ライフサイエンスコーパス: diabetic rat

1 d in vivo (nonhuman primates and healthy and diabetic rats).

2 that prevent retinal capillary demise in the diabetic rat.

3 4 and retinoids were significantly lower in diabetic rats.

4 eroxidase, coenzyme Q(10) and ORAC levels in diabetic rats.

5 2 expression was assessed in nondiabetic and diabetic rats.

6 734 and GSK2193874) resolve BRB breakdown in diabetic rats.

7 as fibrous encapsulation in both normal and diabetic rats.

8 dase level, was also significantly higher in diabetic rats.

9 ameliorates insulin-induced hypoglycemia in diabetic rats.

10 n) in healthy rats was compared with that in diabetic rats.

11 al, Tgf-beta signaling in retinal vessels of diabetic rats.

12 corticosterone secretion to normal levels in diabetic rats.

13 effects in high-fructose diet (HFD)-induced diabetic rats.

14 in both the cerebral cortex and striatum in diabetic rats.

15 nt (TSC2(+/-) ) diabetic rats than wild-type diabetic rats.

16 lin sensitivity and insulin signaling in non-diabetic rats.

17 ponding reduction in blood glucose levels in diabetic rats.

18 promoted dermal wound healing in normal and diabetic rats.

19 genotoxicity induced by streptozotocin (STZ) diabetic rats.

20 n expression in both wild-type and TSC2(+/-) diabetic rats.

21 (EGFP) mice, ZF, ZDF(fa/fa), and STZ-induced diabetic rats.

22 his resulted in restoration of euglycemia in diabetic rats.

23 bility to reduce the blood glucose levels in diabetic rats.

24 us sac with ability to restore euglycemia in diabetic rats.

25 ation were elevated in insulin resistant and diabetic rats.

26 nd pericytes 1 day after SCI compared to non-diabetic rats.

27 comparable to the parent drugs in nonfasted diabetic rats.

28 d other parameters in streptozotocin-induced diabetic rats.

29 acking (OKT) in streptozotocin (STZ)-induced diabetic rats.

30 and RECs, respectively, in both control and diabetic rats.

31 retinal vascular functions and thickness in diabetic rats.

32 A2a receptors are significantly increased in diabetic rats.

33 ect of plasma treatment for wound healing in diabetic rats.

34 en IV NC1 domains isolated from renal ECM of diabetic rats.

35 duced in the cortical endothelium in 6-month diabetic rats.

36 of synaptophysin and drebrin were reduced in diabetic rats.

37 and fibronectin overexpression in retinas of diabetic rats.

38 ote dendritic and synaptic reorganization in diabetic rats.

39 1, were quantified in streptozotocin-induced diabetic rats.

40 d intravitreally into streptozotocin-induced diabetic rats.

41 x, hippocampus, and cerebellum of untreated, diabetic rats.

42 ter myocardial infarction to nondiabetic and diabetic rats.

43 pidly improves insulin sensitivity in type 2 diabetic rats.

44 inal VEGF and inhibition of BRB breakdown in diabetic rats.

45 d and untreated streptozotocin (STZ)-induced diabetic rats.

46 n system mediates these actions of leptin in diabetic rats.

47 tion in the retina of streptozotocin-induced diabetic rats.

48 uences food intake choices in streptozotocin-diabetic rats.

49 ltered nociception in streptozotocin-induced diabetic rats.

50 etabolites were observed between control and diabetic rats.

51 ncreased inosine levels in sciatic nerves of diabetic rats.

52 d thiobarbituric acid-reacting substances in diabetic rats.

53 e changes were recapitulated in the aorta of diabetic rats.

54 levated spinal COX-2 protein and activity in diabetic rats.

55 sed spinal cyclooxygenase (COX)-2 protein in diabetic rats.

56 dyslipidemia, and cardiac PKC activation in diabetic rats.

57 g hypoglycemia effect with a faster onset in diabetic rats.

58 Diazoxide also failed to suppress EGP in diabetic rats.

59 ate inhibited Wnt signaling in the kidney of diabetic rats.

60 e and body weight gain in healthy, obese and diabetic rats.

61 ion, disrupting gastrointestinal function in diabetic rats.

62 is mislocalized in cardiac mitochondria from diabetic rats.

63 d in the peripheral nervous system of type I diabetic rats.

64 ileectomy or sham operation/pair feeding in diabetic rats.

