ライフサイエンスコーパス: diabetic mice

1 terone were investigated using male nonobese diabetic mice.

2 inhibitor increased glomerular FH levels in diabetic mice.

3 quercetin, to prevent NTDs in the embryos of diabetic mice.

4 wild type (WT), but not in insulin-deficient diabetic mice.

5 in the glomeruli of streptozotocin injected diabetic mice.

6 ivity than the hearts of control, non-type 1 diabetic mice.

7 et of miR-25, was significantly increased in diabetic mice.

8 , antedated the loss of insulin secretion in diabetic mice.

9 d GSIS and preserved islet beta-cell mass in diabetic mice.

10 microRNAs, glomerular ECM and hypertrophy in diabetic mice.

11 aster re-epithelialization of skin wounds in diabetic mice.

12 ing neutrophils and rescued wound healing in diabetic mice.

13 that accounts for poor skin host defense in diabetic mice.

14 ere also observed in GLO1-diabetic versus WT-diabetic mice.

15 i that were purified from type I and type II diabetic mice.

16 random as well as fasting glucose levels in diabetic mice.

17 Cs account for 60% of the ATMs in the type 2 diabetic mice.

18 of GSH concentration and Nox4 expression in diabetic mice.

19 uria and less podocyte loss compared with WT diabetic mice.

20 n leakage was observed in anti-VEGF injected diabetic mice.

21 antation, and reduce blood glucose levels in diabetic mice.

22 letion of BMMPhi restored SC mobilization in diabetic mice.

23 njections) to retinal neurons in Ins2(Akita) diabetic mice.

24 -beta1, collagen IV, and fibrosis only in WT diabetic mice.

25 pounds lower blood glucose concentrations in diabetic mice.

26 reased glomerular basement membrane width in diabetic mice.

27 tly accelerated wound healing in STZ-induced diabetic mice.

28 Similar results were found in obese diabetic mice.

29 rular hypertrophy and mesangial expansion in diabetic mice.

30 sensitivity in skeletal muscle of obese and diabetic mice.

31 ich led to increased blood insulin levels in diabetic mice.

32 diabetic mice were attenuated in EGFR(podKO) diabetic mice.

33 generation also was suppressed in Lrat(-/-) diabetic mice.

34 ng S100A8/A9 also decreased atherogenesis in diabetic mice.

35 sis of lesions characteristic of early DR in diabetic mice.

36 ase 3 and Bcl2 expression in glomeruli of WT diabetic mice.

37 ialization compared with vehicle-treated STZ-diabetic mice.

38 nduced angiogenesis is compromised in type 2 diabetic mice.

39 ty is greater in dysfunctional beta cells of diabetic mice.

40 lity in vitro and after transplantation into diabetic mice.

41 g NAPDH oxidase-mediated oxidative damage in diabetic mice.

42 essing but not an AdipoR1-depleted strain of diabetic mice.

43 insulin, and reduces hyperglycemia in Akita diabetic mice.

44 e 2 diabetic (T2D) mice, but not from type 1 diabetic mice.

45 Vascular PAR-1 mRNA was not increased in diabetic mice.

46 tion in cultured human podocytes (hPODs) and diabetic mice.

47 ogical outcomes 24h after reperfusion in the diabetic mice.

48 like structures and support normoglycemia in diabetic mice.

49 glucose tolerance test (OGTT) in normal and diabetic mice.

50 n is increased in WAT and liver of obese and diabetic mice.

51 n Myostatin regulation in skeletal muscle in diabetic mice.

52 ific injury or from the pancreas of nonobese diabetic mice.

53 BK-channel-mediated coronary vasodilation in diabetic mice.

54 well as increased levels of CD in retinas of diabetic mice.

55 functional angiogenesis in adult, aged, and diabetic mice.

56 mia induces hypertension and renal injury in diabetic mice.

57 of these cells ameliorates hyperglycemia in diabetic mice.

58 GF-beta1, and PAI-1) seen in placebo-treated diabetic mice.

59 K3beta) in renal cells and in the kidneys of diabetic mice.

60 ia restored ischemic limb blood flow in aged diabetic mice.

61 otein levels were elevated in the kidneys of diabetic mice.

62 effects were also seen in type 1 and type 2 diabetic mice.

63 ced insulin action in primary hepatocytes of diabetic mice.

