ライフサイエンスコーパス: body weight

1 erage weight loss of 10.5 kg (10% of initial body weight).

2 most important common genetic determinant of body weight.

3 that potently inhibit food intake and reduce body weight.

4 e growth of individual tissues and organs to body weight.

5 d serum corticosterone, as well as decreased body weight.

6 t, these mice displayed decreased growth and body weight.

7 er by total daily dose or adjusted (Adj) per body weight.

8 tion and a drive to accumulate adiposity and body weight.

9 estimated human lethal dose of 0.1-1 mug/kg body weight.

10 s, corresponding to 27.7% reduction in total body weight.

11 ary to other factors that determine abnormal body weight.

12 ed that there is a homeostatic regulation of body weight.

13 Free sugars had no effect on body weight.

14 oss of FTO leads to decreased brain size and body weight.

15 ment significantly decreased food intake and body weight.

16 stological colitis scores, and increased the body weight.

17 cause malnutrition and a severe reduction in body weight.

18 ression, smoking, personality, cognition and body weight.

19 t inhibition of tumor growth without loss in body weight.

20 ed using 2 formulas based on ideal or actual body weight.

21 ight loss corresponding to 10-15% of initial body weight.

22 ucing tidal volume back to 6 mL/kg predicted body weight.

23 rs too, such as increased blood pressure and body weight.

24 action, leading to increased food intake and body weight.

25 n children with overweight/obesity or reduce body weight.

26 nduced a robust reduction in food intake and body weight.

27 and energy expenditure with no net effect on body weight.

28 JNK1/2/3) inhibitor, reduced food intake and body weight.

29 is induces an afferent signal, which reduces body weight.

30 08 mmol/L; 95% CI: -0.14, -0.02 mmol/L), and body weight (-1.40 kg; 95% CI: -2.07, -0.74 kg).

31 ssociated with surprisingly small changes in body weight [1-4].

32 reated with different levels of activity per body weight (10, 15, and 20 MBq/kg).

33 in the medical-therapy group with respect to body weight (-23%, -19%, and -5% in the gastric-bypass,

34 tries of kidney, spleen and liver weights to body weight, 36 of which were imprinted with different i

35 body weight (7.0-9.1) to 6.4 mL/kg predicted body weight (6.1-6.7) and an increase in lung-protective

36 rtment tidal volume from 8.1 mL/kg predicted body weight (7.0-9.1) to 6.4 mL/kg predicted body weight

37 ression in bone, normal postnatal growth and body weight acquisition compared to the littermate contr

38 diet-induced obesity regimens, CR decreased body weight, adiposity, and serum metabolic hormones as

39 x10(6) anti-CD19 CAR T cells per kilogram of body weight after receiving a conditioning regimen of lo

40 in healthy adults while maintaining subject body weights.After a 2-wk provided-food run-in period of

41 ext of a weight-reducing diet did not affect body weight among adolescents with overweight or obesity

42 the association between food insecurity and body weight among adult women, but not to the results ab

43 Toxicity was determined by monitoring body weight, analyzing blood samples for hematologic and

44 or, impaired glucose homeostasis, and higher body weight and abdominal adipose tissue weight were obs

45 ietary MR produced a comparable reduction in body weight and adiposity in both genotypes because of a

46 abolic dysfunction as reflected by increased body weight and adiposity index in adult male offspring

47 between whole-grain consumption and reduced body weight and adiposity.

48 end points included change from baseline in body weight and adverse events.

49 med at tidal volumes 6 and 8 mL/kg predicted body weight and after reducing tidal volume back to 6 mL

50 ur data identify GFRAL as a new regulator of body weight and as the bona fide receptor mediating the

51 ed to statistically significant decreases in body weight and body fat percentage.

52 Secondary end points included change in body weight and cardiometabolic parameters.

53 t of dietary advice and/or food provision on body weight and cardiovascular disease risk factors.

54 a high-fat diet, although no differences in body weight and composition were observed, Lin28aKI(VMH)

55 d mice, HFD-fed mice had a rapid increase in body weight and fat mass and specifically showed an incr

56 sion did not influence high fat diet-induced body weight and fat mass gain throughout the study.

57 e metabolic actions of GDF15 with respect to body weight and food intake in vivo in mice.

58 Body weight and food intake were monitored daily.

59 and MBH TRPC3-deficient mice have increased body weight and food intake.

