ライフサイエンスコーパス: obese mice

1 CK are produced in the endocrine pancreas of obese mice.

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

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

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

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

6 in the same individuals and are increased in obese mice.

7 ntributes to augmented responses to ozone in obese mice.

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

9 of hepatic lipotoxicity and inflammation in obese mice.

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

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

12 oves glucoregulatory control in diet-induced obese mice.

13 otects against cardiomyopathy in chronically obese mice.

14 n sensitivity and decreases hyperglycemia in obese mice.

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

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

17 microenvironment and anti-tumor immunity in obese mice.

18 to substantial and sustained weight loss in obese mice.

19 functional changes in the gut microbiome of obese mice.

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

21 meliorates hepatic steatosis in diet-induced obese mice.

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

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

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

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

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

27 d lymphatic function compared with sedentary obese mice.

28 olic dysfunction in genetic and diet-induced obese mice.

29 of function, improved insulin sensitivity in obese mice.

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

31 sociated with enlarged adipocytes in lean or obese mice.

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

33 iposity, and improves insulin sensitivity in obese mice.

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

35 lycerol accumulation compared with wild type obese mice.

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

37 r of cutaneous hypersensitivity reactions in obese mice.

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

39 reased dermatitis responses in both lean and obese mice.

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

41 the extensive visceral fat necrosis of dying obese mice.

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

43 with improvements in metabolic parameters in obese mice.

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

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

46 GPR120, inhibit mammary tumor progression in obese mice.

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

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

49 tion of these kinases improves metabolism in obese mice.

50 L-induced body weight loss in male or female obese mice.

51 in the process improving glucose handling in obese mice.

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

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

54 reduces steatosis and glucose intolerance in obese mice.

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

56 hepatosteatosis and hypertriglyceridemia in obese mice.

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

58 entiated the defects in insulin signaling of obese mice.

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

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

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

62 proliferation was maintained in diet-induced obese mice.

63 wn-regulated in serum exosomes and islets of obese mice.

64 alter body weight or glucose intolerance of obese mice.

65 ng coincides with adipocyte iron overload in obese mice.

66 pproved calcium channel blocker verapamil to obese mice.

67 detected in plasma from moderately inflamed obese mice.

68 obese mice, a response that is diminished in obese mice.

69 lin resistance and metabolic dysfunctions in obese mice.

70 tosis in high-fat-sucrose diet (HFS) induced obese mice.

71 mmation, but insulin resistance persisted in obese mice.

72 cancer allografts and xenografts even in non-obese mice.

73 angiogenic factor in cancer, in tumors from obese mice.

74 nfiltration and fibrotic injury in livers of obese mice.

75 (RS) has been reported to reduce body fat in obese mice.

76 7) are significantly reduced in the liver of obese mice.

77 anine, are elevated in high-fat diet-induced obese mice.

78 nificantly increased hepatic inflammation in obese mice.

79 verses impaired placental vascularization in obese mice.

80 h the reduced insulin secretion in islets of obese mice.

81 hylation in adipose tissue from diet-induced obese mice.

82 insulin resistance in high-fat-diet-induced obese mice.

83 oncomitant increase of STAT5 co-occupancy in obese mice.

84 ion is altered in the brains of diet-induced obese mice.

85 fat mass loss without calorie restriction in obese mice.

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

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

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

89 stress does not improve glucose tolerance in obese mice, 2) silencing of the Pnpla2 in interscapular

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

91 In obese mice, activation of FXR by obeticholic acid treatm

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

93 RSA (8-log(10) reduction) in infected PUs of obese mice after just four days of treatment.

94 dle cerebral artery occlusion (tMCAO) in T2D/obese mice (after 7 months of high-fat diet [HFD]) and a

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

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

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

98 and PKC (protein kinase C) were measured in obese mice and compared with lean controls.

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

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

101 Here, we show that ATMs isolated from obese mice and humans exhibit markers of increased rate

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

103 rrelated with fasting plasma glucose in both obese mice and humans.

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

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

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

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

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

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

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

111 n, indices of healthy glucose metabolism, in obese mice and obese, prediabetic women.

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

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

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

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

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

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

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

119 n resistance in liver and skeletal muscle of obese mice, and such effects were associated with activa

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

121 were significantly increased in diet-induced obese mice as compared with controls.

122 and reversed atrial fibrosis in diet-induced obese mice as compared with controls.

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

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

125 ponectin supplementation during pregnancy in obese mice attenuates the adverse metabolic outcomes in

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

127 nd low-fat diet improve glucose tolerance in obese mice but these effects do not track with a thermog

128 metabolism and insulin sensitivity in female obese mice, but did not affect CL-induced body weight lo

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

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

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

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

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

134 and females, although they are increased in obese mice compared with lean mice of both sexes.

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

136 Moreover, obese mice conditionally lacking GRIP1 in macrophages de

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

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

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

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

141 In HFD-induced obese mice, daily treadmill exercise during pregnancy re

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

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

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

145 Adult male offspring of obese mice developed obesity, fatty liver, and insulin r

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

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

148 In addition, obese mice displayed heightened dermatitis responses to

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

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

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

152 Silencing Mafg in mouse hepatocytes and obese mice elicits a fasting-like gene expression profil

153 Unexpectedly, depletion of macrophages in obese mice enhanced mammary epithelial cell stem/progeni

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

155 However, obese mice exhibit elevated serum VA.

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

157 Here, we demonstrate that ATM from obese mice exhibit metabolic profiles characterized by e

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

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

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

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

162 In diet-induced obese mice, expression of EAT gene induces weight loss,

163 Knocking out integrin beta6 in obese mice favorably altered the pulmonary environment b

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

165 acetate reduces body weight and adiposity in obese mice fed a high-fat diet.

