ライフサイエンスコーパス: body weight

1 s (final weight ~6 kg, close to the animal's body weight).

2 ndamental role in the control of feeding and body weight.

3 sucrose seeking, ad libitum food intake, or body weight.

4 same dose regardless of the patients' age or body weight.

5 eflect chemically-induced changes in overall body weight.

6 dose of 2x10(6) CAR T cells per kilogram of body weight.

7 l at 3.0 T at a dose of 4 mg per kilogram of body weight.

8 abilized glucose tolerance without affecting body weight.

9 p time for transplantation is not related to body weight.

10 is, and gene-ethnicity interactions on human body weight.

11 OSNs impact larval feeding behavior and its body weight.

12 als who diet and exercise maintain a healthy body weight.

13 e compensatory feedback mechanisms to defend body weight.

14 reased consumption, thereby achieving stable body weight.

15 the LD(50) of LNCs was higher than 100 mg/kg body weight.

16 ng sex, race, income, physical activity, and body weight.

17 ain insight into the mechanisms that control body weight.

18 s were normalized to infant daily intake and body weight.

19 days post-injury at a dose level of 4 mg/kg body weight.

20 lanocortin (POMC)-producing neurons regulate body weights.

21 3877) showed that viscous fiber reduced mean body weight (-0.33 kg; 95% CI: -0.51, -0.14 kg; P = 0.00

22 erienced mean greater increases of 2.1 kg in body weight, 0.8 kg/m2 in BMI, 1.4% in PBF, and 2.0, 1.9

23 Significant between group decreases in body weight (1.3 kg, p < 0.0001), BMI (0.045 kg/m(2), p

24 in the intensive-lifestyle group (change in body weight, -4.99%; 95% confidence interval [CI], -6.02

25 from all trials on blood lipids, 8 trials on body weight, 5 trials on percentage body fat, 4 trials o

26 hort and the recent cohort (combined cohort, body weight 6.3%, BMI 3.6%).

27 inadequately controls for the dependence on body weight - a point made by statisticians for decades,

28 d a more rapid improvement, with recovery of body weight, a dramatic improvement in pulmonary functio

29 otein intake was 0.94 +/- 0.36 g/kg adjusted body weight (aBW)/d in men and 0.95 +/- 0.36 g/kg aBW/d

30 ern diet, Atp7b (-/-) mice exhibited reduced body weight, adiposity, and hepatic steatosis compared w

31 lizumab (at a dose of 0.5 mg per kilogram of body weight) administered subcutaneously at baseline, we

32 l experience and how an experimentally added body weight affects this process.

33 CP diets, but 12% CP significantly decreased body weight after day 21.

34 (6), or 1x10(7) CAR-NK cells per kilogram of body weight) after lymphodepleting chemotherapy.

35 e, omalizumab dosages should be adjusted for body weight alone, independently of total IgE level.

36 ed males early in life led to an increase in body weight, an effect that persisted across life even w

37 factors that contribute to the regulation of body weight, an important first step is to establish the

38 severity also directly correlated to leptin, body weight and adiposity.

39 lthood whereas the small RNA fraction alters body weight and behavioural despair.

40 ontent, fat absorption, chymotrypsin levels, body weight and blood vitamin and glucose levels were de

41 iry was associated with greater increases in body weight and BMI [e.g., for high-fat dairy: beta = 0.

42 Men with information on prepubertal body weight and BMI at 8 y of age and age at peak height

43 ty phenotype of EC-AGO1-KO, evident by lower body weight and body fat, improved insulin sensitivity,

44 tion was associated with a lower increase in body weight and body mass index (BMI).

45 diuretic clearance, the diuretic effects on body weight and BP at lower eGFR were maintained.

46 review is to summarize the effects of TRE on body weight and cardiometabolic disease risk factors in

47 Body weight and composition (4-compartment model) and RM

48 Il10 mRNA in intestine tissues, and reduced body weight and death from neonatal sepsis.

49 IHTG by 31% in the face of a 3% decrease in body weight and decreased hepatic insulin resistance (-5

50 ractions mediate the genetic contribution to body weight and diabetes risk.