60 A relationship between body weight and gastric emptying as well as self-reporte

61 Food intake, body weight and glucose handling were assessed, together

62 4R genotype affected longitudinal changes in body weight and glucose metabolism biomarkers among wome

63 Gpr119(-/-) mice displayed normal body weight and glucose tolerance on a regular chow (RC)

64 lucose tolerance independently of changes in body weight and glucose-induced insulin response.

65 h diet resulted in a significant increase in body weight and impairments in their working memory toge

66 Individuals can lose body weight and improve health status on a wide range of

67 g of myostatin and GDF11, regulates not only body weight and muscle size, but also inhibits neuromusc

68 bese (ob/ob) mice suppresses food intake and body weight and normalizes locomotor activity.

69 nografts without having a negative effect on body weight and showing any sign of clinical toxicity.

70 ved metabolic profile in addition to reduced body weight and total adiposity.

71 heralding improved glycemic control, reduced body weight and total daily insulin dose without an incr

72 persistently elevate ingestive behavior and body weight and ultimately resulted in a doubling of fat

73 chain n-3 PUFAs and subsequent 5-y change in body weight and waist circumference in humans.

74 respectively, (P = 0.048)].There are greater body weight and WC reductions in risk carriers than in n

75 e initial program, 222 lost at least 4 kg of body weight and were randomly assigned to maintenance (n

76 ing lower tidal volumes (4-8 ml/kg predicted body weight) and lower inspiratory pressures (plateau pr

77 ratory lung volume (30.4 +/- 9.1 mL/kg ideal body weight) and oxygenation (273.4 +/- 72.1 mm Hg).

78 Low tidal volume (2.9-4 ml/kg ideal body weight) and poor compliance (12.1-18.7 ml/cm H2O) w

79 ed a low dose (6.7x10(13) vg per kilogram of body weight), and 12 received a high dose (2.0x10(14) vg

80 ravenously with MBKDR (0.03 to 0.08 mL/kg of body weight), and USMI of the lesions was performed star

81 ric disorder presenting with dangerously low body weight, and a deep and persistent fear of gaining w

82 reduces glycemia as well as blood pressure, body weight, and albuminuria in people with diabetes.

83 oidance, anxiety-like behavior, reduction of body weight, and elevated levels of circulating interleu

84 f SGLT2 inhibitors to reduce blood pressure, body weight, and fluid retention as well as to improve r

85 ay mediate postoperative changes in satiety, body weight, and gastrointestinal quality of life.

86 ificantly reduced liver fat independently of body weight, and reduced markers of insulin resistance a

87 Remarkably, although food intake, body weight, and systemic insulin sensitivity were still

88 d the impact of intervention on food intake, body weight, and visceral adipose tissue (VAT) mass; pla

89 or risk factors, baseline lipid levels, mean body weight, and weight change, each increase of 1 SD in

90 However, the predicted body weight approach is imperfect in patients with ARDS

91 avoidance of hypoglycemia and the control of body weight are attractive despite its poor stability.

92 explanation of how food intake behavior and body weight are regulated by endogenous central GLP-1.

93 ters with increased adiposity, FGF21 lowered body weight as a result of both reduced daily food intak

94 istic rationale to prevent or reverse excess body weight as a strategy to reduce HER2-positive breast

95 After return to the same body weight as chow fed control mice, the fasting insuli

96 ficant decrease in the gain of adiposity and body weight as well as an improvement in glucose and ins

97 10% initial weight loss.Regainers had higher body weight at year 4 than did maintainers (mean differe

98 ration of GDF15 to mice with obesity reduces body weight, at least in part, by decreasing food intake

99 6) or ustekinumab (45 or 90 mg, according to body weight, at weeks 0, 4, and 16).

100 wer Vts, the use of Vts of 6 ml/kg predicted body weight (based on sex and height) has been recommend

101 tered PGT121 or 3BNC117 at 10 and 2 mg/kg of body weight before being rectally challenged with a sing

102 Body weights, blood glucose levels were monitored throug

103 Body weight, body composition, energy expenditure, food

104 Possible associations of age, body length, body weight, body surface area, and heart rate on PAAT w

105 hibition with canagliflozin decreases HbA1c, body weight, BP, and albuminuria, implying that canaglif

106 LH-21 did not affect food intake nor body weight but it improved glucose handling, displaying

107 These reductions were unrelated to change in body weight, but correlated with down-regulation of lipo

108 those faunal species that match our typical body weight, but significantly lower than a range of fau

109 obesity risk factor increased significantly body weight (BW) and adiposity, with additive effects af

110 We measured HVPG, body weight (BW) and composition, adipokines, health-rel

111 We found that changes in body weight (BW) and waist circumference (WC) were signi

112 -knockout (Tia1 (-/-)) mice gain significant body weight (BW) during early postnatal development.