64 renal glomeruli from streptozotocin-induced diabetic mice.

65 ortex of control and streptozotocin-injected diabetic mice.

66 (-/-) mice treated with TRAM34 compared with diabetic mice.

67 d improved cardiac structure and function in diabetic mice.

68 rogenase (PDH) were observed in kidneys from diabetic mice.

69 o QT interval prolongation for both types of diabetic mice.

70 ucose uptake and correcting hyperglycemia in diabetic mice.

71 streptozotocin, high-fat diet-fed, and db/db diabetic mice.

72 nd COX-2-dependent mechanisms in male type 2 diabetic mice.

73 x 10(6) splenocytes from 6-week-old nonobese diabetic mice.

74 glucose and insulin sensitivity in obese and diabetic mice.

75 c acid (OCA) and the TGR5 agonist INT-777 in diabetic mice.

76 is significantly downregulated in embryos of diabetic mice.

77 ive stress and calcineurin/NFAT signaling in diabetic mice.

78 lammation, and suppressed atherosclerosis in diabetic mice.

79 eptibility to RA teratogenesis in embryos of diabetic mice.

80 f recombinant GPNMB protein to the wounds of diabetic mice.

81 on increases in nondiabetic mice, but not in diabetic mice.

82 ncidence of autoimmune diabetes in non-obese diabetic mice.

83 l infiltration in the ischemic hind limbs of diabetic mice.

84 ed angiogenesis and arteriogenesis in type 2 diabetic mice.

85 ochondrial bioenergetics in the podocytes of diabetic mice.

86 nd was attenuated by NOX1/NOX4 inhibition in diabetic mice.

87 Metformin and reduce blood glucose levels in diabetic mice.

88 synaptic plasticity, learning, and memory in diabetic mice.

89 f cutaneous wounds in both type 1 and type 2 diabetic mice.

90 hondrial structure in Drp1-null podocytes of diabetic mice.

91 ssessing insulin-sensitizing effect in db/db diabetic mice.

92 n type 1 diabetes in humans and in non-obese diabetic mice.

93 uminuria in streptozotocin-induced and Akita diabetic mice.

94 RvD2 rescued defective revascularization in diabetic mice.

95 lations, accelerating T1D onset in non-obese diabetic mice.

96 beta cells of inflamed islets from non-obese diabetic mice.

97 ischemia/reperfusion injury in obese type 2 diabetic mice.

98 n streptozotocin (STZ)-induced diabetic (STZ-diabetic) mice.

99 ACM was impaired in macrophages from db/db (diabetic) mice.

100 In streptozotocin-induced diabetic mice, 1,25-VitD3 also promoted reendothelializa

101 eased CD levels were found in the retinas of diabetic mice (3-fold) and serum samples of patients wit

102 d the effects of PI3Kgamma ablation in db/db diabetic mice, a genetic model of obesity-driven beta-ce

103 regulates the blood glucose level of type-1 diabetic mice, achieving a reduction for over 10 h.

104 ntly decreased MRI signals were confirmed in diabetic mice after streptozotocin (STZ) injection.

105 anti-inflammatory macrophages, increased in diabetic mice after treatment.

106 In STZ-diabetic mice, albuminuria, increased Src pTyr-416, TACE

107 Thus, male nonobese diabetic mice allow for translational studies on the met

108 tal autoimmune encephalomyelitis in nonobese diabetic mice, an experimental model that resembles seve

109 oved overall retinal and visual functions in diabetic mice and acute treatment with DA D1 or D4 recep

110 bition on stroke recovery were restricted to diabetic mice and appeared to worsen BBB permeability in

111 to improve angiogenesis in the wounds of STZ-diabetic mice and blunted angiogenesis in the wounds of

112 l cells was maintained in the hearts of GLO1-diabetic mice and corresponded to less myocardial cell d

113 neal nerve regeneration and wound healing in diabetic mice and could potentially be exploited as a th

114 When isolated from diabetic mice and cultured in high glucose, Drp1-null po

115 nerve regeneration in the wounded corneas of diabetic mice and healthy animals, in which DCs had been

116 a switch between autophagy and apoptosis, in diabetic mice and high glucose-treated H9c2 cardiac myob

117 its expression is up-regulated in obese and diabetic mice and humans.

