ライフサイエンスコーパス: diabetic mice

1 ress in the retina of streptozotocin-induced diabetic mice.

2 GLP-1R in healthy and streptozotocin-induced diabetic mice.

3 G6PD activity was also reduced in diabetic mice.

4 sulfate in the liver, reduces albuminuria in diabetic mice.

5 o improved wound closure and angiogenesis in diabetic mice.

6 ed in the duodenum of streptozotocin-induced diabetic mice.

7 tion, and the accelerated atherosclerosis in diabetic mice.

8 empagliflozin improves plaque regression in diabetic mice.

9 ed the role of IL-23 in diabetes in nonobese diabetic mice.

10 he intraperitoneal (IP) space of healthy and diabetic mice.

11 terone were investigated using male nonobese diabetic mice.

12 is significantly downregulated in embryos of diabetic mice.

13 ed angiogenesis and arteriogenesis in type 2 diabetic mice.

14 uminuria in streptozotocin-induced and Akita diabetic mice.

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

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

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

18 nduced angiogenesis is compromised in type 2 diabetic mice.

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

20 glucose and insulin sensitivity in obese and diabetic mice.

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

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

23 lammation, and suppressed atherosclerosis in diabetic mice.

24 eptibility to RA teratogenesis in embryos of diabetic mice.

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

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

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

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

29 ochondrial bioenergetics in the podocytes of diabetic mice.

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

31 Metformin and reduce blood glucose levels in diabetic mice.

32 pithelial wound healing and nerve density in diabetic mice.

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

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

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

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

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

38 RvD2 rescued defective revascularization in diabetic mice.

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

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

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

42 ction and augmented vascular regeneration in diabetic mice.

43 inhibitor increased glomerular FH levels in diabetic mice.

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

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

46 in the glomeruli of streptozotocin injected diabetic mice.

47 ly) had slower healing ratios than wild-type diabetic mice.

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

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

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

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

52 microRNAs, glomerular ECM and hypertrophy in diabetic mice.

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

54 ing neutrophils and rescued wound healing in diabetic mice.

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

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

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

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

59 of GSH concentration and Nox4 expression in diabetic mice.

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

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

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

63 letion of BMMPhi restored SC mobilization in diabetic mice.

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

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

66 pounds lower blood glucose concentrations in diabetic mice.

67 reased glomerular basement membrane width in diabetic mice.

68 cumulation, and improved cardiac function in diabetic mice.

69 ntrol early-stage vascular disease in type I diabetic mice.

70 th diabetes correction in chemically induced diabetic mice.

71 l beta-cells in streptozotocin (STZ)-induced diabetic mice.

72 umulation of Mo/MPhi and impaired healing in diabetic mice.

73 of antigen presenting cells in the lungs of diabetic mice.

74 pithelial wound healing and nerve density in diabetic mice.

75 achieve a glucose-lowering effect in type 1 diabetic mice.

76 eeks-, and 24 weeks-old male Akita/+ and non-diabetic mice.

77 on of PTEN improved the survival of infected diabetic mice.

78 sangial expansion and glomerular fibrosis in diabetic mice.

79 synthase expression and plasma NO levels of diabetic mice.

80 g to reduced islet autoimmunity in non-obese diabetic mice.

81 d and remained attenuated in both normal and diabetic mice.

82 al tubular cell (RPTC) apoptosis and loss in diabetic mice.

83 y T cells negatively affect wound healing in diabetic mice.

84 prevented oxidative stress in the retina of diabetic mice.

85 latory T cells in cutaneous wound healing in diabetic mice.

86 e-related changes on the volatile profile of diabetic mice.

87 ivation in the podocytes and renal cortex of diabetic mice.

88 betes, PNES inhibited disease progression in diabetic mice.

89 romoted general health and survival of obese diabetic mice.

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

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

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

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

94 liorated chronic progressive EAE in nonobese diabetic mice, a model which resembles some aspects of s

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

96 ry environment of atherosclerotic plaques of diabetic mice after cholesterol lowering and may represe

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

98 pecific cyclin D1 deficiency protected obese/diabetic mice against hepatic tumorigenesis, whereas lea

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

100 Consequently, CCR4(-/-) diabetic mice also presented with alteration on T cells

101 VDR(-/-) and VDD diabetic mice also showed significantly decreased nerve

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

103 CXCR2 was able to reverse delayed healing in diabetic mice and accelerate ex vivo human skin wound he

104 CXCL12 showed enhanced insulin secretion in diabetic mice and accelerated the normalization of hyper

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

106 e region of the wound at a higher density in diabetic mice and associate with endothelial cells at th

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

108 pitulated in the brains of db/db (Lepr(db) ) diabetic mice and corresponds with recognition memory de

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

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

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

112 nal microvessels from streptozotocin-induced diabetic mice and human donors with diabetic retinopathy

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

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

115 n significantly accelerated wound healing in diabetic mice and may be a potential therapeutic target

116 regulated blood glucose in insulin-deficient diabetic mice and minipigs (for minipigs >25 kg, glucose

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

118 ed gene product, is increased in the eyes of diabetic mice and patients with DME.