51 LP-1R agonists achieves greater reduction in body weight and fat mass than monotherapies by promoting

52 ally modified mice gained significantly less body weight and fat mass when on high-fat diets compared

53 Using body weight and feed intake data for Iberian lynx (Lynx

54 the POMC(ARH)->VTA circuit in mice increases body weight and food intake, and reduces depression-like

55 low up for approx. 180 weeks showed a stable body weight and health state of the animals with normal

56 ereas N-ERalphaKO females exhibited a higher body weight and increased body and bone length compared

57 The relationship between body weight and lung function is complex.

58 ture, are in fact a normalization to a lower body weight and not drivers of weight regain.

59 erventions resulted in a similar decrease in body weight and NT-proBNP.

60 Rgs4 gene locus is associated with increased body weight and obesity susceptibility phenotypes, and t

61 6x10(12) vector genomes [vg] per kilogram of body weight and one who had received 2x10(13) vg per kil

62 us fiber modestly yet significantly improved body weight and other parameters of adiposity independen

63 PV was defined as Vt <=8 ml/kg predicted body weight and positive end-expiratory pressure >=8 cm

64 ral administration increased food intake and body weight and preserved fat mass and lean mass during

65 dpoints were percent change from baseline in body weight and proportion of patients with >=10% weight

66 flozin also caused significant reductions in body weight and serum urate at week 6.

67 in the regulation of energy expenditure and body weight and suggest that VSG can improve alterations

68 PA reduced the body weight and systolic blood pressure, lowered fasting

69 e knockout strain for FOXI3 revealed smaller body weights and relatively lower thymus weights in hete

70 n for 45 days (3 injections of LAmB, 5 mg/kg body weight, and 100 mg/day MIL).

71 ow-fat dairy on glycated hemoglobin (HbA1c), body weight, and cardiovascular disease risk factors in

72 ively related to mission duration, preflight body weight, and clinical manifestations of SANS.

73 mice impaired glucose homeostasis, increased body weight, and decreased energy expenditure without ch

74 o 31 QTLs for milk yield and its components, body weight, and residual feed intake traits.

75 ci (QTLs) for milk yield and its components, body weight, and residual feed intake within 1 Mb of sig

76 s relapse or a normalization towards a lower body weight, and to explore alternative hypotheses that

77 g-term leptin treatment reduces fat mass and body weight, and transiently alters circulating free fat

78 sed mice, however, had high nest scores, low body weights, and increased sucrose and food consumption

79 lecular mechanisms by which metformin lowers body weight are unknown.

80 come was the percent change from baseline in body weight at 24 months.

81 the simplified measures, SUV normalized for body weight at 50 and 67 min after injection correlated

82 he energy balance equation that try to bring body weight back to its original state: this is the Comp

83 Both body weight (beta: -0.24 SD/SD increase in weight; 95% C

84 o significant differences in food intake and body weight between all groups.

85 ed no relationship between the similarity in body weight between the dog pairs and the overall accura

86 enase 2 (COX2) inhibitor ibuprofen (30 mg/kg body weight) blocked tooth injury-induced bone loss in S

87 trically with CO-EtOAc for last 6 weeks, and body weight, blood biochemical parameters as well as hep

88 arrow transplantation did not further affect body weight, blood pressure, creatinine, or hematocrit i

89 no differences in the mean changes in HbA1c, body weight, BMI, body composition or lipid parameters,

90 We evaluated HbA1c, body weight, BMI, body composition parameters, blood pre

91 Primary outcomes were changes in body weight, BMI, waist circumference (WC), waist-to-hei

92 and quantify the effects of viscous fiber on body weight, BMI, waist circumference, and body fat, ind

93 was associated with significant increases in body weight, body circumferences, and fat percentages, c

94 ated at 0, 6, and 12 weeks, including HbA1c, body weight, body composition by dual-energy X-ray absor

95 atified to either VSG or sham surgery before body weight, body composition, diet preference, and gluc

96 aining energy intake has no effect on HbA1c, body weight, body composition, lipid profile, or BP.

97 collected data on age, sex, race/ethnicity, body weight, body mass index (BMI), diabetes, smoking st

98 Body weight, body mass index (BMI), percentage body fat

99 enta, C57BL6J mouse dams were fed 200 mug/kg body weight BPA or BPS daily for 2 wk and then bred.

100 s of dietary protein restriction on reducing body weight, but not on improving insulin sensitivity in

101 effects including increased food intake and body weight, but the underlying mechanisms remain unknow

102 he primary outcomes were 12-month changes in body weight (BW) and body fat percentage (BF%).

103 t kisspeptin signaling is also important for body weight (BW) and metabolism.