65 reased in proteinuric streptozotocin-induced diabetic rats.

66 increases whole body glucose disposal in non-diabetic rats.

67 first time for bFGF delivery to the heart of diabetic rats.

68 costerone responses to hypoglycemic clamp in diabetic rats.

69 A control group was made up of non-diabetic rats.

70 hed in the wound fluids collected from day 2 diabetic rats.

71 oxidative-nitrative stress in streptozotocin diabetic rats.

72 ng diabetic insults in the livers of STZ-NIC diabetic rats.

73 elations with reductions in visual acuity in diabetic rats.

74 ed in the retina from streptozotocin-induced diabetic rats.

75 Neurological deficit was greater in diabetic rats.

76 failure in recurrently hypoglycemic (RH) and diabetic rats.

77 ated in the retina of streptozotocin-induced diabetic rats.

78 comparison with those of control HFD-induced diabetic rats.

79 the one-month period in both the normal and diabetic rats.

80 ct of a high-fat-diet (HFD) on the retina of diabetic rats.

81 cells (RECs) of streptozotocin (STZ)-induced diabetic rats 3 months after the onset of diabetes and m

82 SOCS1 transgenic rats, 3) insulin-deficient diabetic rats, 4) retinal cells depleted of SOCS6 or ove

83 Streptozotocin-diabetic rats 8 weeks duration were treated with or with

84 and 10.8%, respectively, in the HFD-induced diabetic rats administered with vescalagin at 30 mg/kg b

85 aled a decrease in RPE65 in the RPE layer of diabetic rats after 3 months of hyperglycemia.

86 egulated in the retina of ZDF(fa/fa) and STZ diabetic rats after 4 months of disease.

87 tween ER stress and the integrity of BSCB in diabetic rats after SCI remains unclear.

88 ific-inhibitor, pegsunercept, was applied to diabetic rats after the onset of periodontal disease.

89 In streptozotocin-diabetic rats, all cocoa autolysates significantly decre

90 VPL neurons from diabetic rats also display enhanced spontaneous activity

91 ith the decrease of SCAI protein expression, diabetic rat and mouse kidneys with unilateral ureteral

92 thrombin biologic scaffold, was evaluated in diabetic rat and nonhuman primate (NHP) models.

93 nt with SA-PAE enhances bone regeneration in diabetic rats and accelerates bone regeneration in normo

94 microvascular cell loss in type 1 and type 2 diabetic rats and can be linked to the effect of high gl

95 ressed (P < 0.01) in the retinas and RECs of diabetic rats and controls, respectively.

96 gulation of retinal vascular permeability in diabetic rats and cultured retinal endothelial cells.

97 enged low-dosed streptozotocin (STZ)-induced diabetic rats and db/db mice.

98 ruvate carboxylase flux were normal in newly diabetic rats and elevated in older rats.

99 ncreata from neonatal streptozotocin-induced diabetic rats and improved glucose levels in mice with h

100 ge and leukostasis in streptozotocin-induced diabetic rats and in Akita mice.

101 ies were conducted in streptozotocin-induced diabetic rats and in cultured retinal cells.

102 reduced in aortas of streptozotocin-induced diabetic rats and in human coronary arterial smooth musc

103 y reported an increase in Grx1 in retinae of diabetic rats and in rat retinal Muller glial cells (rMC

104 plantation had a positive systemic effect in diabetic rats and induced regression of the established

105 expression in streptozotocin-induced type 1 diabetic rats and insulin-treated diabetic rats at 4 and

106 retina was harvested from control and type 1 diabetic rats and mice and analyzed for VEGF mRNA and pr

107 l infusion of autologous blood is greater in diabetic rats and mice compared to nondiabetic controls

108 Kidneys of diabetic rats and mice with unilateral ureteral obstruct

109 ing and podocyte numbers in the glomeruli of diabetic rats and mice.

110 ciatic nerve, spinal cord) of streptozotocin diabetic rats and mice.

111 se were similar in the retinas of Zx-treated diabetic rats and normal control rats, and these values

112 or OX lowered VMH GABA levels in both RH and diabetic rats and restored the counterregulatory respons

113 etinas from human and streptozotocin-induced diabetic rats and retinal ganglion cells (RGCs).