113 d 2 years in this population is 0.104 mug/kg body weight (BW)/day.

114 rs in this population is [Formula: see text] body weight (BW)/day.

115 = 1.07-1.35), and people who increased their body weight by 10 kg or more had an RR of 1.72 (95% CI =

116 raditional view of homeostatic regulation of body weight by mainly the hypothalamus to include hedoni

117 ndicate that MANF influences food intake and body weight by modulating hypothalamic insulin signaling

118 regulation of muscular lipid metabolism and body weight by repressing estrogen receptor alpha (ERalp

119 de (cumulative dose, 12 mmol per kilogram of body weight) by using inductively coupled plasma-mass sp

120 th reduced adiposity, the effect of FGF21 on body weight, caloric intake and fat oxidation were signi

121 constituents when considering the effects on body weight, cardiometabolic disease risk, and bone heal

122 mediator have yielded somewhat disappointing body weight changes, often leading to the hormone/mediat

123 le grains for refined grains, independent of body weight changes, on energy-metabolism metrics and gl

124 insulin resistance and bone metabolism, and body weight changes.

125 JAK2 knockout (M-JAK2(-/-)) mice gained less body weight compared to wildtype littermate control (M-J

126 ffects translate into long-term benefits for body weight control and insulin sensitivity in the obese

127 (GLP-1R), which are critical to feeding and body weight control, we tested the hypothesis that PVT G

128 portance of systemic inhibition of DGAT1 for body weight control.

129 ein diets (HPDs) are frequently consumed for body-weight control, little is known about the consequen

130 t gain and promoting maintenance of a normal body weight could reduce incidence of psoriasis.

131 w point, and temperature) and self-monitored body weight data simultaneously.

132 Results In the dietary group, fat intake and body weight decreased (all P < .001).

133 pecific differences in muscle metabolism and body weight development.

134 HFD resulted in higher body weight, development of insulin resistance, lower br

135 tained during tidal volume 6 mL/kg predicted body weight did not predict fluid responsiveness.

136 rphyrin IX significantly reduces the loss of body weight due to hRSV-induced disease.

137 index >/=30 kg/m2) who lost 4 kg or more of body weight during a 16-week, group-based weight loss pr

138 oride (CH3HgCl) (0, 0.125, 0.5, or 2.0 mg/kg body weight each) 4 days before and 4 days after concept

139 y 87 and 69%, respectively, without altering body weight, energy expenditure, respiratory quotient, o

140 vascular lung water was indexed to predicted body weight (EVLWPBW).

141 e to BPA affect the obesity-related outcomes body weight, fat (pad) weight, and circulating and tissu

142 icant, albeit clinically modest, benefits on body weight, fat mass, and markers of oxidative stress a

143 Fenugreek did not alter body weight, fat mass, or food intake in either group, b

144 Body-weight fluctuation is a risk factor for death and c

145 Body weight, food intake, adiposity index, fasting insul

146 t salmon calcitonin dose-dependently reduces body weight, food intake, and motivated feeding behavior

147 ion, we extracted information on weather and body weight for each user located in each of several geo

148 e determined intraindividual fluctuations in body weight from baseline weight and follow-up visits an

149 in-expressing astrocytes induced exaggerated body weight gain and glucose intolerance in mice exposed

150 atory ratio controlled inflammation, reduced body weight gain and protected from hyperglycemia on hig

151 or fluid intake, physical activity levels or body weight gain in the rat, whereas it depleted muscle

152 y 9 was found to be effective in suppressing body weight gain relative to control in a diet-induced o

153 ranosyl cytidine (AraC) blunted food intake, body weight gain, and adiposity.

154 TRF prevents excessive body weight gain, improves sleep, and attenuates age- an

155 Alcohol intake prevented body weight gain, induced the formation of uncoupling pr

156 ipulation can result in a robust and chronic body weight gain.