104 breaking point between the 25 and 250 mug/kg body weight (BW) per day doses.

105 s fed with LP had lower feed intake (FI) and body weight (BW) throughout the study, but those fed wit

106 ein intake recommendations advise >=0.8 g/kg body weight (BW)/d, whereas experts propose a higher int

107 of BPA [0, 25, 250, 2,500, or 25,000 mug/kg body weight (BW)/d] or 2 doses of 17alpha - ethynylestra

108 /d was associated with a smaller increase in body weight by 0.23 kg (95% CI: -0.46, -0.01 kg).

109 , administration of exogenous rGDF11 reduced body weight by 3-17% and significantly improved glucose

110 e that bilirubin strongly affects organismal body weight by reshaping the PPARalpha coregulator profi

111 (36 or 74 mg gallic acid equivalent (GAE)/kg body weight) by gavage from week 6 to week 14 (end-point

112 parameters showed no significant changes in body weight, cell blood count, nor plasma biomarker indi

113 Body weight change was described by using linear mixed m

114 um; disease severity was determined based on body weight, colon length, and histopathology analysis o

115 nce, delayed gastric emptying, and increased body weight compared to controls.

116 21 and APS20 recorded the highest (P < 0.05) body weight compared to other treatments, but it was not

117 Postdiagnosis weight gain (> 5% of body weight), compared with stable weight (+/- < 3%), wa

118 Body weight/composition and RMR were measured at baselin

119 riction of energy intake, leading to lowered body weight, constant fear of gaining weight, and psycho

120 Offspring were assessed for body weight; cortical volume, gene expression, and cellu

121 Then melatonin (10 mg/kg body weight/day, 14 days), and the vehicle was administe

122 posure was measured in dose area product per body weight (dose area product/kg; uGy*m(2)/kg) and repo

123 ured outcomes include behavioral assessment, body weight, dual-energy X-ray absorptiometry (DEXA) for

124 nally, we found that, when mice had elevated body weight due to chronic G(q) signaling in AgRP neuron

125 This work reconciles the similar preclinical body weight effects of GIPR antagonists and agonists in

126 erage contemporary group effects on yearling body weight equal to 159.40, 228.6 and 297.6 kg, respect

127 difference, -4.64 percentage points) and for body weight (estimated difference, -4.50 kg [for absolut

128 vinacumab at a dose of 15 mg per kilogram of body weight every 4 weeks (39 patients) or 5 mg per kilo

129 venously at a dose of 1000 U per kilogram of body weight every 48 hours for a total of six doses, fol

130 inacumab (at a dose of 15 mg per kilogram of body weight) every 4 weeks or placebo.

131 Body weight explained more of the variance in age at PHV

132 ormally present in males resulted in reduced body weight, fat content, and food intake to a degree si

133 nistered weekly (each molecule at 1 mg/kg of body weight), followed 2 days later by AZD5582 (0.1 mg/k

134 cid (TUDCA) causes long-term amelioration of body weight, food intake, glucose homeostasis, and pro-o

135 Wounds, body weights, food consumption, nest scores, sucrose con

136 ly 5-kg/m2 lower BMI (approximately 14 kg of body weight for a 1.7-m-tall person) than those with a h

137 There were no influences of body weight for efficacy, safety, and immunological resp

138 nhibitor teprotumumab (10 mg per kilogram of body weight for the first infusion and 20 mg per kilogra

139 57BL/6 mice were administered with UA (10 mg/body weight) for 12-16 weeks.

140 e meglumine (0.6 or 2.5 mmol per kilogram of body weight), gadodiamide (0.6 or 2.5 mmol/kg), or salin

141 of male breeders reduced their week-on-week body weight gain and altered NR3C1 and CRH gene expressi

142 tected diet-induced obese (DIO) mice against body weight gain and improved multiple metabolic paramet

143 neurons is necessary for protection against body weight gain and induction of UCP1 in adipose tissue

144 ised C57BL/6J-mouse dams were protected from body weight gain and NAFLD in adulthood (postnatal day (

145 howed no significant changes in food intake, body weight gain and relative weight of vital organs.

146 MFGM-PL treatment to HFD dams decreased the body weight gain and WAT mass as well as lowered the ser

147 f body weight, we found that the decrease in body weight gain in mice treated with metformin is not d

148 The risk of poor body weight gain increased in FPIES triggered by cow's m

149 eatment groups consistently displayed higher body weight gain than the untreated chicks.

