ライフサイエンスコーパス: diet-induced obesity

1 n weight gain and energy balance in high fat diet induced obesity.

2 ion of Hdac3 (Hdac3(IKO)) protects mice from diet induced obesity.

3 at diet (HFD), IRMOE mice are protected from diet-induced obesity.

4 sion of miR-26a protected mice from high-fat diet-induced obesity.

5 decreased energy expenditure, and increased diet-induced obesity.

6 deficiency-induced colitis, and ameliorates diet-induced obesity.

7 ation of hepatic Dpp4 in young mice prone to diet-induced obesity.

8 electrophysiological properties observed in diet-induced obesity.

9 hat mediate the resistance of female mice to diet-induced obesity.

10 rvention protects offspring against high-fat diet-induced obesity.

11 al white adipose tissue (WAT) in response to diet-induced obesity.

12 a marked increase in their susceptibility to diet-induced obesity.

13 2 diabetes, and C57BL/6J mice with high-fat diet-induced obesity.

14 d insulin resistance despite protection from diet-induced obesity.

15 lin and leptin receptors in animal models of diet-induced obesity.

16 ic reticulum contacts in POMC neurons during diet-induced obesity.

17 ylcholinesterase (BChE), in a mouse model of diet-induced obesity.

18 s control pancreatic dysfunction in high-fat-diet-induced obesity.

19 f Bmal1 also worsens chronic inflammation in diet-induced obesity.

20 deletion exerts a protective effect against diet-induced obesity.

21 increased oxygen consumption during high-fat-diet-induced obesity.

22 inflammation in the NAcc in animal models of diet-induced obesity.

23 nd appetitive motivation under conditions of diet-induced obesity.

24 tervention in dealing with the prevalence of diet-induced obesity.

25 is in the beta-cell compensatory response to diet-induced obesity.

26 tion prior to high calorie feeding prevented diet-induced obesity.

27 des in adipocytes and protected animals from diet-induced obesity.

28 erexpression inhibits lipolysis and promotes diet-induced obesity.

29 n resistance, particularly in the context of diet-induced obesity.

30 f alternative splicing to the development of diet-induced obesity.

31 adipose remodeling and adipocyte survival in diet-induced obesity.

32 tained glucose tolerance and did not develop diet-induced obesity.

33 stance and as a novel therapeutic target for diet-induced obesity.

34 iR-155 (-5p and -3p) in female mice prevents diet-induced obesity.

35 7 also prevented kidney disease in mice with diet-induced obesity.

36 a central mechanism for beta cell failure in diet-induced obesity.

37 ate during and after development of high-fat diet-induced obesity.

38 oc in mice (Noc KO) results in resistance to diet-induced obesity.

39 itochondrial oxidation and susceptibility to diet-induced obesity.

40 rature and energy expenditure and preventing diet-induced obesity.

41 ivation precipitates vascular dysfunction in diet-induced obesity.

42 repression increased with aging and high-fat diet-induced obesity.

43 ts may define a prothrombotic risk factor in diet-induced obesity.

44 and, as adults, were protected from high fat diet-induced obesity.

45 sm in the TME, detailing how it changes with diet-induced obesity.

46 display reduced adiposity and resistance to diet-induced obesity.

47 bitor decreased adipogenesis and ameliorated diet-induced obesity.

48 cient mice were also evaluated in a model of diet-induced obesity.

49 oding MGAT2 (Mogat2(-/-)) are protected from diet-induced obesity.

50 iture, decreased fat mass, and resistance to diet-induced obesity.

51 IF-1alpha and its target genes in ATM during diet-induced obesity.

52 o evidence for its involvement in developing diet-induced obesity.

53 ds and undergoes extensive remodeling during diet-induced obesity.

54 me, and glucose metabolism in the context of diet-induced obesity.

55 ic lymphangiogenesis during 16-week high-fat diet-induced obesity.

56 ssue inflammation has on metabolic health in diet-induced obesity.

57 ythmicity in metabolism and is implicated in diet-induced obesity.

58 impairs adaptive thermogenesis and promotes diet-induced obesity.

59 d adipocyte mitochondrial quality control in diet-induced obesity.

60 arged beta cell area and hyperinsulinemia in diet-induced obesity.

