ライフサイエンスコーパス: obese mice

1 fat mass loss without calorie restriction in obese mice.

2 ibition of TF-PAR2 signaling in diet-induced obese mice.

3 r of cutaneous hypersensitivity reactions in obese mice.

4 as the FXR acetylation site in diet-induced obese mice.

5 reased dermatitis responses in both lean and obese mice.

6 ulator of inflammation, NF-kappaB, in KCs in obese mice.

7 ose and insulin tolerance at 16 weeks HFD in obese mice.

8 the extensive visceral fat necrosis of dying obese mice.

9 ave been observed only during weight loss in obese mice.

10 with improvements in metabolic parameters in obese mice.

11 e action of Gly-MCA in high-fat diet-induced obese mice.

12 betes, and hepatic steatosis in diet-induced obese mice.

13 GPR120, inhibit mammary tumor progression in obese mice.

14 also downregulated in high-fat diet-induced obese mice.

15 hesis and oxidation in the livers of HFD-fed obese mice.

16 tion of these kinases improves metabolism in obese mice.

17 in the process improving glucose handling in obese mice.

18 d hepatic steatosis in high-fat diet-induced obese mice.

19 ion, and maintained normal blood pressure in obese mice.

20 idney mass on glucose metabolism in lean and obese mice.

21 reduces steatosis and glucose intolerance in obese mice.

22 for fermentation of faeces from diet-induced obese mice.

23 hepatosteatosis and hypertriglyceridemia in obese mice.

24 mic IT tolerance in aged compared with young obese mice.

25 entiated the defects in insulin signaling of obese mice.

26 rent is blunted in neurons from diet-induced obese mice.

27 have silenced hepatic SREBP-1 in normal and obese mice.

28 ) did not affect food intake or body mass in obese mice.

29 proliferation was maintained in diet-induced obese mice.

30 alter body weight or glucose intolerance of obese mice.

31 n the augmented effects of ozone observed in obese mice.

32 ng coincides with adipocyte iron overload in obese mice.

33 pproved calcium channel blocker verapamil to obese mice.

34 ophages and in ATMs of high-fat diet-induced obese mice.

35 ation score (P < 0.0001) than nontreated OVA-obese mice.

36 tolerance parallel to insulin sensitivity in obese mice.

37 improves insulin sensitivity in diet-induced obese mice.

38 ith robust systemic insulin sensitization in obese mice.

39 hanges that underlie diabetes development in obese mice.

40 immune cell composition of adipose tissue in obese mice.

41 d intestine and induced in adipose tissue of obese mice.

42 glucose and insulin homeostasis in lean and obese mice.

43 with beta-cell compensation (or failure) in obese mice.

44 lucose intolerance and insulin resistance in obese mice.

45 ue, and the expression level is decreased in obese mice.

46 s detected specifically in the adipocytes of obese mice.

47 ion of Npy was limited to purified ATMs from obese mice.

48 erived macrophages and high-fat diet-induced obese mice.

49 nst hyperglycemia and glucose intolerance in obese mice.

50 vity and glucose homeostasis in diet-induced obese mice.

51 cerbates glucose intolerance in diet-induced obese mice.

52 eripheral leptin sensitivity in diet-induced obese mice.

53 e in selective hepatic insulin resistance in obese mice.

54 CTRP1 are strikingly reduced in diet-induced obese mice.

55 were markedly suppressed in dietary-induced obese mice.

56 ted for its effects on insulin resistance in obese mice.

57 ralizing activities were markedly reduced in obese mice.

58 ose inflammation in established diet-induced obese mice.

59 ance and insulin sensitivity in diet-induced obese mice.

60 ntributes to augmented responses to ozone in obese mice.

61 pe, leptin-deficient ob/ob, and diet-induced obese mice.

62 es response to IFNalpha in insulin-resistant obese mice.

63 atment with oseltamivir enhanced survival of obese mice.

64 upregulated in metabolic tissues of HFD-fed obese mice.

65 ions and to reverse the phenotype in already obese mice.

66 rease proinflammatory cytokine production in obese mice.