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

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

168 e 1 enzymes at myoendothelial projections in obese mice generated higher levels of nitric oxide and s

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

170 e compared cancer aggressiveness in lean and obese mice grafted with prostate tumors.

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

172 Furthermore, obese mice had fewer bronchoalveolar macrophages and reg

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

174 Obese mice have fewer IgA(+) immune cells and less secre

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

176 We found that the lungs of obese mice have increased expression of the epithelial i

177 Of interest, obese mice have increased lung beta6 integrin levels at

178 n resistance, with adult female offspring of obese mice having a less pronounced metabolic phenotype.

179 Previous studies show that in obese mice, hyperinsulinemia plays a crucial role in bet

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

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

182 ng metabolic reprogramming by tumor cells in obese mice improves anti-tumor immunity.

183 Administration of FGF21 in obese mice improves defective autophagy and hepatosteato

184 aptive visceral adipose tissue plasticity in obese mice in response to cold stress and antibody-based

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

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

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

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

189 Diet-induced obese mice, including wild-type or whole body knockout (

190 Inducible AF in obese mice is mediated, in part, by a combined effect of

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

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

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

194 In contrast, obese mice lacking hepatic activating transcription fact

195 Diet-induced obese mice lacking lncOb show increased fat mass with re

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

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

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

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

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

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

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

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

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

205 ability to slow post-traumatic OA (PTOA) in obese mice models.

206 unction in the intestinal epithelium renders obese mice more susceptible to dextran sulfate sodium-in

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

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

211 lic fatty liver disease (NAFLD) patients and obese mice, occupancy of SHP and DNMT3A and DNA methylat

212 alcoholic fatty liver disease (NAFLD) and in obese mice, occupancy of SHP is reduced and that of AHR

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

214 In obese mice on a high-fat diet, the effects of metformin

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

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

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

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

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

220 estinal BCRP functions and that diet-induced obese mice recapitulate these outcomes.

221 f healthy and prediabetic/glucose-intolerant obese mice remains unknown.

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

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

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

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

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

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

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

229 Islets from prediabetic obese mice show significantly higher CypD-dependent prot

230 ce, as well as leptin-resistant diet-induced obese mice, show significant reductions of sympathetic i

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

232 All obese mice showed higher AHR at 30 mg/ml of methacholine

233 Obese mice showed significant increases in lung IL-1 bet

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

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

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

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

238 In HFD-fed obese mice systemic glucose tolerance and insulin sensit

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

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

241 2(+) Tregs in VAT was severely diminished in obese mice that had been fed a high-fat/sucrose diet, an

242 In diet-induced obese mice, the coadministration of a peripheral CB1R in

243 These studies demonstrate that in obese mice, the combination of liraglutide and phentermi

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

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

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

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

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

249 In obese mice, treatment with cGAMP significantly decreases

250 Here we show that cold exposure of obese mice triggers an adaptive tissue remodeling in vis

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

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

253 Pacing-induced AF in 100% of diet-induced obese mice versus 25% in controls (P<0.01) with increase

254 latable food consumption in the offspring of obese mice was a change in taste function.

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

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

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

258 model of sepsis in lean and in diet-induced obese mice, we demonstrate that obese diabetic mice have

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

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

261 ction, memory T-cell subsets in the lungs of obese mice were decreased compared to lean mice.

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

263 At the same time, T cells from obese mice were found to have altered cellular metabolis

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

265 metabolic abnormalities in offspring born to obese mice were largely prevented by normalization of ma

266 stitial macrophages in high-fat diet induced obese mice were lower than regular chow diet-fed mice ch

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

268 Diet-induced obese mice were randomized to VSG or sham surgery, with

269 , body weight, and adiposity in diet-induced obese mice when administered once daily for 6 days.

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 lly identical 10-week-old female New Zealand Obese mice, which differ in their degree of hyperglycemi

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

274 of NRG4 reduced weight gain in diet-induced obese mice, while overexpression of ANGPTL8 resulted in

275 imulus gradually increases, liver cells from obese mice will reach the state of saturated cytosolic C

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

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

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

279 crophages and decorin expression, we treated obese mice with either IgG control or anti-F4/80 antibod

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

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

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

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

284 chow diet-fed mice or high-fat diet induced obese mice with lipopolysaccharide (LPS) or vehicle via

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

286 Previously we reported that obese mice with low circulatory APN levels exhibited pul

287 We further found that diet-induced obese mice with mild hyperbilirubinemia have reduced WAT

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

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

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

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

292 ucing synovitis and cartilage destruction in obese mice with PTOA.

293 Furthermore, treatment of obese mice with putative NURR1 agonists increases energy

294 Injection of obese mice with recombinant helminth-derived Schistosoma

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

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

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

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

299 In obese mice, Wnt5a ablation ameliorates insulin resistanc

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