61 gene Cd36 and promoting lipid absorption and diet-induced obesity.

62 impaired glucose homeostasis associated with diet-induced obesity.

63 at mass loss on a normal diet after high fat diet-induced obesity.

64 hR-deficient females (VEH) were resistant to diet-induced obesity.

65 Thy1-knockout mice are prone to diet-induced obesity.

66 s in reduced weight gain and protection from diet-induced obesity.

67 nd increases food intake leading to high-fat diet-induced obesity.

68 the MARC2 KO mice were resistant to high-fat diet-induced obesity.

69 mma activity enhanced insulin sensitivity in diet-induced obesity.

70 se fails to correct metabolic dysfunction in diet-induced obesity.

71 eta cell function and islet compensation for diet-induced obesity.

72 t-reducing effects of leptin in rodents with diet-induced obesity.

73 5(-/-) (double knock-out (DKO)) mice show HF diet-induced obesity, adipocyte hypertrophy, and present

74 Maternal diet-induced obesity alters muscle mitochondrial functio

75 Diet-induced obesity alters the biophysical, pharmacolog

76 he comorbidities of Pb exposure and high-fat diet-induced obesity amplify skeletal deficits independe

77 mice were completely protected from high-fat diet-induced obesity and accompanying metabolic impairme

78 define whether activated calpains influence diet-induced obesity and adipose tissue macrophage accum

79 O) was sufficient to protect adult mice from diet-induced obesity and associated metabolic alteration

80 enes in BAT, and are protected from high-fat diet-induced obesity and development of insulin resistan

81 ve therapeutic potential in the treatment of diet-induced obesity and dyslipidemia.

82 y weight but specifically prevents excessive diet-induced obesity and ensuing metabolic impairments.

83 n this tissue are strongly protected against diet-induced obesity and exhibit increased energy expend

84 male zebrafish increased the propensity for diet-induced obesity and fasting hyperglycemia in adulth

85 Diet-induced obesity and food allergies increase in tand

86 fuel oxidation and thermogenesis, leading to diet-induced obesity and glucose intolerance.

87 The knock-out mice were resistant to diet-induced obesity and had abnormal lipid metabolism i

88 issues were resistant to developing high-fat diet-induced obesity and had significantly reduced white

89 Mice globally lacking Them2 are resistant to diet-induced obesity and hepatic steatosis, and exhibit

90 lism and thermogenesis, and protects against diet-induced obesity and hepatic steatosis.

91 ally reducing dietary BCAAs rapidly reverses diet-induced obesity and improves glucoregulatory contro

92 Importantly, loading relieves diet-induced obesity and improves glucose tolerance.

93 1)R deletion (B(1) (-/-)) protects mice from diet-induced obesity and improves insulin and leptin sen

94 tivation of Hh signaling suppresses high-fat-diet-induced obesity and improves whole-body glucose tol

95 In addition, diet-induced obesity and insulin resistance are exacerba

96 nd adipose tissue mass and were resistant to diet-induced obesity and insulin resistance due to a com

97 NSG mice were completely protected from diet-induced obesity and insulin resistance with signifi

98 homeostasis in a preclinical murine model of diet-induced obesity and insulin resistance, making the

99 ial fatty acid oxidation, thereby preventing diet-induced obesity and insulin resistance.

100 ound, lymphocytes, and cytokine signaling in diet-induced obesity and insulin resistance.

101 roved metabolic profiles and protection from diet-induced obesity and insulin resistance.

102 for 15 weeks, after which the mice exhibited diet-induced obesity and insulin resistance.

103 Mice lacking PEMT are protected against diet-induced obesity and insulin resistance.

104 ases energy expenditure and protects against diet-induced obesity and insulin resistance.

105 Aifm2, thus, can ameliorate diet-induced obesity and insulin resistance.

106 t Opn3-knockout (Opn3-KO) mice were prone to diet-induced obesity and insulin resistance.

107 ed energy expenditure and are protected from diet-induced obesity and insulin resistance.

108 ion of Tst in adipocytes protected mice from diet-induced obesity and insulin-resistant diabetes.

109 overexpression of the IR protects mice from diet-induced obesity and its effects on glucose metaboli

110 pothesis that Nnmt deletion protects against diet-induced obesity and its metabolic consequences in m

111 e that LCN2 is dispensable for both high fat diet-induced obesity and its therapeutic reduction by ce

112 epresents a promising approach to ameliorate diet-induced obesity and leptin resistance.