67 2,344 were detected uniquely in healthy and obese mice.

68 t results in inhibition of carcinogenesis in obese mice.

69 of hepatic lipotoxicity and inflammation in obese mice.

70 teins involved in BCAA metabolism but not in obese mice.

71 istance and fat accumulation in diet-induced obese mice.

72 oves glucoregulatory control in diet-induced obese mice.

73 n sensitivity and decreases hyperglycemia in obese mice.

74 nd lipid metabolism in high-fat diet-induced obese mice.

75 rate and energy expenditure in diet-induced obese mice.

76 IL-33 drives augmented responses to ozone in obese mice.

77 to substantial and sustained weight loss in obese mice.

78 nd improve glucose tolerance in diet-induced obese mice.

79 functional changes in the gut microbiome of obese mice.

80 pression in response to exercise in lean and obese mice.

81 meliorates hepatic steatosis in diet-induced obese mice.

82 ion of BiP protein, and was also observed in obese mice.

83 es weight gain and adiposity in diet-induced obese mice.

84 f lean mice to more closely resemble that of obese mice.

85 so reduced hepatic steatosis in diet-induced obese mice.

86 st growth factor 21 (FGF21) in both lean and obese mice.

87 e, was significantly reduced in diet-induced obese mice.

88 d lymphatic function compared with sedentary obese mice.

89 of function, improved insulin sensitivity in obese mice.

90 , including Sirt1, within the hippocampus of obese mice.

91 sociated with enlarged adipocytes in lean or obese mice.

92 ct pre-existing adiposity and body weight in obese mice.

93 iposity, and improves insulin sensitivity in obese mice.

94 and counter strains and the low fertility of obese mice.

95 lycerol accumulation compared with wild type obese mice.

96 ta1 (TGF-beta1) in mammary adipose tissue in obese mice activates SMAD3 signaling, causing phospho-SM

97 In obese mice, adipocyte-specific gp130 deletion reduced ba

98 erulein pancreatitis was induced in lean and obese mice, alone or with the lipase inhibitor orlistat

99 Notably, nonsensitized obese mice already exhibited increased lung ILC counts a

100 macological inhibition of Notch signaling in obese mice ameliorates obesity, reduces blood glucose an

101 sion of SULT2B1b in the liver was induced in obese mice and during the transition from the fasted to

102 the severity of pandemic influenza virus in obese mice and evaluated antiviral effectiveness.

103 environmental temperature, and is altered in obese mice and human patients.

104 Moreover, in obese mice and humans, both the number of exosomes secre

105 L) are significantly reduced in the liver of obese mice and humans.

106 significantly induced in adipose tissue from obese mice and humans.

107 pression is upregulated in the adipocytes of obese mice and humans.

108 evels of FGF21 in both high-fat diet-induced obese mice and in genetically obese-diabetic Lepr(db)mic

109 osphorylation at serine 793 was increased in obese mice and in palmitate-treated HepG2 cells.

110 the RBP vigilin is upregulated in livers of obese mice and in patients with fatty liver disease.

111 ) is the most highly elevated hepatic miR in obese mice and is also substantially elevated in patient

112 In obese mice and obese individuals, Gpnmb expression was i

113 enhance the IKKbeta activity in the liver of obese mice and observed increased XBP1s activity, reduce

114 ntigen-presenting cells in adipose tissue of obese mice and patients with insulin resistance.

115 CD40/IL-2 prevented cytokine storms in young obese mice and protected from lethality.

116 treatment also reversed VAT inflammation in obese mice and resulted in a reduction of hyperinsulinem

117 in the 5 + 5 schedule induced weight loss in obese mice and reversed the progression of metabolic dis

118 was to analyse lymphatic vascular changes in obese mice and to determine whether these pathological e

119 ic NAS DBS was also examined in diet-induced obese mice and was found to acutely reduce caloric intak

120 we observed that in leptin-knockout (ob/ob) obese mice, and in mice with diet-induced obesity, orexi

121 Expression of both genes was elevated in obese mice, and induction of Cadm1 in excitatory neurons

122 inflammatory mediator in the hypothalamus of obese mice, and its hypothalamic inhibition improves ene

123 Monocytes from obese mice are not programmed to become inflammatory ATM

124 When obese mice are removed from their high-fat diet to regai

125 OX-A and alpha-MSH serum levels was found in obese mice as well as in human obese subjects (body mass

126 ligation, nonalcoholic steatohepatitis, and obese mice, as well as EVs released from hepatocytes exp

127 rway hyperresponsiveness and inflammation in obese mice but had no effect in lean mice.