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

120 hibition of DUSP26 improves hyperglycemia in diabetic mice and protects human islet cells from cell d

121 When hindlimb ischemia is induced in diabetic mice and QKI-7 is knocked-down in vivo in ECs,

122 vation in the kidney cortex and glomeruli of diabetic mice and rats, respectively.

123 e found that TSP2 expression was elevated in diabetic mice and skin from patients with diabetes.

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

125 s were isolated from adult male db/db type 2 diabetic mice and their healthy corresponding control db

126 VEZF1 expression was reduced in aortae of diabetic mice and upregulated in diabetic murine aortae

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

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

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

130 highly expressed in kidneys of type 1 and 2 diabetic mice, and AP4 is a major transcription factor t

131 ors, CCL2 levels were increased in wounds of diabetic mice, and subsequent experiments showed that lo

132 contractile activity is disordered in type 2 diabetic mice, and this appears to be a consequence of e

133 xpression is highly increased in islets from diabetic mice as well as in plasma of diabetic patients.

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

135 In diabetic mice, both pre- and post-wounding, topical MCS-

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

137 -controlling islet implants in the kidney of diabetic mice but not in failing implants.

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

139 dedifferentiation and intimal hyperplasia in diabetic mice by decreasing PDGFRbeta expression in VSMC

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

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

142 ifficult to heal, differently from CCR4(-/-) diabetic mice (CCR4(-/-) diabetic), and also from anti-C

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 S. aureus infection in diabetic mice compared with nondiabetic controls, correl

146 Phi proliferate at higher rates in wounds of diabetic mice compared with nondiabetic mice, leading to

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

148 When transplanted into diabetic mice, converted human alpha-cells reverse diabe

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

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

151 insulin deficiency in streptozotocin-induced diabetic mice decreased mitochondrial ATP production and

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

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

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

155 the retinal microvasculature from untreated diabetic mice demonstrated a nearly threefold increase i

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

157 Despite normoglycemia, CaMKIIdelta-deficient diabetic mice developed the full picture of diabetic nep

158 VDR(-/-) and VDD diabetic mice (diabetic for 8 and 20 weeks, respectively

159 Remarkably, CaMKIIdelta-deficient diabetic mice did not develop hyperglycemia.

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

161 Diabetic mice displayed decreased survival in a collagen

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

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

164 Platelets from STZ-induced diabetic mice exhibited increased activation after admin

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

166 Diabetic mice fed a high-fiber diet were significantly l

167 tore glucose homeostasis in immune-competent diabetic mice for 50 days.

168 s restore normal glycemia in immunocompetent diabetic mice for at least 6 weeks, can be visualized us

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

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

171 Diabetic mice had increased expression of Txnip in the s

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

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

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

175 ce, we observed that S. aureus isolated from diabetic mice had significant increases in the levels of

176 from the pancreatic infiltrates of nonobese diabetic mice have been shown to recognize epitopes form

177 nduced obese mice, we demonstrate that obese diabetic mice have decreased "emergency hematopoiesis" a

178 Neutrophils isolated from obese diabetic mice have decreased transcripts of Axl and Mert

179 ly, both neutrophils and monocytes in obese, diabetic mice have functional defects, with decreased ph

180 imal models of sepsis have shown that obese, diabetic mice have lower survival rates compared with no

181 In diabetic mice, higher levels of citrullinated histone H3

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

183 ein expression is elevated in Muller glia of diabetic mice; however, the mechanisms responsible for t

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

185 Here, we find that a 28-day IF regimen for diabetic mice improves behavioral impairment via a micro

186 ft ventricle (LV) dysfunction in hearts from diabetic mice, improving contractility and relaxation wh

187 tes liver metabolism and glycemic control in diabetic mice in a LKB1-dependent manner.

188 d in the glomerular mesangial area of type 1 diabetic mice in two different models (streptozotocin-in

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

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

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

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

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

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

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

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

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

198 od sugar level in diet-induced obesity (DIO) diabetic mice, it reduced osteoclast numbers and alveola

199 In diabetic mice, knockout or topically applied nanoconstru

200 In diabetic mice, macrophage depletion followed by reconsti

201 studied lung and kidney ACE2 and TMPRSS2 in diabetic mice mimicking host factors linked to severe CO

202 In diabetic mice model we detected alterations in skeletal

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

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

205 ls were decreased in the wounds of CCR4(-/-) diabetic mice on day 2.