118 ing enzyme, was reduced in kidneys from both diabetic mice and humans.

119 n (STAT) and target gene expression, both in diabetic mice and in cultured cells under hyperglycemic

120 umans) levels are lower in islets taken from diabetic mice and in humans with type 2 diabetes; knockd

121 llobaculum bacteria that were abundant in HF diabetic mice and increased butyrate-producing bacteria.

122 patients with non-alcoholic steatohepatitis, diabetic mice and mice fed a high-fat diet.

123 e cardiac function of streptozotosin-induced diabetic mice and on advanced glycation end products (AG

124 Dicer levels were altered in platelets from diabetic mice and patients, a change that could be attri

125 ) is a known target that is overexpressed in diabetic mice and responsible for causing insulin resist

126 r levels (BGLs) of chemically induced type-1 diabetic mice and stabilize BGLs at a reduced level for

127 Ins2(Akita) diabetic mice and streptozotocin-induced diabetic rats e

128 ion was observed in NOX4 transgenic mice and diabetic mice and was attenuated by NOX1/NOX4 inhibition

129 es in animals (streptozotocin-induced type 1 diabetic mice) and cellular models to investigate canoni

130 BKS.Cg-Dock7m+/+ Leprdb/J db/db mice (diabetic mice) and db/+ mice, as well as C57BL/6J IL6-kn

131 puncture (EA) on cerebral ischemic injury in diabetic mice, and explored the role of NADPH oxidase-me

132 ased accumulation of apoptotic thymocytes in diabetic mice, and stimulated diabetic macrophage phagoc

133 2 expression was reduced in the glomeruli of diabetic mice as well as TGF-beta-treated mouse mesangia

134 in vivo decreases NTD rate in the embryos of diabetic mice, as well as Caspase-8 activation and cell

135 Cortices from diabetic mice (both CTGF +/+ and CTGF +/-) manifested hi

136 GTPCH1 activity in the aortas and hearts of diabetic mice, both of which were attenuated by the inhi

137 d mitochondria in the podocytes of wild-type diabetic mice but a marked improvement in mitochondrial

138 ncreases blood flow recovery in obese type 2 diabetic mice by an endothelial nitric oxide synthase/Ak

139 1D via kidney-pancreas transplantation or in diabetic mice by treatment with an ecto-TMEM219 recombin

140 tudy was performed in streptozotocin-induced diabetic mice (C57BL/6).

141 fic inducible repletion of angiopoietin-1 in diabetic mice caused a 70% reduction of albuminuria and

142 trate that SHP-1 is elevated in podocytes of diabetic mice, causing insulin unresponsiveness and DN.

143 ased colocalization of SHP-1 with nephrin in diabetic mice compared with control littermates.

144 gg1 was found to be highly O-GlcNAcylated in diabetic mice compared with controls.

145 Studies in diabetic mice confirmed these findings (6.0 +/- 0.4-fold

146 n expression and the onset of proteinuria in diabetic mice correlate with an increased accumulation o

147 ucible podocyte-specific deletion of Drp1 in diabetic mice decreased albuminuria and improved mesangi

148 Dietary supplementation of d-glucarate in diabetic mice decreased MIOX expression, attenuated tubu

149 ivation of insulin in streptozotocin-induced diabetic mice decreased mitochondrial ATP production, re

150 full-thickness wounds in diet-induced obese diabetic mice decreases local GM3S expression by >80% at

151 Nevertheless, nondiabetic and diabetic mice deficient in MCs have delayed wound healin

152 augmented remodeling response was absent in diabetic mice deficient in PAR-4.

153 ue kallikrein-1 protein (DM199) to non-obese diabetic mice delayed the onset of T1D, attenuated the d

154 The diabetic mice demonstrate an early decrease in renal red

155 Here we report that the hearts of type 1 diabetic mice, despite having increased Ogg1 protein lev

156 Ligated carotid arteries from diabetic mice developed more extensive neointimal hyperp

157 Although naturally occurring Th17 cells in diabetic mice did not contribute to diabetes development

158 Additionally, STZ-injected wild-type (WT) diabetic mice displayed an altered gut microbiota compar

159 e cardiac biopsies of streptozotocin-induced diabetic mice displayed impaired angiogenic capacity (P=

160 Pax3 expression is inhibited in embryos of diabetic mice due to hyperglycemia-induced oxidative str

161 t increasing plasma MG to levels observed in diabetic mice either using an exogenous source (1% in dr

162 In diabetic mice, erlotinib-treated mice had evidence of in

163 this study, we demonstrate that Akita type 1 diabetic mice exhibit hyperacetylation.

