimia nervosa (n = 6), and binge-eating disorder (n = 1), published between January

175 The best treatment options for binge-eating disorder are unclear.

176 Eligible adults met DSM-IV-R binge-eating disorder criteria and had moderate to sever

177 Binge-eating disorder is characterized by excessive, unc

178 binge-eating behavior.SIGNIFICANCE STATEMENT Binge-eating disorder is the most common eating disorder

179 Binge-eating disorder is the most common eating disorder

180 n circuits and neurotransmitters involved in binge-eating disorder pathology and identify RXFP3 as a

181 on across the genome of anorexia nervosa and binge-eating disorder patients.

182 ther eating disorders (OED: bulimia nervosa, binge-eating disorder, and eating disorder not otherwise

183 f efficacy in adults with moderate to severe binge-eating disorder.

184 and topiramate reduced weight in adults with binge-eating disorder.

185 he characteristic symptomatology observed in binge-eating disorder.

186 as a potential pharmacological treatment for binge-eating disorder.

187 ic substrate for observed sex differences in binge-eating disorder.

188 ramate also increased abstinence and reduced binge-eating frequency and related psychopathology.

189 Finally, in a model of binge-eating in female rats, RXFP3 blockade within the P

190 lso showed flexibility in foraging patterns, binge-eating less and using feeders more when they exper

191 Risk of binge-eating relapse over 6 months was lower in particip

192 PC1 ('binge-eating'), accounting for 38% of variation, capture

193 Using a model of binge-eating, we demonstrated that relaxin-3/RXFP3 signa

194 GAs (MD, -3.84 [CI, -6.55 to -1.13]) reduced binge-eating-related obsessions and compulsions, and SGA

195 vy drinking, defined as 60 or more days with binge episodes in a year.

196 ide a potential mechanism for severe cocaine binge episodes, which occur even after sustained abstine

197 Utilizing the Gao-binge ethanol feeding protocol, matched mLipin-1KO mice

198 C57BL/6-Ly5.1 mice were fed chronic plus binge ethanol to create a model of ALD.

199 Effects of binge EtOH exposure on brain volumes and neurometabolite

200 Brain changes in response to binge EtOH treatment were more pronounced in young relat

201 sion in an effortful T-maze task following a binge exposure to methamphetamine, and no such changes i

202 erve as a target to treat adolescent alcohol binge exposure-induced mental disorders, such as anxiety

203 vioral addictions, and eating disorders with binge features.

204 Simulations demonstrated the ability to binge-feed increased cumulative consumption (16-32%) and

205 vlmJ as a strain that exhibits low levels of binge feeding behavior and suggests that this strain cou

206 We found that after chronic plus binge feeding of Lieber-DeCarli liquid diet in male C57B

207 restriction (CR) induces bouts of compulsive binge feeding separated by prolonged fasting intervals,

208 The degree of binge-feeding by bull trout in the field was slightly re

209 nd food availability influence the degree of binge-feeding by comparing field observations with labor

210 Binge-feeding has important implications for energy budg

211 fied mice, with the exception of the chronic binge-feeding model.

212 sis), but this phenomenon of hyperphagia (or binge-feeding) is largely overlooked.

213 uence of genetic variation in the control of binge food intake.

214 , moderate drinkers (60-229 drinks/year) who binged had a higher risk (HR = 1.25, 95% CI: 1.08, 1.44)

215 Weekly binge in this new hybrid feeding model shifts chronic AS

216 Binge-induced changes in VTA CRF system protein and mess

217 identify the premorbid transcriptome and the binge-induced transcriptome to inform molecular mechanis

218 prepotent responses (motor impulsivity) and binge intake of high-fat food (HFF) seen in binge eating

219 nd development of drug-seeking habits in the binge/intoxication stage involve changes in dopamine and

220 During the binge/intoxication stage, alcohol intoxication leads to

221 extended period within a three-stage cycle: binge/intoxication, withdrawal/negative affect, and preo

222 Low, moderate to high, or binge-level alcohol exposure in the first trimester or t

223 es, midface, chin, and parietal region), and binge-level exposure in the first trimester (chin).

224 were associated with the rate of achieving a binge-level exposure.

225 so demonstrated that ERs in the VTA regulate binge-like alcohol drinking by female, but not male, mic

226 Early binge-like alcohol drinking may promote the development

227 e inhibitory DREADD by CNO injection reduced binge-like alcohol drinking, but CNO injection did not a

228 he chronic regulation of food intake and the binge-like consumption of a palatable HCD.

229 of fetal alcohol spectrum disorder (FASD) is binge-like consumption of alcohol before pregnancy aware

230 tration of the KOR agonist U50,488 increased binge-like drinking (Experiment 1) while, conversely, sy

231 in/kappa opioid receptor (DYN/KOR) system in binge-like drinking has not been fully explored.

232 asynaptic delta-GABA(A)Rs to male and female binge-like drinking in a critical area of mesolimbic cir

233 downregulated delta-GABA(A)Rs and decreased binge-like drinking in females.

234 semble only partially contributed to alcohol-binge-like drinking in nondependent rats.

235 pha in the VTA had a more dramatic effect on binge-like drinking than reducing ERbeta, consistent wit

236 kout (KO) mice selectively increased ethanol binge-like drinking, without affecting ethanol metabolis

237 gnature for genetic risk for high intensity, binge-like drinking.

238 toxicating blood alcohol levels (BALs) after binge-like drinking.