114 tributes to retinal vascular dysfunctions in diabetic rats and that the combination of diabetes and i

115 Diabetic rats and their non-diabetic littermates were ho

116 this further, type 1 streptozotocin-induced diabetic rats and type 2 Zucker diabetic fatty rats were

117 Inflammation was prolonged in diabetic rats and was reversed by the TNF inhibitor, whi

118 vivo studies were undertaken in STZ-induced diabetic rats and Zucker diabetic fatty rats using the t

119 BB rat and the streptozotocin (STZ)-induced diabetic rat, and compared them with nondiabetic control

120 ch day for 2 weeks to streptozotocin-induced diabetic rats, and BRB breakdown was quantified.

121 was significantly increased in retinas from diabetic rats, and this acetylation was inhibited in dia

122 etinas increased approximately 4-fold in STZ diabetic rats, and this increase was prevented by ISO an

123 inal abnormalities in streptozotocin-induced diabetic rats are alleviated by preventing the rods from

124 of action on intravenous bolus injection in diabetic rats are indistinguishable from wild-type (WT)

125 h DJB and jejunal resection normalized SI in diabetic rats as shown by SI levels equivalent to those

126 significantly reduced BRB breakdown in aged diabetic rats at 10 weeks after STZ treatment.

127 n blot in control and streptozotocin-induced diabetic rats at 3-6 weeks of diabetes.

128 ced type 1 diabetic rats and insulin-treated diabetic rats at 4 and 8 weeks following diabetes onset.

129 (nitroglycerin) agonists in nondiabetic and diabetic rats before and during inhibition of oxidative

130 e injected 4CIN or OX into the VMH of RH and diabetic rats before inducing hypoglycemia.

131 lin were assayed for receptor binding and in diabetic rats, before and after conversion by saponifica

132 eover, the activity of PKC was increased, in diabetic rat brain, in a tissue fraction composed primar

133 allodynia were present in type 1 and type 2 diabetic rats but not in rats with type 1 diabetes recei

134 s in a myocardial infarction model of type 1 diabetic rats by intramyocardial administration of an ad

135 ion were evaluated in streptozotocin-induced diabetic rats by leukostasis assay and Western blot anal

136 e effect of gaseous ozone on bone healing in diabetic rat calvarial defects treated with xenografts.

137 t 4 and 12weeks in SA-PAE/bone graft-treated diabetic rats compared to diabetic rats receiving bone g

138 lysine-acetylated proteins in the kidneys of diabetic rats compared with 11 in control kidneys.

139 significantly higher in cortical tissues of diabetic rats compared with control rats, indicating tha

140 (24 h postinjection) to a greater extent in diabetic rats compared with nondiabetic control rats.

141 oconstriction was observed in the venules of diabetic rats compared with the baseline (81.4% +/- 4.6%

142 and epinephrine responses were attenuated in diabetic rats compared with their nondiabetic control co

143 th that of nondiabetic controls, vitreous of diabetic rats contained decreased PEDF, increased VEGF,

144 These studies suggest that in type 1 diabetic rats decreased innervation of the cornea epithe

145 At 5 weeks after STZ treatment, STZ-treated diabetic rats demonstrated significantly elevated vitreo

146 Within 4 to 5 weeks of STZ treatment, the diabetic rats demonstrated significantly less retinal fu

147 In diabetic rats, depletion of EZH2 decreased histone 3 lys

148 Further characterization showed that the diabetic rats develop liver steatosis, abdominal fat acc

149 ic nerves and DRG from sulfasalazine-treated diabetic rats displayed a decrease in NF-kappaB p50 expr

150 However, the diabetic rats exhibited decreased intensity and delayed

151 ta) diabetic mice and streptozotocin-induced diabetic rats exhibited marked reductions in retinal pro

152 Diabetic rats exhibited significantly reduced visual fun

153 myocardium, compared diabetic HIP rats with diabetic rats expressing endogenous (nonamyloidogenic) r

154 nd organ histology in streptozotocin-induced diabetic rats fed a high fat (HF) diet.