113 y regulated in white and brown fat depots of diet-induced obesity and leptin-deficient ob/ob mouse mo

114 rgy expenditure and amelioration of high-fat-diet-induced obesity and markedly improved glucose toler

115 geted activation of Hh signaling ameliorates diet-induced obesity and may be explored for pharmaceuti

116 endothelial dysfunction, occurs early during diet-induced obesity and may serve as a mediator of athe

117 potential therapeutic targets for combating diet-induced obesity and metabolic disease.

118 crobial community structure can protect from diet-induced obesity and metabolic disease.

119 dy suggests that blocking of CB1 ameliorates Diet-Induced Obesity and metabolic disorder by modulatin

120 ies additional novel therapeutic targets for diet-induced obesity and metabolic disorder.

121 KKbeta-deficient mice were also resistant to diet-induced obesity and metabolic disorders.

122 egulated microbiota protect BALB/c mice from diet-induced obesity and metabolic dysfunction.

123 Finally, moderate alcohol prevented high-fat diet-induced obesity and metabolic dysfunction.

124 xpression of SH2B1 protects against high fat diet-induced obesity and metabolic syndromes.

125 pe mice, NaHS treatment ameliorates high fat diet-induced obesity and metabolism disorders, indicatin

126 ockout of Maf1 in mice confers resistance to diet-induced obesity and nonalcoholic fatty liver diseas

127 lacking hepatic ZFP36L1 were protected from diet-induced obesity and steatosis.

128 ntrolling the proliferation of beta cells in diet-induced obesity and suggest that selective targetin

129 DZ-RhoGEF-deficient mice were protected from diet-induced obesity and T2D.

130 results of VSG surgery applied to mice with diet-induced obesity and targeted genetic disruption of

131 ver, the transgenic mice were protected from diet-induced obesity and type 2 diabetes.

132 Shp inactivation may be beneficial to combat diet-induced obesity and uncover that hepatic SHP is nec

133 to test the role of high dietary fat intake, diet-induced obesity, and associated changes in gut micr

134 a therapeutic target for insulin resistance, diet-induced obesity, and associated metabolic dysfuncti

135 proves insulin sensitivity, protects against diet-induced obesity, and elicits the browning of white

136 at they were protected from atherosclerosis, diet-induced obesity, and insulin resistance.

137 ic insulin resistance and hepatosteatosis in diet-induced obesity are associated with various metabol

138 aling and insulin action that manifests with diet-induced obesity, as insulin action is preserved to

139 Mice lacking LR11 are protected from diet-induced obesity associated with an increased browni

140 confers long-term metabolic protection from diet-induced obesity at the cost of moderate skin oxidat

141 role in different models of NCDs, including diet-induced obesity, atherosclerosis, and inflammation-

142 Since diet-induced obesity attenuates the responsiveness of ga

143 effector protein SMAD3 are protected against diet-induced obesity because of browning of their white

144 Following diet-induced obesity, biochemical analysis of livers rev

145 ting) and excessive energy storage (high-fat diet-induced obesity) blunt the effect of leptin.

146 lin resistance and insulin resistance due to diet-induced obesity both depend on muscle TRIB3.

147 The 16 week HF/HS diet induced obesity, but did not significantly affect t

148 ansfer in mice suppressed the development of diet-induced obesity, but did not affect pre-existing ad

149 om brain cells is known to protect mice from diet-induced obesity, but the effects on HCD-induced inf

150 ient mice have been shown to be resistant to diet-induced obesity, but the mechanism behind this rema

151 r steady state and under metabolic stress by diet-induced obesity, but we observed increases in both

152 r steady state and under metabolic stress by diet-induced obesity, but we observed increases in proli

153 mproves insulin sensitivity substantially in diet-induced obesity by both peripheral and central mech

154 se tissue LPL improves glucose metabolism in diet-induced obesity by improving the adipose tissue phe

155 in proopiomelanocortin neurons and prevented diet-induced obesity by increasing WAT browning and ener

156 R in adipose tissue controls the response to diet-induced obesity by promoting adipose tissue expansi

157 esults implicate a new class of compounds in diet-induced obesity-C18 epoxide and diol oxylipins.