164 STZ-induced diabetic mice exhibited distinct cardiac dysfunction, da

165 Low-dose streptozotocin-induced diabetic mice exhibited increased aortic O-GlcNAcylation

166 GT in HF-fed diabetic mice exhibited parallel decreases in insulin an

167 Macrophage from nonobese diabetic mice failed to provide signals necessary for be

168 y in immune competent streptozotocin-induced diabetic mice for therapeutic efficacy evaluation.

169 aeruginosa in the wounds of insulin-treated diabetic mice from antibiotic treatment.

170 neutrophils was prevented by pretreatment of diabetic mice given MS with compound 48/80.

171 We also show that in diabetic mice, Glo1 overexpression completely prevents d

172 ted into the liver of streptozotocin-induced diabetic mice (H-2) via the portal vein.

173 In response to 8Br-cAMP treatment, diabetic mice had impaired inotropic and lusitropic resp

174 Diabetic mice had increased expression of Txnip in the s

175 Islets from diabetic mice had increased levels of IL1B and IL6, comp

176 Furthermore, EGFR(podKO) diabetic mice had less TGF-beta1 expression, Smad2/3 pho

177 Streptozotocin-induced diabetic mice had reduced blood flow recovery and neoves

178 Alveolar macrophages from diabetic mice had reduced expression of CD14 and macroph

179 expectedly, we observed that insulin-treated diabetic mice had significantly more biofilm in their wo

180 reased monocyte recruitment into arteries of diabetic mice has emerged as an important mediator of th

181 betes have increased M1 macrophages, whereas diabetic mice have increased CD169(+) BMMPhi with SC-ret

182 ompared with nondiabetic mice, wounds in STZ-diabetic mice healed more slowly.

183 In diabetic mice, higher levels of citrullinated histone H3

184 units that also suppressed hyperglycemia in diabetic mice, highlighting the potential for developmen

185 nt hyperlipidemic and streptozotozin-induced diabetic mice, hyperglycemia and hyperlipidemia acted re

186 cyte-specific overexpression (OE) of Tug1 in diabetic mice improved the biochemical and histological

187 o skeletal muscle of either young or old and diabetic mice improved the recovery of blood flow in the

188 Plasma levels of HDL were reduced in diabetic mice in a RAGE-dependent manner.

189 ass B type I (SR-BI) in vitro and SR-BI(-/-) diabetic mice in vivo attenuated rHDL rescue of diabetes

190 cification and worsened aortic compliance of diabetic mice in vivo.

191 In the hearts of db/db diabetic mice, in which Akt phosphorylation was decrease

192 Furthermore, angiopoietin-1 repletion in diabetic mice increased Tie-2 phosphorylation, elevated

193 In diabetic mice, increased islet levels of IL6 and IL1B mi

194 In tubules of diabetic mice, increased MIOX expression and mitochondri

195 In HFD-fed diabetic mice, increasing miR-30c expression by lenti-mi

196 Thus, FGF21 corrects hyperglycemia in diabetic mice independently of insulin action in the liv

197 on of CB1 and CB2 receptors was decreased in diabetic mice, indicating reduced endocannabinoid signal

198 late blood glucose in streptozotocin-induced diabetic mice, indicating that additional MSC-derived fa

199 eeks starting from 3 weeks of age, and to HF diabetic mice induced by high fat diet (HFD) plus strept

200 Oral dosing of these compounds in diabetic mice induces beta-cell proliferation, increases

201 Similar events were observed in DCs from diabetic mice infected with MRSA.

202 ansfer of infected alveolar macrophages from diabetic mice into nondiabetic recipients confirmed an i

203 oantibodies in young diabetes-prone nonobese diabetic mice is associated with reduced inflammation in

204 germ-free mice, that the oral microbiota of diabetic mice is more pathogenic.

205 In diabetic mice, knockout or topically applied nanoconstru

206 In diabetic mice model we detected alterations in skeletal

207 rally in normal, type 1 diabetic, and type 2 diabetic mice models.