150 ced the formation of hepatic lipid droplets, body weight gain, blood glucose, and improved serum bioc

151 ss of CTR in POMC neurons leads to increased body weight gain, increased adiposity, and glucose intol

152 CBC reduced body weight gain, inflammation, hepatic steatosis, hyper

153 -biased skin inflammation before significant body weight gain.

154 and banana as triggers were at risk of poor body weight gain.

155 ity, family history, food aversion, and poor body weight gain.

156 ar dose, as seen by longer survival, greater body-weight gain and better preservation of motor neuron

157 mice fed a chow diet presented with blunted body-weight gain over time, had lower fat mass, and were

158 sufficient to protect mice from diet-induced body-weight gain.

159 glycemic efficacy and ability to reduce the body weight, glucagon-like peptide 1 receptor (GLP-1R) a

160 ertainty of evidence was graded moderate for body weight, high for waist circumference and body fat,

161 gest that it acts developmentally to program body weight homeostasis.

162 gest that it acts developmentally to program body weight homeostasis.

163 ssessed in relation to effects on metrics of body weight, hyperlipidemia, and glucose tolerance.

164 These changes are associated with higher body weight, hyperlipidemia, and severe insulin and gluc

165 s tissue (IEQ/g) and digest IEQ per kilogram body weight (IEQ/kg), using multiple regression to adjus

166 his ABA-enriched extract, at 0.125 ug ABA/kg body weight, improves glucose tolerance, insulin sensiti

167 butable to the ability of metformin to lower body weight in a sustained manner(3).

168 An association between body weight in adolescence and future cardiomyopathy amo

169 To assess the polygenic contribution to body weight in carriers of normal weight and carriers wi

170 e (HDM) SLIT-tablet treatment in relation to body weight in children.

171 se-stimulated insulin secretion and decrease body weight in diet-induced obese (DIO) mice.

172 vation of neuronal ERalpha did not alter the body weight in males, whereas N-ERalphaKO females exhibi

173 ng significant reductions in food intake and body weight in mice.

174 ) rate should be prescribed based on patient body weight in millilitres per kilogramme per hour with

175 take, improved glucose profiles, and reduced body weight in mouse models of type 1 and 2 diabetes.

176 R) agonists effectively improve glycemia and body weight in patients with type 2 diabetes and obesity

177 ignaling within peripheral immune cells, and body weight in pigs provide both evidence and insight in

178 ody weight-sensing homeostatic regulation of body weight in postpubertal rodents and humans.

179 increases insulin sensitivity and decreases body weight in rodents.

180 tional supplements, was reported to increase body weight in some trials, but evidence remains limited

181 e leads to enlarged adipocytes and increased body weights in transgenic mice.

182 ociated with improvements in appetite and/or body weight include progesterone analogs and corticoster

183 Body weight, insulin resistance (homeostatic model asses

184 of either tocilizumab (8 mg per kilogram of body weight intravenously) or placebo.

185 In conclusion, prepubertal body weight is a more robust inverse predictor of pubert

186 weight hypothesis and tested if prepubertal body weight is a more robust inverse predictor of pubert

187 Body weight is a potential contributing risk factor.

188 Maintaining healthy body weight is increasingly difficult in our obesogenic

189 Body weight is regulated by interoceptive neural circuit

190 ween the salivary microbiome composition and body weight is unclear.

191 UV at 60 min after injection, normalized for body weight, is an accurate simplified parameter for upt

192 changes in individual histological features, body weight, liver enzymes, dyslipidemia, markers of oxi

193 In the training set of 61 patients, excess body weight loss >95% (odds ratio [OR] 6.73, 95% confide

194 uten-dependent enteropathy (in model 3), and body weight loss (in model 3).

195 The primary endpoint was 6-month total body weight loss (TBWL).

196 racteristics, YAC84Q mice showed a rescue of body weight loss and extended survival upon calpain-1 kn

197 le obese mice, but did not affect CL-induced body weight loss in male or female obese mice.

198 I of 34.07 +/- 3.73 kg/m, representing total body weight loss of 25.13 +/- 4.44% and excess weight lo

199 describe salivary microbiome changes during body weight loss on an individual-specific level, and to

200 preoperative requirements were met: 7% total body weight loss or 6 months of counseling and no weight

201 -wk low-calorie diet (LCD) resulting in >=8% body weight loss, during which changes in body compositi

202 0 mg/kg daily o.s.) was able to decrease the body weight loss, macroscopic damage, colon length, hist

203 allenge, though they experienced viremia and body weight loss.