158 eered mice on different diets, we found that diet-induced obesity caused a loss of guanylin expressio

159 Diet-induced obesity causes chronic macrophage-driven in

160 Diet-induced obesity causes hyperinsulinemia and diminis

161 In diet-induced obesity, cellular Ca(2+) handling propertie

162 of Dennd5b results in resistance to western diet induced obesity, changes in plasma lipids, and redu

163 Diet-induced obesity compromises the excitability and re

164 We hypothesized that diet-induced obesity could lead to alterations of the NR

165 In this study, we show that diet-induced obesity did not impact the maintenance of p

166 improves diabetic dyslipidemia in mice with diet-induced obesity (DIO mice).

167 B1) antagonists have been shown to attenuate diet-induced obesity (DIO) and associated inflammation,

168 lin sensitivity and fasting blood glucose in diet-induced obesity (DIO) and db/db mouse models.

169 Global deletion of Ip6k1 protects mice from diet-induced obesity (DIO) and insulin resistance, but t

170 t protein-coding mRNAs, are repressed during diet-induced obesity (DIO) and refeeding, whilst nutrien

171 genic enzymes and spare lipogenic enzymes in diet-induced obesity (DIO) are obscure.

172 However, obese humans and mice with diet-induced obesity (DIO) are resistant to leptin becau

173 Its reduced levels in diet-induced obesity (DIO) contribute to hyperleptinemia

174 stemically quenched the blood sugar level in diet-induced obesity (DIO) diabetic mice, it reduced ost

175 th regular chow, increased susceptibility to diet-induced obesity (DIO) in males but not in females,

176 We report that diet-induced obesity (DIO) in mice increased plasma and

177 ought to establish whether the propensity to diet-induced obesity (DIO) is associated with addictive-

178 ic distribution, 17- to 18-week-old lean and diet-induced obesity (DIO) mice were studied.

179 In db/db or diet-induced obesity (DIO) mice, hepatic expression of A

180 Here we use a diet-induced obesity (DIO) mouse model and compare metab

181 In the diet-induced obesity (DIO) mouse model, activation of li

182 reduces obesity and insulin resistance in a diet-induced obesity (DIO) mouse model.

183 HGA(273-301)) by investigating the effect of diet-induced obesity (DIO) on insulin sensitivity of the

184 Impaired adipogenic differentiation during diet-induced obesity (DIO) promotes adipocyte hypertroph

185 t received low perinatal n-6/n-3 ratios were diet-induced obesity (DIO) resistant and had a lower pos

186 und that withaferin-A treatment of mice with diet-induced obesity (DIO) resulted in a 20-25% reductio

187 gh behavioural rhythmicity was maintained in diet-induced obesity (DIO), gene expression profiling re

188 othelial explants excised from mice modeling diet-induced obesity (DIO), in which they were fed a "We

189 sing three different mouse models of obesity-diet-induced obesity (DIO), leptin receptor (LepR)-null,

190 a cannabinoid receptor 1 (CB1) antagonist on Diet-Induced Obesity (DIO), specifically whether such a

191 in resistance in C57Bl6/J mice with high-fat diet-induced obesity (DIO), using JD5037, a peripherally

192 In mice subjected to diet-induced obesity (DIO), we observed similar increase

193 , pADORA(1) signaling facilitates a high-fat diet-induced obesity (DIO).

194 TNF receptor-associated factors (TRAFs), in diet-induced obesity (DIO).

195 ular mechanisms underlying susceptibility to diet-induced obesity (DIO).

196 sis was tested by comparing the wild-derived diet-induced obesity- (DIO-) resistant mouse strain WSB/

197 Here we show that mice with diet-induced obesity display mislocalization of Par3, a

198 We found that rats susceptible to diet-induced obesity displayed heightened conditioned ap

199 We show that diet-induced obesity does not impair NRG1 signalling in

200 Diet-induced obesity drove early production of interleuk

201 d muscle glucose metabolism and resistant to diet-induced obesity due to increased energy expenditure

202 dipose tissue development, but its effect on diet-induced obesity during postnatal life is not known.