208 In the embryos of diabetic mice, OGT is highly activated in association wi

209 letal pathology in leptin receptor-deficient diabetic mice on a C57BLKS background (db).

210 s, and increased cell death in the wounds of diabetic mice on insulin therapy.

211 levels of lysed neutrophils in the wounds of diabetic mice on insulin, combined with fewer macrophage

212 hibitors reduced retinal vascular leakage in diabetic mice on insulin.

213 roles, we mated Cav2.2(-/-) mice with db/db (diabetic) mice on the C57BLKS background.

214 In diabetic mice, OSM neutralization prevented CXCL12 induc

215 ith diabetes and in unwounded dorsal skin of diabetic mice (P < 0.05).

216 In ERV1-transgenic and ERV1-transgenic diabetic mice, phagocytosis was significantly increased.

217 In diabetic mice, plasma H2S levels were decreased while RO

218 uated with optokinetic tracking response) of diabetic mice, potentially via improvement of retinal fu

219 p66Shc knockout (KO) in diabetic mice prevented DAN in the BM, and rescued defec

220 ing CD4 T cell clones isolated from nonobese diabetic mice recognize epitopes formed by covalent cros

221 Reconstituted HDL (rHDL) infusions in diabetic mice restored blood flow recovery and capillary

222 Chronic administration of SR1555 to obese diabetic mice resulted in a modest reduction in food int

223 sEH in the retinal Muller glial cells of non-diabetic mice resulted in similar vessel abnormalities t

224 reported that tuberculosis susceptibility in diabetic mice results from a delay in innate immune resp

225 deletion of IRS-1 expression in VSMCs in non-diabetic mice results in dedifferentiation, SHPS-1 activ

226 In the retinas of streptozotocin-induced diabetic mice, retinal apoptosis was dramatically elevat

227 In diabetic mice, Sema3a(+) exacerbates laminin and collage

228 Diabetic mice show an increased number of active OCLs.

229 Diabetic mice showed increased skin lesion size and bact

230 Diabetic mice showed parallel changes in cardiac Klf5 an

231 Ten weeks after streptozotocin injection, diabetic mice showed significant decreases of corneal se

232 Additionally, only WT diabetic mice showed significant increases in oxidative

233 the expression of MMP-9 within the wounds of diabetic mice, significantly accelerating the wound heal

234 unds as demonstrated by the increased LC3 in diabetic mice skin or patients' chronic wounds.

235 rs by diseased kidneys causes the CKD-MBD in diabetic mice subjected to renal injury to induce stage

236 einforce the previously published studies in diabetic mice supporting GM3-depleting strategies as an

237 Type 1 diabetic mice that are genetically deficient in IL-17A d

238 Using non-obese diabetic mice that are genetically susceptible to T1D, w

239 ulin-dependent lowering of glucose levels in diabetic mice that is dose-dependent but does not lead t

240 We then administered 1 microg/day leptin to diabetic mice that underwent transplantation of 50 or 12

241 utes to DNA damage in skeletal muscle of the diabetic mice that would lead to myofiber degeneration.

242 In diabetic mice, the outer retinal Delta1/T1rho pattern su

243 In streptozotocin-induced type 1 diabetic mice, there was a substantial reduction in sens

244 antly accelerated cutaneous wound healing in diabetic mice through facilitating angiogenesis.

245 /-), Rag2(-/-), Il2r(-/-) mice with nonobese diabetic mice to create FRGN mice, whose livers can be f

246 Ang 1-7 on diabetic cardiomyopathy in db/db diabetic mice to elucidate the therapeutic effects and m

247 ed the capacity of alveolar macrophages from diabetic mice to phagocytose M. tuberculosis ex vivo and

248 Rat islets were transplanted into diabetic mice to the intraadrenal transplant site and co

249 Replenishment of adipsin to diabetic mice treated hyperglycemia by boosting insulin

250 Although regression was impaired in diabetic mice treated with control oligonucleotides, ant

251 In contrast, diabetic mice treated with MK-0626 exhibited modest card

252 Leukocytes isolated from diabetic mice treated with Ret-NH2 caused significantly

253 In streptozotocin diabetic mice, TRIB3 MOE exacerbated, whereas MKO preven

254 In streptozotocin-induced diabetic mice, TXNIP knockdown to nondiabetic levels res

255 In diabetic mice, VDAC1 activity was altered, resulting in

256 reased NHE3 activity and fluid absorption in diabetic mice via an insulin-independent pathway.