128 osis and glucose intolerance in diet-induced obese mice, but these beneficial effects were not observ

129 al cell proliferation in the hypothalamus of obese mice, but this proliferation is not required for e

130 binding sites of FXR in healthy and dietary obese mice by chromatin immunoprecipitation sequencing (

131 mplete restoration of insulin sensitivity in obese mice by the thiazolidinedione drug pioglitazone.

132 F-alpha or osteopontin in epididymal ATMs of obese mice caused significant improvement in glucose tol

133 ith glucagon and GLP-1 activity to diabetic, obese mice causes enhanced weight loss and improves gluc

134 pr120 agonist treatment of high-fat diet-fed obese mice causes improved glucose tolerance, decreased

135 ation that accumulates in the VAT of HFD-fed obese mice causes VAT inflammation by producing large am

136 We found that genetically and diet-induced obese mice challenged with either 2009 influenza A virus

137 sed during feeding; however, in diet-induced obese mice, Clk2 protein remains elevated through both f

138 significantly lower in skeletal muscle from obese mice compared to that from lean mice.

139 tration led to more BrdU(+) cells in PDGs of obese mice compared with lean mice.

140 in the brains of diet-induced or genetically obese mice compared with their respective lean controls

141 nd ILC3s further increased in HDM-challenged obese mice compared with those in HDM-challenged lean mi

142 highly induced in AT from high-fat diet-fed obese mice, concurrent with insulin resistance.

143 Moreover, obese mice conditionally lacking GRIP1 in macrophages de

144 Injection of ATS-9R into obese mice confirmed specific binding of ATS-9R to fat v

145 capitulated the memory deficits exhibited by obese mice, consistent with the hypothesis that the high

146 ns and is upregulated in the hypothalamus of obese mice, contributing to insulin and leptin resistanc

147 Reductions in organ VA signaling in obese mice correlate with increasing adiposity and fatty

148 -defective SIRT3-K57R mutant in diet-induced obese mice decreased acetylation of mitochondrial long-c

149 Silencing of NF-kappaB expression in KCs in obese mice decreased cytokine secretion and improved ins

150 Deficiency of E-FABP in obese mice decreased recruitment of CD11c(+) macrophages

151 Consistent with diet-induced obese mice, desensitization of leptin receptors caused b

152 Indomethacin administration to obese mice did not reduce adipose tissue mass, and the c

153 lly, we observed that the skeletal muscle of obese mice displayed decreased expression of muscular ma

154 In addition, obese mice displayed heightened dermatitis responses to

155 Here, we show that hepatocytes from obese mice displayed significantly diminished SOCE as a

156 phosphorylation is enhanced in the liver of obese mice displaying insulin resistance.

157 nt of obesity as weight matched diet induced obese mice do not display systolic dysfunction.

158 pair glucose homeostasis in lean mice and in obese mice during weight loss.

159 glucose tolerance and insulin sensitivity to obese mice, even as they continue to consume a high-fat,

160 However, obese mice exhibit elevated serum VA.

161 In addition, skeletal muscles from HFD-fed obese mice exhibit low levels of miR-149 and high levels

162 Ab protection was absent in this model, but obese mice exhibited a significantly lower level of nonn

163 High-fat diet-induced and genetic-induced obese mice exhibited greater pH1N1 mortality, lung infla

164 Young obese mice exhibited greater ratios of M1/M2 macrophages

165 Previously, obese mice exhibited improved glucose and insulin tolera

166 Furthermore, AT from obese mice exhibits an increased sensitivity to IL-4 sti

167 The lung endothelium from obese mice expressed higher levels of leukocyte adhesion

168 Obese mice fed a diet supplemented with the SIRT1-activa

169 Infection of obese mice fed the HFD reduced body weight and adipose t

170 pressed in the white adipose tissue (WAT) of obese mice fed with a choline-deficient high-fat diet.