157 n and glucose concentrations associated with body weight gain.

158 Minimal intermittent stimulation led to body weight gain; ZI GABA neuron ablation reduced weight

159 te concentration and alleviated diet-induced body-weight gain and adiposity in mice.

160 E4, animals with dietary n-3 PUFAs decreased body-weight gain, plasma lipids, and insulin (P < 0.05)

161 otype with reduced microglial activation and body-weight gain.

162 Body weight, glucose test tolerance, and insulin test to

163 significantly reduces adiposity index, whole body weight, glucose, triacylglycerol, cholesterol and b

164 SI values of pancreas change with age, body weight, height, and BMI in the pediatric population

165 tigate the relationship between age, gender, body weight, height, body mass index (BMI), and elastici

166 w-dose crizanlizumab (2.5 mg per kilogram of body weight), high-dose crizanlizumab (5.0 mg per kilogr

167 actions of JNK in the control of feeding and body weight homeostasis.

168 se findings demonstrate a leptin-independent body weight homeostat ("gravitostat") that regulates fat

169 d into three groups based on stimulation and body weight (i.e., lean nonstimulated, obese nonstimulat

170 e of 5x10(11) vector genomes per kilogram of body weight in 10 men with hemophilia B who had factor I

171 teract with homeostatic controls to regulate body weight in a flexible and adaptive manner that takes

172 in the quintile with the lowest variation in body weight in adjusted models.

173 Chronic liraglutide treatment reduced body weight in chow-fed GLP-1RKD(DeltaNkx2.1cre) mice, b

174 c studies in diabetic db/db mice and reduced body weight in diet-induced obese (DIO) mice.

175 haride (LPS) decreased food/water intake and body weight in ethanol-naive and ethanol-trained wild-ty

176 n between perceived food insecurity and high body weight in humans.

177 ability of GDF15 to decrease food intake and body weight in mice.

178 ive growth of multiple tissues and organs to body weight in mice.

179 4, a clinically used GLP-1 analog, to reduce body weight in rats, suggesting that serotonin is a crit

180 egulates food intake, energy expenditure and body weight in response to metabolic and toxin-induced s

181 and organs are significantly associated with body weight in terms of phenotypic relative growth.

182 The adjusted mean change from baseline in body weight in the surgery group was -45.0 kg (95% confi

183 In the Whitehall II study, body weight increased by 2.96 +/- 6.5 kg during a follow

184 y despite an order of magnitude variation in body weight; increased weight is supported solely throug

185 Both diets resulted in similar body weight increases.

186 Body weight influenced clearance and volume parameters s

187 The maintenance of normal body weight is disrupted in patients with anorexia nervo

188 rimary cause or secondary effect of abnormal body weight is uncertain.

189 PET/MRI examination from 3 to 0.5 MBq/kg of body weight (kgBW) in intervals of 0.25.

190 KL(fl/fl) ) mice both responded with reduced body weight, kidney atrophy, hyperphosphatemia, and incr

191 GTx-026 significantly increased body weight, lean mass and grip strength by 60-80% over

192 ed significant additive genetic variance for body weight, leg length, parasite burden, horn length, a

193 , both of which occurred prior to changes in body weight, lending support to a causal relationship be

194 ften surpass the expected improvement due to body weight loss alone.

195 PINTA745 reduced body weight loss and improved body weight recovery after

196 tor (+)-JQ1 protects tumor-bearing mice from body weight loss and muscle and adipose tissue wasting.

197 Body weight loss at 6 weeks and 3 months postoperatively

198 ated suppression of FGF21 was independent of body weight loss or improved hepatic insulin sensitivity

199 ns attenuated cisplatin-induced anorexia and body weight loss significantly.

200 ns attenuated cisplatin-induced anorexia and body weight loss significantly.

201 s a multifactorial syndrome characterized by body weight loss, atrophy of adipose tissue (AT) and sys

202 stration from 5 to 11 weeks of age prevented body weight loss, skeletal muscle atrophy, muscle weakne

203 improves glucose tolerance independently of body weight loss.

204 sistant to chemotherapy-induced anorexia and body weight loss.

205 le TNBC xenograft models without significant body weight loss.

206 otor performance, accompanied by progressive body weight loss.

207 ling mediates cisplatin-induced anorexia and body weight loss.