203 PQQ, provided prenatally in a mouse model of diet-induced obesity during pregnancy, could protect obe

204 and suggest a novel mechanism through which diet-induced obesity during puberty imposes its long-las

205 exercise on type II diabetes risk under a HF diet-induced obesity environment.

206 Monoacylglycerol lipase deficiency affects diet-induced obesity, fat absorption, and feeding behavi

207 -) mice would exhibit altered progression of diet-induced obesity, fatty liver, and insulin resistanc

208 control region mice on a high fat diet with diet-induced obesity following single oral doses of 3 an

209 Whey protein has been indicated to curb diet-induced obesity, glucose intolerance and delay the

210 aches of leptin therapy for the treatment of diet-induced obesity have been ineffective.

211 ke receptor 4 expression was observed in the diet-induced obesity HCC animal model.

212 We developed a diet-induced obesity HCC mouse model and examined TnC ex

213 lays a protective role in the progression of diet-induced obesity, hepatosteatosis, and atheroscleros

214 This study evaluates the role of cafeteria diet-induced obesity/hyperlipidemia (CAF) on alveolar bo

215 Diet-induced obesity impaired AT1-ILC killing ability.

216 MH-specific inhibition of TBK-1 in mice with diet-induced obesity impaired glucose metabolism and AKT

217 nfirmed in both serum and liver of mice with diet-induced obesity, implying that such a metabolic alt

218 cific deletion of P2Y(6)R protects mice from diet-induced obesity, improving glucose tolerance and in

219 paralleled profiles from long-term high-fat diet induced obesity in males.

220 to the gut microbiota retards development of diet induced obesity in wild-type mice.

221 ggerated the detrimental effects of maternal diet-induced obesity in adipose tissue.

222 logy and satellite cell dynamics compared to diet-induced obesity in irradiated muscle, and have impl

223 Pharmacological inhibition of CBR1 in diet-induced obesity in mice results in more marked gluc

224 oting AgRP neurons during the development of diet-induced obesity in mice.

225 on of Id1 causes age-associated and high-fat diet-induced obesity in mice.

226 mide N-methyltransferase (NNMT)-ASO prevents diet-induced obesity in mice.

227 and deletion of theNrf2gene protects against diet-induced obesity in mice.

228 odulates traits of the metabolic syndrome in diet-induced obesity in mice.

229 ative stress in the metabolic alterations in diet-induced obesity in rats.

230 Estrogens protect against diet-induced obesity in women and female rodents.

231 Maternal diet-induced obesity increased miR-126 expression howeve

232 In mice with a GSNOR deletion, diet-induced obesity increases lysosomal nitrosative str

233 According to our previous results, diet-induced obesity induces epigenetic modifications to

234 nvestigated the effects of Lcn2 depletion on diet-induced obesity, inflammation, and PDAC development

235 y, microbial and dietary factors incurred by diet-induced obesity influence underlying innate and ada

236 Here, we demonstrate that resistance to diet-induced obesity inNrf2(-/-)mice is associated with

237 w that intestinal PPARdelta protects against diet-induced obesity, insulin resistance and dyslipidemi

238 er of the EAT gene to mice prevents high-fat diet-induced obesity, insulin resistance and fatty liver

239 Importantly, CD81 loss causes diet-induced obesity, insulin resistance, and adipose ti

240 tion, transgenic mice were protected against diet-induced obesity, insulin resistance, and inflammati

241 rexpression (Adipo-TFEB) were protected from diet-induced obesity, insulin resistance, and metabolic

242 Additionally, in mice with diet-induced obesity, INT-767 prevented mitochondrial dy

243 High-fat diet-induced obesity is a major risk factor for osteoart

244 Diet-induced obesity is associated with strong circadian

245 ate and testing its effectiveness to prevent diet-induced obesity later in life.

246 Diet-induced obesity leads to devastating and common chr

247 Previous studies have shown that maternal diet-induced obesity leads to increased risk of type 2 d

248 rovide mechanistic insights of MGL's role in diet-induced obesity, lipid metabolic disorder, and regu

249 During high fat diet-induced obesity, macrophages are activated by lipid

250 suggest that the memory-impairing effects of diet-induced obesity may potentially be mediated by neur

251 our unique gut microbiota with resistance to diet-induced-obesity-mediated alteration of the gut micr

252 e receptor (Drd1)-null mice are resistant to diet-induced obesity, metabolic disease, and circadian d

253 ce but increased over time in overweight and diet-induced obesity mice, suggesting CR obviates epigen

254 der to determine whether miR-146a influences diet-induced obesity, mice that were either wild type (W

255 We used a diet-induced obesity model to show that Thy1-null mice g

256 e metabonomics data and microbiome data in a diet-induced obesity model using C57BL/6 mice.