204 ctor VIII at a dose of 25 IU per kilogram of body weight (lower-dose group) or 65 IU per kilogram (hi

205 were evaluated post hoc in three subgroups (body weight < 30kg, 30-44kg, >= 45kg) of patients from a

206 its beneficial effects on energy balance and body weight, major contributors to its action as a chemo

207 le interventions (regular physical exercise, body weight management and healthy dietary patterns), as

208 ion models were used to jointly analyse live body weight measured in different time points throughout

209 er 14 days, no evidence of adverse effect on body weight, mortality and clinical signs were observed.

210 oup) or a tidal volume of 10 mL/kg predicted body weight (n = 592; conventional tidal volume group).

211 receive a tidal volume of 6 mL/kg predicted body weight (n = 614; low tidal volume group) or a tidal

212 ve gadolinium dose, 7.2 mmol per kilogram of body weight; n = 6) or saline (n = 6) was examined with

213 we describe a novel way to manage excessive body weight; namely, prescribing personalized diets with

214 as provided to match the reduction in EI and body weight observed in eTRF.

215 lation to a maximum of 20 mg per kilogram of body weight occurred in 22 participants.

216 DA SGK1 KO significantly decreased body weight of adult mice as well as increased general l

217 e administration of 0.2 mmol per kilogram of body weight of gadobenate dimeglumine, with 19 patients

218 teparin (at a dose of 200 IU per kilogram of body weight once daily for the first month, followed by

219 hole-body REE was higher, without changes in body weight or composition.

220 gron to human subjects was without effect on body weight or fat mass, but improved several measures o

221 Energy expenditure adjusted for body weight or lean mass was increased (P < .05) in male

222 EC gene number in 26 species, independent of body weight or phylogeny.

223 at a dose of 1.00 to 1.25 mg per kilogram of body weight) or placebo for at least 48 weeks.

224 efalin (at a dose of 0.5 mug per kilogram of body weight) or placebo three times per week for 12 week

225 a dose of 1.0 up to 1.75 mg per kilogram of body weight) or placebo, administered subcutaneously eve

226 of either tocilizumab (8 mg per kilogram of body weight) or placebo.

227 80, 100 and 120 steps min(-1), normalised to body weight (p > 0.05).

228 ed dose (approximately 20 mg per kilogram of body weight per day) with dose escalation (approximately

229 mount of glucose metabolized per kilogram of body weight per minute (Mbw) assessed during steady-stat

230 y, single dose (50, 300, 1000 and 2000 mg/kg body weight) pigment was administered to female Wistar r

231 elor in elderly patients or those with a low body weight presenting with an acute coronary syndrome (

232 TG was accompanied by an increased LV weight/body weight ratio and LV end diastolic volume (WT, 50.8

233 ere were no significant differences in organ/body weight ratio for most of the organs, the testis/bod

234 alculate the relative organ weight (organ to body weight ratio), but this inadequately controls for t

235 examination of internal organs and organ-to-body weight ratio.

236 hile CDH fetuses undergoing TO had a lung-to-body-weight ratio comparable to that of controls (2.5 +/

237 The lung-to-body-weight ratio was significantly reduced in sham-CDH

238 nificantly reduced lung-, heart-, and liver: body weight ratios and prevalence of ascites in 8 rabbit

239 ficantly increased lung-, heart-, and liver: body weight ratios, and decreased I(p) relative to that

240 OT-12 exhibited more potent anorexigenic and body weight reducing effects than carbetocin.

241 evealed a nonlinear inverse relation between body weight reduction and gastric volume, confirming tha

242 The effects of oxytocin on food intake and body weight reduction have been demonstrated in both ani

243 tumor growth inhibition with acceptable host body weight reduction is therefore needed.

244 taneous BFKB8488A injection caused transient body weight reduction, sustained improvement in cardiome

245 Stratification identified greater body weight reductions in overweight subjects (1.88%, p

246 enting other innate mechanisms implicated in body weight regulation.

247 d in the nanoparticle-treated mice and their body weight remained stable.

248 Maintaining a healthy body weight requires an exquisite balance between energy

249 returned to baseline levels within 1 wk, and body weight returned to baseline levels within 60 d.