171 xpression profile in diverse tissue sites in obese mice following the induction of colitis.

172 ired glucose homeostasis in lean mice and in obese mice following weight loss.

173 rtantly, short-term knockdown of BIM rescued obese mice from insulin resistance, evidenced by reduced

174 We demonstrate that obese mice, generated from a high fat diet (HFD) or by g

175 Transfer of the FGF21 gene in HFD-induced obese mice greatly increased the expression of thermogen

176 Further, obese mice had elevated viral titers, greater lung infla

177 Furthermore, obese mice had fewer bronchoalveolar macrophages and reg

178 We found that sedentary obese mice had markedly decreased collecting lymphatic v

179 Although obese mice had more regulatory T cells (Tregs) in the lu

180 We found that obese mice have impaired lymphatic function, characteriz

181 alpha was also measured in insulin-resistant obese mice (high fat diet and ob/ob mice) untreated and

182 y, the activation of FcgammaRIIB by IgG from obese mice impaired endothelial cell insulin transcytosi

183 Long-term fluvastatin treatment of obese mice impaired insulin-stimulated glucose uptake in

184 atory effects on macrophages in vitro and in obese mice in vivo.

185 antibody reduced appetite and body weight in obese mice, in addition to improving their glycemic prof

186 SIRT3 is hyperacetylated in aged and obese mice, in which SIRT1 activity is low, and SIRT3 ac

187 in allergic airway inflammatory features in obese mice, including TH2 and TH17 infiltration.

188 Finally, apigenin administration to obese mice increases NAD(+) levels, decreases global pro

189 profile of macrophages in adipose tissue of obese mice, indicating the presence of an interaction be

190 CD11c(high)F4/80(low) DCs from obese mice induced Th17 differentiation.

191 ing ILC2 or type I or type II NKT cells into obese mice induces transient weight loss and stabilizes

192 PVAT from obese mice inhibits insulin-induced vasodilation, which

193 Type 2 diabetes in humans and in obese mice is polygenic.

194 found that attenuated muscle regeneration in obese mice is rescued by AICAR, a drug that specifically

195 lamps revealed no significant differences in obese mice lacking ceramide de novo synthesis machinery

196 In contrast, obese mice lacking hepatic activating transcription fact

197 Examination of adipose tissue from obese mice lacking macrophage Tgr5 revealed enhanced inf

198 Conversely, over-expression of STIM1 in obese mice led to increased SOCE, which was sufficient t

199 h1a1 knockdown conferred this BAT program in obese mice, limiting weight gain and improving glucose h

200 VAT Tregs in obese mice lose the signature typical of lean individual

201 iver-specific depletion of RetSat in dietary obese mice lowers hepatic and circulating TGs and normal

202 y, liver-specific overexpression of GSNOR in obese mice markedly enhances lysosomal function and auto

203 ndrial dysfunction in the skeletal muscle of obese mice may be because of, at least in part, miR-149

204 bolic syndrome, produced 3 groups of equally obese mice: mice with normal glucose tolerance, hyperins

205 study was to test whether muscle ERRgamma in obese mice mitigates weight gain and insulin resistance.

206 eficial effects in both animal xenograft and obese mice models could be a direct consequence of its m

207 rved in other extra-oral tissues of lean and obese mice, most strikingly in the duodenum where obesit

208 al glucose tolerance tests with diet-induced obese mice, NTE-1 treatment improved the glucose excursi

209 In particular, in obese mice, O(3) induces IL-13 and IL-13 synergizes with

210 found in the fibers projecting to the ARC of obese mice (ob/ob and high-fat diet fed) concurrently wi

211 In genetically obese mice (ob/ob), 45h was as effective as a dipeptidyl

212 is in response to PCB-77 was not observed in obese mice of either genotype.