208 zed serum metabolomic profiles of breed- and body weight-matched, diabetic (n = 6) and healthy (n = 6

209 s 50 to 79 years at WHI enrollment had their body weights measured and body mass indices calculated a

210 d metabolic environment related to excessive body weight might bear consequences on the WJ MSCs.

211 Clinical parameters (gestational age, birth body weight, mode of delivery and feeding, immunizations

212 ale offspring of dams treated with 2.0 mg/kg body weight of Cd and Hg suggested insulin resistance.

213 ds A total dose of 13.2 mmol per kilogram of body weight of each GBCA was administered in healthy Wis

214 ells (p < 0.001) than controls, and the mean body weight of gene-edited fry increased by 29.7%.

215 IV infusion of 1, 2, 3, or 4 mL/Kg (body weight) of crystalloid over 5 minutes.

216 (LPS) administration at a dose of 2 ng/kg of body weight on motivation in 21 healthy human subjects i

217 ravenously at a dose of 3 mg per kilogram of body weight once every 2 weeks) or platinum-based chemot

218 eceived IMGN853 at 6.0 mg/kg (adjusted ideal body weight) once every 3 weeks.

219 nsulin sensitivity without changing maternal body weight or composition.

220 mprovements were not associated with reduced body weight or food intake.

221 HFD did not affect body weight or glucose metabolism in atERalphaKO- compar

222 inhibited tumor formation without effects on body weight or liver function.

223 ly nor appreciably associated with change in body weight or waist circumference.

224 dose of either VA (6 mug retinyl palmitate/g body weight) or canola oil (control), both containing 1.

225 b (at a dose of 20 mg or 40 mg, according to body weight) or placebo, administered subcutaneously eve

226 IVIg, 0.5 g/kg of body weight, or visually indistinguishable placebo of 0.

227 me [in milliliters per kilogram of predicted body weight]: OR, 1.12, 95% CI, 1.01-1.24) factors.

228 Our results reveal that body weight, organ development and integrity were not im

229 ounds and characterized them with respect to body weight, organ integrity, behavioral and memory perf

230 Body weight, organ mass, fasting blood glucose, energy e

231 ty score was associated with a 0.13-kg lower body weight (P < 0.001) and a 0.26-cm(3) lower AFA (P <

232 as positively associated with age (p=0.005), body weight (p=0.004), height (p=0.003), and BMI (p=0.00

233 rs, in milliliters per kilogram of predicted body weight (PBW).

234 iding DHA at a dose of 60 mg per kilogram of body weight per day or a control (soy) emulsion without

235 After 4 wk of oral CRMP (2 mg/kg body weight per day) or vehicle treatment, mice underwen

236 trial of amitriptyline (1 mg per kilogram of body weight per day), topiramate (2 mg per kilogram per

237 , at a dose of 0.7 to 1.0 mg per kilogram of body weight per day, or itraconazole capsules (221 patie

238 cinogenic dose range from 1.5 to 2.0mg/kg of body weight per day.

239 evel or urine output <0.5 ml per kilogram of body weight per hour for >/=12 hours) and was assessed f

240 mendan (at a dose of 0.2 mug per kilogram of body weight per minute for 1 hour, followed by a dose of

241 ularitide at a dose of 15 ng per kilogram of body weight per minute or matching placebo for 48 hours,

242 gen consumption (milliliters per kilogram of body weight per minute) increased more in the combinatio

243 nagement [body mass index (BMI; in kg/m(2)), body weight, percentage of body fat, and waist circumfer

244 nivolumab at a dose of 1 mg per kilogram of body weight plus ipilimumab at a dose of 3 mg per kilogr

245 ing tidal volume from 6 to 8 mL/kg predicted body weight predicted fluid responsiveness with areas un

246 Whole body biomarkers (body weight, protein, chitobiase, catalase, xenobiotic m

247 (r=0.871), body surface area (r=0.856), and body weight (r=0.825) and negatively with heart rate (r=

248 ney results were replicated in terms of lung/body weight ratio (45/0 > 45/10 approximately 30/0 appro

249 es in systolic blood pressure, kidney weight/body weight ratio, urinary albumin, and urinary thiobarb

250 In contrast to all other organs, liver-to-body-weight ratio needs to be maintained always at 100%

251 d mice displayed reduced LV and lung mass to body weight ratios and improved ejection fraction at d5