250 In subacute-toxicity of LNCs (1 and 10 mg/kg body weight) revealed no mortality with no morphological

251 e-toxicity of LNCs (0.1, 1, 10 and 100 mg/kg body weight) revealed that the LD(50) of LNCs was higher

252 Mice were administered 3 mug/kg of body weight RvD1 intraperitoneally on days 5, 10, and 15

253 It is possible that body weight sensing also might be involved in the regula

254 We propose that body weight sensing constitutes a feedback mechanism to

255 Recent findings indicate that there is a body weight-sensing homeostatic regulation of body weigh

256 lts showed that: (1) subjects with increased body weight showed significantly higher BP, BFM, total b

257 y, 28 days sub-acute studies (250-1000 mg/kg body weight) showed no significant changes in food intak

258 On normal chow, IRMOE mice have body weight similar to that of controls but an increase

259 incidence of ADRs was decreased in the lower body weight subgroup.

260 Surprisingly, lesions did not alter body weight, suggesting that this system is not involved

261 e allele mutants are fertile and have normal body weights, suggesting a high degree of redundance for

262 Body weight, systemic blood pressure, and ocular perfusi

263 efore administering streptozotocin, 30 mg/kg body weight (T2D), and compared with age- and duration-m

264 ts for 8 months, during which energy intake, body weight, the onset of diabetes circulating hormones,

265 s been shown to reduce food intake and lower body weight through a brain-stem-restricted receptor.

266 ing that they might exert their influence on body weight through eating-related behaviors.

267 depth percentage, implantation cell number, body weight, tissue source, and the type of cartilage da

268 The mechanisms linking age and body weight to cancer are incompletely understood, but r

269 han 80% 6-month survival rate and comparable body weight to control mice.

270 ve approach to reduce excess fat storage and body weight to improve metabolic health.

271 ad libitum or food restricted to match their body weight to VSG-operated mice.

272 g the removal of ligatures, melatonin (10 mg/body weight) to Ep-Mel group, and vehicle (saline) to Ep

273 fusion (cohort A), or 2 x 10(6) cells per kg body weight, to a maximum dose of 2 x 10(8) cells per in

274 dose level of either 1 x 10(6) cells per kg body weight, to a maximum of 1 x 10(8) cells per infusio

275 mean), SUV(peak), and SUV(max) normalized to body weight; tumor volume; and total lesion uptake (TLU)

276 non-toxic IV dose of the INPs (7 g iodine/kg body weight), tumors showed a heavily iodinated rim surr

277 esity, but it does not affect food intake or body weight under normal chow consumption.

278 tibodies reduce blood glucose, appetite, and body weight, validating asprosin as a therapeutic target

279 the genetic effects of smoking cessation on body weight vary from different populations.

280 metabolic receptors modulate food intake and body weight via reciprocal functional interactions.

281 one of the specific BSH inhibitors (25 mg/kg body weight) via oral gavage for 17 days.

282 After 6 mo, body weight, waist circumference (WC), systolic and dias

283 25(OH)D and body weight were assessed, while body weight was assessed again at a later date.

284 ence was below the third percentile, and his body weight was at the 10th percentile.

285 Body weight was not a clinically relevant predictor of c

286 The body weight was not different between the CON and 18% CP

287 ated with age at PHV but the association for body weight was significantly more pronounced than the a

288 Successful weight loss (-11+/-5% body weight) was associated with improvement of these en

289 (68)Ga-NeoBOMB1 (3 MBq/kg of body weight) was injected intravenously, and safety para

290 of smoking on genetic architecture of human body weight, we conducted a genome-wide association stud

291 ls, metformin treatment leads to the loss of body weight, we found that the decrease in body weight g

292 und the time of diagnosis, serum 25(OH)D and body weight were assessed, while body weight was assesse

293 dapted to conditions and maintained a stable body weight were characterized as resilient.

294 al study, 43 subjects of normal or increased body weight were examined in order to determine the corr

295 Greater reductions in body weight were observed in overweight individuals and

296 fat diet, the effects of metformin to reduce body weight were reversed by a GFRAL-antagonist antibody

297 Body weights were measured, and fecal, blood, and liver

298 yopathy, starting already at mildly elevated body weight, whereas severe obesity entailed an almost 5

299 We found that cADORA(1) signaling reduces body weight while also inducing adipose tissue lipolysis

300 of LS(Nts) neurons decreases food intake and body weight, without altering locomotion and anxiety.