213 d quantified with a 4.7-T MR imager in ob/ob obese mice on the basis of the signal variance of adipos

214 Adoptive transfer of iNKT cells into obese mice or in vivo activation of iNKT cells via their

215 In obese mice, ozone increased lung IL-13+ innate lymphoid

216 , in vivo antisense inhibition of miR-34a in obese mice partially restored betaKL levels and improved

217 In obese mice, PCB-77 had no effect on glucose homeostasis,

218 re we show that in hypercaloric diet-induced obese mice, persistently activated microglia in the MBH

219 GM3S knockout in diet-induced obese mice prevents the diabetic wound-healing defect.

220 Data herein show B cells from obese mice produce a proinflammatory cytokine profile co

221 AMP levels in subcutaneous adipose depots of obese mice, promoting the synthesis and secretion of the

222 Overexpression of hIGFBP1 in obese mice reduced blood pressure, improved insulin sens

223 in oral and extra-oral tissues from lean and obese mice, remains poorly characterized.

224 demonstrate that 4 weeks of VWR exercise in obese mice rescued high-fat diet-induced decreased muscl

225 tes were identified in livers of healthy and obese mice, respectively, after a short 1-hour treatment

226 -miR-34a treatment in primary hepatocytes of obese mice restored FGF19-activated ERK and glycogen syn

227 roduction of VEGF-A specifically into BAT of obese mice restored vascularity, ameliorated brown adipo

228 Hypoxia develops in white adipose tissue in obese mice, resulting in changes in adipocyte function t

229 r-infiltrating cell populations in lean, and obese mice revealed that cancer induces a six-fold incre

230 FSF11A or NDUFAB1 in the MBH of diet-induced obese mice reverses mitochondrial elongation and reduces

231 ow that adipose tissue macrophages (ATMs) in obese mice secrete miRNA-containing exosomes (Exos), whi

232 on of siRNA encapsulated by glucan shells in obese mice selectively silences genes in epididymal ATMs

233 Organs from obese mice show impaired VA transcriptional signaling, i

234 visceral adipose tissue of hyperinsulinemic, obese mice showed a similar specific decrease in IL-10 p

235 Obese mice showed increased susceptibility to allergic s

236 istration of PS10 (70 mg/kg) to diet-induced obese mice significantly augments pyruvate dehydrogenase

237 GM-CSF neutralization in diet-induced obese mice significantly reduced immunosuppression, intr

238 gic inhibition of hepatic Notch signaling in obese mice simultaneously improves glucose tolerance and

239 were differentially altered in the lungs of obese mice such as fatty acid, phospholipid, and nucleot

240 of genomic FXR-binding sites in healthy and obese mice suggested that FXR transcriptional signaling

241 andomly selected genes from both healthy and obese mice suggested that more FXR-binding sites are lik

242 sufficient to improve glucose homeostasis in obese mice, suggesting that the resveratrol-mediated cha

243 In diet-induced obese mice, TF tail signaling independent of PAR2 drives

244 ng virus titers were significantly higher in obese mice than in lean controls after challenge.

245 proximately sixfold higher number of RHMs in obese mice than in lean mice, whereas the number of KCs

246 2(+) Tregs in VAT was severely diminished in obese mice that had been fed a high-fat/sucrose diet, an

247 s to FGF19 were severely impaired in dietary obese mice that have elevated miR-34a.

248 phoid cell populations are largely intact in obese mice, the upregulation of IL-23, a cytokine upstre

249 affecting pulmonary inflammation; whereas in obese mice, TNFR2 deficiency augmented O(3)-induced AHR

250 We randomized obese mice to either aerobic exercise (treadmill running

251 ng assays and in vivo metabolic profiling in obese mice to investigate the effects of IGFBP-1 and its

252 Upon exposing isolated pancreatic islets of obese mice to normal glucose concentrations, beta-cells

253 Ovalbumin-obese mice treated with NK1-R antagonist had lower weigh

254 Here, we examined obese mice treated with salidroside at the dosage of 50

255 In obese mice, treatment with cGAMP significantly decreases

256 in the cortex of db/db and high fat diet-fed obese mice, two mouse models of IR.