155 Diabetic rats fed GLP-1-secreting bacteria showed signif

156 bone marrow of streptozotocin (STZ)-induced diabetic rats following treatments that prevent experime

157 baseline to a greater extent (P = 0.017) in diabetic rats (from 193 +/- 10 mum to 223 +/- 13 mum) co

158 Nine-month diabetic rats had a threefold increase in vascular leaka

159 immunized with adjuvant alone, KLH-immunized diabetic rats had decreased levels of glycated peptides

160 Both RH and diabetic rats had higher baseline GABA levels and were u

161 Compared with control rats, diabetic rats had more apoptotic cells in the kidney cor

162 m age-matched nondiabetic and streptozotocin-diabetic rats, half of which received the test compound

163 In diabetic rat hearts, expression of RAGE and its ligands

164 n and an impairment in diastolic function in diabetic rat hearts, which were normalized by all three

165 Relative to nondiabetic rats, diabetic rats (IgG-treated) manifested 3.9- and 7.9-fold

166 istered intramyocardially in nondiabetic and diabetic rats immediately after myocardial infarction.

167 Compared with diabetic rats immunized with adjuvant alone, KLH-immuniz

168 nduced renal glucose excretion in normal and diabetic rats, improved glucose tolerance in normal rats

169 immunostaining pattern in the beta-cells of diabetic rats in contrast to the nuclear and cytoplasmic

170 ntaneous excitatory synaptic transmission in diabetic rats in greater degree than in healthy age-matc

171 d as well as in high-fat-diet-streptozotocin diabetic rats, in which CREB is constitutively activated

172 ley rats studied for 8 months: control rats, diabetic rats, insulin-treated diabetic rats with modera

173 dry weights were significantly decreased in diabetic rats; insulin prevented these decreases.

174 Lastly, in a manner akin to the ZDF diabetic rat islets, Rac1 expression, JNK1/2, and caspas

175 insulin B:9-23-reactive T cells in nonobese diabetic rat islets.

176 The diabetic rats lacked the flicker induced increase in art

177 Removal of islet graft-bearing venous sac in diabetic rats led to recurrence of hyperglycemia.

178 neuronal and glial changes when compared to diabetic rats maintained in a standard 12:12 hour light-

179 e analyzed in the retina from streptozotocin-diabetic rats maintained in poor glycemic control (PC, g

180 e analyzed in the retina from streptozotocin-diabetic rats maintained in poor or good control for 12

181 e previously seen in the glio-pial tissue of diabetic rats may be due to the selective upregulation o

182 RVP and retinal blood flow abnormalities in diabetic rats measured at 4 weeks' diabetes duration.

183 1.5 mg/eye/d) was assessed in an STZ-induced diabetic rat model by determining retinal leukostasis an

184 A streptozotocin-treated diabetic rat model was used to study localization of (18

185 his hypothesis, we used the BBZDR/Wor type 2 diabetic rat model, as well as REC and Muller cells cult

186 These studies suggest that in a type 2 diabetic rat model, changes in corneal nerve innervation

187 ced murine models of obesity and in an overt diabetic rat model, oral administration of 29 normalized

188 Using cultured human keratinocytes and a diabetic rat model, the current study shows that a high-

189 diabetes onset in the streptozotocin-induced diabetic rat model, there is a large loss of trabecular

190 tivity and to improve glucose tolerance in a diabetic rat model.

191 ucose tolerance in normal rats and a genetic diabetic rat model.

192 for wound fluid analysis demonstrated with a diabetic rat model.

193 stems were studied in streptozotocin-induced diabetic rat model.

194 dy gene expression in pancreatic islets in a diabetic rat model.

195 ere transplanted in the PDLLCL scaffold in a diabetic rat model.

196 Both diabetic rat models exhibited an ~50% increase in GAD(65

197 extracellular GABA levels in the VMH of two diabetic rat models, the diabetic BB rat and the strepto

198 impairment of angiogenesis in the infarcted diabetic rat myocardium by proangiogenic gene therapy.

199 Streptozotocin diabetic rats (n = 19), previously subjected to five hyp

200 In the diabetic rats, no significant flicker-induced changes we

201 Diabetic rats of both sexes exhibit a reduction in cardi

202 revented the increase observed in untreated, diabetic rats of both sodium-dependent and sodium-indepe

203 O, VEGF, TNF-alpha and RAGE in the retina of diabetic rats on HFD than in controls and diabetics fed

204 In diabetic rats only, there was a transmural gradient of c

205 observed in ventricular cardiomyocytes from diabetic rats or high-glucose-treated H9c2 cells while Z

206 unterregulatory responses to hypoglycemia in diabetic rats or rats exposed to recurrent bouts of hypo

207 a enhanced the wound-healing rate in the non-diabetic rats (P < 0.05), and significant wound contract

208 respectively, in pegsunercept-treated type 1 diabetic rats (P < 0.05).