257 Using a diet-induced obesity model, we show that TLR3-deficient

258 Diet-induced obesity modulates the excitability and resp

259 oside A and sucralose on NASH using high fat diet induced obesity mouse model by substituting fructos

260 sulin sensitivity and glucose control in the diet-induced obesity mouse model after both acute and ch

261 In a diet-induced obesity mouse model, daily subcutaneous adm

262 ong-acting GLP-1 analog is demonstrated in a diet-induced obesity mouse model.

263 , are present in naive CD4(+) T cells from a diet-induced obesity murine model and that elevated O-Gl

264 y of LCN2 altered neither the development of diet-induced obesity, nor the ability of celastrol to pr

265 recapitulates the leanness and resistance to diet-induced obesity of RIIbeta KO mice.

266 f increased susceptibility to the effects of diet-induced obesity on amygdala function.

267 tatively contributing to protection from the diet-induced obesity phenotype.

268 y robust to alter the effects of fibrates on diet-induced obesity phenotypes.

269 e long-term impact of transient peripubertal diet-induced obesity (ppDIO, induced between 4 and 10 we

270 oreover, betaine administration to mice with diet-induced obesity prevents the development of impaire

271 by increased intestinal permeability during diet-induced obesity promotes insulin resistance in mice

272 zed to receive a CR, overweight-inducing, or diet-induced obesity regimen (n = 27/group).

273 Relative to the overweight and diet-induced obesity regimens, CR decreased body weight,

274 TTR-ASO treatment of mice with genetic or diet-induced obesity resulted in an 80-95% decrease in c

275 Diet-induced obesity resulted in increased muscle fibros

276 In a rat model of breast cancer driven by diet-induced obesity, STAT3 blockade suppressed the CSC-

277 Recent studies revealed that diet-induced obesity suppressed guanylin and uroguanylin

278 ocytic genes from islets of rodent models of diet-induced obesity that significantly overlap with clo

279 Our study indicates that, in diet-induced obesity, these circadian fluctuations in ga

280 We used a mouse model of maternal-diet induced obesity to define predictive correlations b

281 l of individual susceptibility to junk-foods diet-induced obesity to determine whether there are pre-

282 the current study, we used a mouse model of diet-induced obesity to identify putative cellular mecha

283 use models of a regular diet and of high-fat-diet-induced obesity to investigate the role of dietary

284 Maternal diet-induced obesity, together with androgen excess, aff

285 In a model of diet-induced obesity, Tregs from the visceral adipose ti

286 ssels as a basis for vascular dysfunction in diet-induced obesity via a mechanism involving type 2 pr

287 h was slightly inhibited and protection from diet-induced obesity was less complete.

288 Here, a rat model of diet-induced obesity was used to explore changes in brai

289 Here, using a murine model of diet-induced obesity, we determined that obesity causes

290 he consequences of hepatic BIM deficiency in diet-induced obesity, we generated liver-specific BIM-kn

291 In a mouse model of diet-induced obesity, we show that adipose tissue macrop

292 ceptor 4 mutant mice (C3H/HeJ) with high-fat-diet-induced obesity were not protected against insulin

293 mice have increased food intake and greater diet-induced obesity when fed high-fat diet.

294 ptive response is the complete resistance to diet-induced obesity when POLG mice are placed on a high

295 In mice, diet-induced obesity, which decreases insulin sensitivit

296 ssions in the mutant pedigrees and mice with diet-induced obesity, which showed that each obesity mou

297 pha in the MeA partially prevented mice from diet-induced obesity, while chemogenetic activation of S

298 ator (SRA) (SRAKO) are resistant to high fat diet-induced obesity with a phenotype that includes impr

299 Our findings suggest that the combination of diet-induced obesity with other risk factors may increas

300 duces WAT lipolysis in vivo but also reduces diet-induced obesity without affecting LPL activity.