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

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

208 evented transcellular induction of Cxcl12 In diabetic mice, pioglitazone treatment downregulated Osm,

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

210 est whether raising functional HDL levels in diabetic mice prevents monocytosis, reduces the quantity

211 In diabetic mice, PRR knockdown decreased urine albumin to

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

213 Administration of AFSE to diabetic mice reduced total cholesterol, triglycerides,

214 ion of mmu-miR-483* in B6.BKS(D)-Lepr(db) /J diabetic mice rescued diabetes-associated impairment of

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

216 encapsulated in the device and implanted in diabetic mice restored normoglycaemia in the mice for ov

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

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

219 ed the increased hepatic Apoc3 expression in diabetic mice - resulting in lower levels of TRLs - with

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

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

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

223 Stimulation of AgRP neurons in diabetic mice reversed leptin's ability to inhibit feedi

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

225 Diabetic mice show an increased number of active OCLs.

226 At the end of study, diabetic mice showed increased expressions of PRR and NO

227 Diabetic mice showed increased incidence of spontaneous

228 Diabetic mice showed increased skin lesion size and bact

229 Diabetic mice showed parallel changes in cardiac Klf5 an

230 In addition, renal mitochondria of diabetic mice showed reduced protein expression and acti

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

232 as corroborated by immunoblotting results in diabetic mice showing that BBM DMT1 expression was incre

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 Cx36 coupling is decreased in pre-diabetic mice, suggesting a role for altered coupling in

236 hich resulted in improved visual function in diabetic mice, suggesting that chromophore deficiency pl

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

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

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

240 tify a population of neutrophils in infected diabetic mice that correlated with decreased survival an

241 studies, we used our chronic wound model in diabetic mice that has similar characteristics as human

242 lso from anti-CCL17/22 or anti-CD25-injected diabetic mice that presented with accelerated wound heal

243 In alloxan-induced diabetic mice, the AFS methanol extract (AFSE) rich in c

244 In healthy, hyperglycaemic and diabetic mice, the oral delivery of 10 U kg(-1) insulin

245 In the retina of diabetic mice, the repressor of mRNA translation, eIF4E-

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

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

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

249 nto either wild-type, diabetic wild-type, or diabetic mice transgenic for human apolipoprotein AI, wh

250 By contrast, obese-diabetic mice treated with a small-molecule PGRMC2 activ

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 ed insulin levels were measured in recipient diabetic mice upon implantation of the islet-seeded biom

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

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

259 Through an unbiased, systematic screen in diabetic mice, we identified selective, safe, and effect

260 y minor changes between infected control and diabetic mice, we observed that S. aureus isolated from

261 SCFA-treated diabetic mice were protected from nephropathy, but not i

262 Diabetic mice were randomized to high-fiber, normal chow

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

264 Diabetic mice were transplanted with syngeneic islets pl

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

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

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

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

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

270 tidome of the pancreatic islets in non-obese diabetic mice, which spontaneously develop autoimmune di

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

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

273 l sensitivity was significantly decreased in diabetic mice, which was prevented by fenofibrate.

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

275 Treating diabetic mice with a calpain inhibitor prevented loss of

276 Treating diabetic mice with a specific sEH inhibitor prevented th

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

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

279 Analyses in human cells and diabetic mice with cardiomyocyte-specific FOXO1 (Forkhea

280 Diabetic mice with cardiomyocyte-specific FOXO1 deletion

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

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

283 as able to identify unique differences among diabetic mice with different duration of diabetes.

284 Of note, non-obese diabetic mice with high blood glucose levels displayed a

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

286 e and less frequent injections, in non-obese diabetic mice with insulin resistance symptoms.

287 Treatment of diabetic mice with insulin restored intestinal NHE3 acti

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

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

290 Intriguingly, diabetic mice with PKCalpha deficiency did not show incr

291 mental MI or sham surgery in nondiabetic and diabetic mice with preexisting atherosclerosis.

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

293 tosis and ROS generation abilities in obese, diabetic mice with sepsis.

294 Treatment of diabetic mice with the NFAT blocker A-285222 reduced NFA

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

296 the diabetic heart, we crossed OVE26 type 1 diabetic mice with transgenic mice expressing a constitu

297 Treatment of chronic skin wounds in diabetic mice with VEGF-A165 and PDGF-BB incorporated wi

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

299 rough comparison of BMSCs from wild-type and diabetic mice, with a known redox and metabolic disorder

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