257 the kidney capsule of streptozotocin-induced diabetic mice; viability, function, and criteria for gra

258 of isolated brain MAM from long-term type 2 diabetic mice vs. non-diabetic controls.

259 sed macrophage content in anti-miR33 treated diabetic mice was associated with a blunting of hypergly

260 pplication of the maneuver in HFD-fed type 2 diabetic mice was found to lead to near total disappeara

261 Increased albumin/creatinine ratio in diabetic mice was markedly attenuated by erlotinib treat

262 The mortality rate of diabetic mice was reduced to 57% after the depletion of

263 is TDDS to a pressure-induced ulcer model in diabetic mice, we found that transdermal delivery of DFO

264 alter the severity of the renal phenotype in diabetic mice, we have generated mice that are type 1 di

265 d caspase 3 and downregulation of Bcl2 in WT diabetic mice were attenuated in EGFR(podKO) diabetic mi

266 Control and streptozotocin-induced diabetic mice were therefore administered 8-bromo-cAMP (

267 of serum insulin and IGF1 were observed when diabetic mice were transplanted with rat islets precondi

268 Diabetic mice were transplanted with syngeneic islets pl

269 After diabetic mice were wounded in the right eye and treated

270 the pathogenicity of the oral microbiota in diabetic mice; when transferred to recipient germ-free m

271 he slit diaphragm and reduced proteinuria in diabetic mice, whereas overexpression of CIN85 in zebraf

272 ts precursor were significantly decreased in diabetic mice, whereas primary miR-25 levels were signif

273 CL in adipocytes isolated from obese/type 2 diabetic mice, whereas the basal (unstimulated) adiponec

274 , BBB permeability was markedly increased in diabetic mice, which could not be prevented with insulin

275 d BDC2.5 T-cell receptor transgenic nonobese diabetic mice, which experience development of type 1 di

276 eaminase (AMPD) is activated in the liver of diabetic mice, which parallels with a significant reduct

277 pore (mPTP) opening in brain mitochondria of diabetic mice, which was further confirmed by mitochondr

278 stently, hepatic Sort1 was down-regulated in diabetic mice, which was partially restored after the ad

279 ameliorated podocyte and glomeruli injury in diabetic mice, which were associated with reduction of R

280 2 expression were increased in arteries from diabetic mice, which were restored after NF-kappaB inhib

281 Treatment of diabetic mice with 17-dimethylaminoethylamino-17-demetho

282 Treating diabetic mice with a calpain inhibitor prevented loss of

283 Treating diabetic mice with a specific sEH inhibitor prevented th

284 Furthermore, treatment of non-obese diabetic mice with a Y1 receptor antagonist delays the o

285 In contrast, Akita type 1 diabetic mice with below-normal Elmo1 expression have re

286 -alpha was not detected in Muller cells from diabetic mice with CD40(+) Muller cells.

287 Consistently, diabetic mice with cilnidipine, an N-/L-type calcium cha

288 After diabetes, streptozotocin-diabetic mice with heterozygous ATGL deficiency displaye

289 n normal mice and high fat (HF) diet-induced diabetic mice with hyperinsulinemia in ECIRS1 TG versus

290 Treating diabetic mice with insulin immediately after stroke resu

291 Treatment of diabetic mice with insulin restored intestinal NHE3 acti

292 of NMI was detected in islets from nonobese diabetic mice with insulitis and in rodent or human beta

293 mprovement of glomerular changes compared to diabetic mice with nitrendipine.

294 Nevertheless, chronic treatment of diabetic mice with P5 increased adipogenesis, reduced ad

295 imilar vessel abnormalities to those seen in diabetic mice with retinopathy.

296 Topical treatment of diabetic mice with the PGE analog misoprostol improved h

297 ft function 30 days after transplantation in diabetic mice, with a glucose tolerance comparable to tr

298 is altered in streptozotocin-induced type 1 diabetic mice, with decreased angiopoietin-1 levels, VEG

299 ic apoCIII knockout islets transplanted into diabetic mice, with high systemic levels of the apolipop

300 hen applied to full thickness skin wounds in diabetic mice, wounds treated with SDF1-ELP nanoparticle