257 hoid cells and CD4(+) T cells is impaired in obese mice under various immune challenges, especially i

258 aired oral glucose tolerance in diet-induced obese mice was also improved by ghrelin preadministratio

259 le mice were comparable, while that of adult obese mice was distinct, indicating a possible impact of

260 he compensatory increase in GSIS observed in obese mice was not affected by treatment with indomethac

261 Consistent with our findings in obese mice, we show that increasing severity of fatty li

262 ing the pH1N1 challenge, Tregs isolated from obese mice were 40% less suppressive than Tregs isolated

263 s in pulmonary endothelial cells observed in obese mice were associated with enhanced susceptibility

264 Lean or obese mice were fed a high-fat diet (HFD) for five days

265 In follow-up studies, diet-induced obese mice were food restricted for 5 weeks to achieve F

266 Lean and obese mice were infected with influenza A/Puerto Rico/8/

267 glucose homeostasis and oxidative stress in obese mice were investigated for the first time.

268 Furthermore, RHMs from obese mice were more inflamed and expressed higher level

269 However, in obese mice, where metabolic tissues exhibited insulin re

270 activity was observed in isolated ATMs from obese mice, which coincided with increased nuclear MITF

271 BP) was significantly upregulated in skin of obese mice, which coupled lipid droplet formation and NL

272 nscriptional signaling is altered in dietary obese mice, which may underlie aberrant metabolism and l

273 educed fasting glucose and insulin levels in obese mice while improving insulin sensitivity, a result

274 Treatment of diet-induced obese mice with a REV-ERB agonist decreased obesity by r

275 Treatment of obese mice with amlexanox elevates energy expenditure th

276 Treatment of obese mice with ATS-9R/shFABP4 led to metabolic recovery

277 Systemic treatment of diet-induced obese mice with BMP7 resulted in increased energy expend

278 the metabolic impact of exercise training in obese mice with cardiac and skeletal muscle disruption o

279 Blocking IKKepsilon in the hypothalamus of obese mice with CAYMAN10576 or small interfering RNA dec

280 ering body weight by switching to LF diet in obese mice with heart failure is associated with decreas

281 Treating obese mice with IL-25 induces weight loss and improves g

282 formed lipidomics on quadriceps muscles from obese mice with impaired glucose tolerance.

283 s were selectively reduced in hypothalami of obese mice with leptin deficiency and leptin resistance.

284 ith pleiotropic immune disorders reported in obese mice with leptin or LepR deficiency, we found that

285 Finally, in obese mice with liver-specific IRE1alpha deficiency, rec

286 Moreover, HDL isolated from obese mice with moderate inflammation and humans with sy

287 Treating obese mice with NAT3 or AAT3 decreases adiposity and inc

288 Treatment of obese mice with PAHSAs lowers glycemia and improves gluc

289 mprove blood glucose control in diet-induced obese mice with pre-existing metabolic syndrome.

290 Injection of obese mice with recombinant helminth-derived Schistosoma

291 ent failed to improve muscle regeneration in obese mice with satellite cell-specific AMPKalpha1 knock

292 Moreover, we treated obese mice with SPM precursors and investigated the effe

293 inhibition of these kinases by treatment of obese mice with the drug amlexanox reversed obesity-indu

294 Treatment of obese mice with the ERK inhibitor U0126 rescued Baf60c a

295 Finally, treating mildly obese mice with the IP6K inhibitor TNP enhanced thermoge

296 Treatment of lean and obese mice with this inhibitor shows that IDE regulates

297 Treatment of ob/ob (obese) mice with a cannabinoid receptor 1 (Cnr1) antagon

298 In obese mice, Wnt5a ablation ameliorates insulin resistanc

299 ough increased blood and lymphatic volume in obese mice would play a role in increased hematopoiesis,

300 ulator of insulin sensitivity in chronically obese mice, yet systemic deletion of Map4k4 did not impr