252 The heart/body weight ratios were greater in Hfe-deficient mice at

253 gh-iron diet demonstrated increased heart-to-body weight ratios, alpha myosin heavy chain and cardiac

254 tly between treated and untreated mice after body weight rebound, suggesting that BChE gene transfer

255 In addition, body weight records and a glucose tolerance test reveale

256 NTA745 reduced body weight loss and improved body weight recovery after cerebral ischemia, as well as

257 ed a significant improvement in survival and body weight recovery associated with a significant ameli

258 Homozygous S999A mice exhibited low body weight, reduced adipose tissue mass, and increased

259 h controls, Ati-CB1-KO mice showed decreased body weight, reduced total adiposity, improved insulin s

260 GFR and body weight reduction were correlated.

261 The identified homeostat for body weight regulates body fat mass independently of fat

262 literature regarding effects of brain NRs on body weight regulation and discuss mechanisms underlying

263 an rhythmicity may affect sleep duration and body weight regulation in Africans Americans.

264 As such, loci involved in body weight regulation may also be relevant for AN and v

265 ced nutrient sensing, ceramide distribution, body weight regulation, and glucose metabolism.

266 f normal food reinforcement, food intake and body weight regulation.

267 A connection between GDF15 and body-weight regulation was initially suggested on the ba

268 nucleus (DRN) is an important brain area for body-weight regulation.

269 The mechanisms through which GDF15 reduces body weight remain poorly understood, because the cognat

270 To prospectively characterize changes in body weight, satiety, and postprandial gut hormone profi

271 anx1 (-/-) Apoe (-/-) mice displayed reduced body weight, serum cholesterol, triglycerides and free f

272 rably impact energy intake and reprogram the body weight set point.

273 Bace1(-/-) mice and rats further differed in body weight, spontaneous locomotor activity, and prepuls

274 ice and control db/db mice developed similar body weight, steatosis, glycemia, and insulin levels aft

275 rrection for age, sex, birth weight, height, body weight, Tanner stage of pubertal development, axial

276 21, both male and female offspring had lower body weight than controls, and pooled subsets of 3 male

277 -/-) mice were viable and fertile, had lower body weight than wild-type (wt) littermates and gray fur

278 in tidal volume from 6 to 8 mL/kg predicted body weight, that is, "tidal volume challenge," the chan

279 n the quintile with the highest variation in body weight, the risk of a coronary event was 64% higher

280 her 40 IU or 60 IU of CSL830 per kilogram of body weight twice weekly followed by placebo, or vice ve

281 ning" phenotype, with a smaller increases in body weight under high-fat diet, smaller fat deposits, i

282 ere orally administered 0.3 and 3 mug PFOS/g body weight until term.

283 and weight change, each increase of 1 SD in body-weight variability (measured according to average s

284 asures at baseline and 12 and 24 mo included body weight, waist circumference, fat mass (FM), fat-fre

285 rting dose of 50 mug daily, or 25 mug if the body weight was <50 kg or the patient had coronary heart

286 Body weight was also recorded but was not a primary outc

287 Body weight was measured.

288 Individual feed intake and body-weight was measured on 144 steers during 105 d on a

289 riglycerides, blood lipoproteins, HbA1c, and body weight.We included 14 comparison arms from 11 trial

290 ing tidal volume from 6 to 8 mL/kg predicted body weight were 3.5% and 2.5%, respectively.

291 and a significant negative association with body weight were estimated [MD=-0.22 (95% CI: -0.37, -0.

292 Tumor sizes and body weights were monitored for up to 49 d.

293 ections of ethyl carbamate (urethane, 1 g/kg body weight) were established and lung tumorigenesis ass

294 macrocyclic GBCA gadobutrol (0.1 mmol/kg of body weight) were retrospectively included in this regio

295 re were almost no changes in food intake and body weight when wortmannin injection (into the third ve

296 loss of Tmem18 in mice resulted in increased body weight, which was exacerbated by high fat diet and

297 Toxicity analysis included body weight, white blood cell count, and hematocrit.

298 Conversely, wing velocity increases with body weight within species, compensating for lower relat

299 who consumed OI had significant decreases in body weight z-score (decrease of 3.1%), percent body fat

300 testinal microbiota and significantly reduce body weight z-score, percent body fat, percent trunk fat