239 nt models of chronic, dependence-driven, and binge-like drinking.

240 R+ mPFC neurons projecting to the BLA blunts binge-like drinking.

241 n in the drinking-in-the-dark (DID) model of binge-like drinking.

242 RF2R signaling, and CRF2R activation reduces binge-like drinking; 2) inhibiting VTA-projecting BNST C

243 g VTA-projecting BNST CRF neurons attenuates binge-like drinking; and 3) binge-like ethanol drinking

244 Thus, inherent motor impulsivity and binge-like eating are linked and the vmPFC to NAcSh path

245 he present results show that OSU6162 reduces binge-like eating behavior and attenuates the impact of

246 action time task and employed a rat model of binge-like eating behavior.

247 d identify RXFP3 as a therapeutic target for binge-like eating disorders.

248 Our results show that RO5256390 blocked binge-like eating in rats responding 1 h per day for a h

249 e relationship between motor impulsivity and binge-like eating in rodents, we identified high (HI) an

250 ere, the effects of OSU6162 on consummatory (binge-like eating) and appetitive (cue-controlled seekin

251 urons immediately (in 2 to 3 seconds) evoked binge-like eating.

252 not prelimbic, subregion of the mPFC-reduced binge-like eating.

253 t core, microinfusion of memantine decreased binge-like eating.

254 ed that TAAR1 may have a role in compulsive, binge-like eating; we tested this hypothesis by assessin

255 ntributions of these receptors in modulating binge-like ethanol consumption (n = 89).

256 nd NPY2R, respectively) is known to modulate binge-like ethanol consumption in rodents.

257 The effects of binge-like ethanol consumption on the VTA CRF system wer

258 We provide novel evidence that 1) blunted binge-like ethanol consumption stemming from CRF1R block

259 nce that NPY signaling in the mPFC modulates binge-like ethanol consumption.

260 urons attenuates binge-like drinking; and 3) binge-like ethanol drinking alters protein and messenger

261 nockdown of each receptor in the VTA reduced binge-like ethanol drinking in female, but not male, mic

262 However, the effects of binge-like ethanol drinking on this system have not been

263 f local CRF neurons in the VTA did not alter binge-like ethanol drinking, but inhibition of VTA-proje

264 We provide novel evidence that (1) binge-like ethanol intake reduces NPY levels in the mPFC

265 nd antagonism of NPY2R resulted in decreased binge-like ethanol intake.

266 o-VTA CRF projections is critical in driving binge-like ethanol intake.

267 projecting to the BLA, significantly reduced binge-like ethanol intake.

268 vation of NPY1R or blockade of NPY2R reduces binge-like ethanol intake; and (3) chemogenetic inhibiti

269 Repeated binge-like exposure to alcohol during adolescence has be

270 Thus, through a paradigm that promoted binge-like food intake through intermittent access to hi

271 gnificantly suppressed motor impulsivity and binge-like intake for high-fat food.

272 OSU6162 significantly reduced binge-like intake of chocolate-flavored sucrose pellets

273 0-) were exposed to either a methamphetamine binge (METH+) or saline (METH-), then tested in the atte

274 al Institute on Alcohol Abuse and Alcoholism binge model) or chow diets along with water containing 0

275 Compared with low-level drinkers who never binged, moderate drinkers (60-229 drinks/year) who binge

276 minant states (great tits, males and adults) binged more than subordinate birds (blue tits, females a

277 ter alcohol binge drinking and in mice after binge or chronic alcohol consumption.

278 , which was assessed for harmful patterns of binge or frequent drinking.

279 pment of alcohol use disorder (AUD) involves binge or heavy drinking to high levels of intoxication t

280 trial fibrillation (AF) following an alcohol binge or the "holiday heart syndrome" is well characteri

281 Rates of abstention mirrored trends in binge outcomes for both sexes, limiting concerns about i

282 trocytes, and microglia) following a cocaine binge paradigm.

283 iagnosis of anorexia nervosa (restricting or binge-purging subtype) and a demonstrated history of chr

284 HFF binge rats consumed significantly greater calories relat

285 Compulsive eating characterizes many binge-related eating disorders, yet its neurobiological

286 ation between moderate lifetime drinking and binging (relative excess risk due to interaction = 0.33,

287 In addition, the 3-day cocaine binge significantly reduced [(11)C]GR103545 binding by 1

288 tes, to cause loss or creation of new ligand binging sites and to alter post-translational modificati

289 After 2 weeks of daily alcohol binges, synaptic plasticity was profoundly altered.

290 porter sites may be efficacious in promoting binge termination following relapse.

291 l three risk factors had the highest rate of binging throughout the session compared with the lowest

292 1.37) were associated with a higher rate of binging throughout the session.

293 ergic interneurons were subjected to a 3 day binge-type 5% w/w ethanol consumption regimen from embry

294 ession in the VTA tunes ethanol intake under binge-type conditions: the more GIRK3, the less ethanol

295 ntrol deficits associated with addiction and binge-type eating disorders.

296 First, we demonstrate that a time-delimited binge-type ethanol exposure in utero during early gestat

297 Our binge-type regimen increased the density of MGE-derived

298 lated cocaine self-administration in a 24 h "binge." VTA CRF continues to influence cocaine seeking i

299 Project, we identified 177 young adults who binged weekly and 309 nonbingers.

300 nge in KOR binding following a 3-day cocaine binge, which is thought to represent a change in endogen