209 mulation and formalin-evoked hyperalgesia in diabetic rats, prevented elevated spinal COX-2 protein a

210 lycemia in response to overinsulinization in diabetic rats previously exposed to recurrent hypoglycem

211 tical impact in the treatment of STZ-induced diabetic rats, producing normalization of fasting hyperg

212 y rats as well as RH or streptozotocin (STZ)-diabetic rats received bilateral VMH microinjections of

213 bone graft-treated diabetic rats compared to diabetic rats receiving bone graft alone.

214 e data show that inflammatory changes in the diabetic rat retina are highly strain dependent, and SD

215 lycemia as well as in streptozotocin-induced diabetic rat retinas.

216 treatment improved the contractility of the diabetic rat's heart concomitant with upregulation of TH

217 hondria from normal and streptozocin-treated diabetic rats show increased mitochondrial O-GlcNAc tran

218 Streptozotocin-induced diabetic rats showed decreased a- and b-wave amplitudes

219 The retinal vessels of diabetic rats showed differential expression of 20 genes

220 Here we observed that diabetic rats showed increased extravasation of Evans Bl

221 Diabetic rats showed significantly increased levels of g

222 Diabetic rats showed significantly increased plasma 1-de

223 overexpression of PPARalpha in the retina of diabetic rats significantly alleviated diabetes-induced

224 Inhibition of H-Ras, both in diabetic rats (simvastatin) and in isolated endothelial

225 In addition, diabetic rat skin showed enhanced EGFR, ERK, and IL-8 ex

226 Streptozotocin-induced diabetic rats (STZ-rats) were treated with 15 mug/kg GHR

227 .Trx1 gene therapy in streptozotocin-induced diabetic rats subjected to infarction.

228 n of synaptic proteins in the spinal cord of diabetic rats, suggesting that ILK and PINCH contribute

229 lized to choriocapillaris PO2, was higher in diabetic rats than in age-matched controls, which was op

230 ormal tissue was significantly higher in non-diabetic rats than in diabetic ones.

231 protein showed significantly lower levels in diabetic rats than those in nondiabetic controls.

232 in partially tuberin-deficient (TSC2(+/-) ) diabetic rats than wild-type diabetic rats.

233 the cause of altered behavioral responses in diabetic rats that occur after short-term diabetes, but

234 Following subcutaneous injection in a diabetic rat, the analog effected glycemic control with

235 After a 14-day administration in diabetic rats, the chloroform extract recorded the highe

236 In the renal cortex of diabetic rats, the increase in Akt phosphorylation is as

237 glucose-exposed podocytes and the kidneys of diabetic rats, the lower EZH2 expression detected coinci

238 In the inner medulla (IM) of diabetic rats, the more abundant 117-kDa UT-A1 in lipid

239 For type 2 diabetic rats, the number of endothelial cells and peric

240 In contrast, in diabetic rats, they were colocalized with upregulated Ra

241 eurons were observed in DRG from STZ-induced diabetic rats; this decrease was confirmed and quantifie

242 We assessed BRB protection in diabetic rats through use of species-specific analogs of

243 iabetic (control) and streptozotocin-induced diabetic rats to elicit a granulation tissue response an

244 ats with moderate or mild hyperglycemia, and diabetic rats transplanted with microencapsulated islets

245 Streptozotocin diabetic rats treated daily with heparin showed similar

246 Diabetic rats treated with periocularly administered cel

247 Diabetic rats treated with SSTR2a needed little or no gl

248 In diabetic rats, TRIB3 expression in skeletal muscle was i

249 icrovasculature was evaluated in control and diabetic rats using three-dimensional images.

250 tes-induced changes in retinal blood flow in diabetic rats, using two distinctly different methods.

251 and pericyte ghosts were measured in control diabetic rats versus nondiabetic controls, and topical N

252 and pericyte ghosts were measured in control diabetic rats versus those in nondiabetic control animal

253 el for control rats was 104.8+/-2.9, and for diabetic rats was 420.1+/-42.0.

254 rogression of early retinal abnormalities in diabetic rats was assessed by monitoring the ERG b-wave

255 inal cord of non-diabetic and streptozotocin-diabetic rats was assessed by Western-blot analysis and

256 e increased retinal vascular permeability in diabetic rats was associated with a decrease in vascular

257 Another group of diabetic rats was infused with the MC3/4R agonist MTII (

258 ecrease in brain DNA and protein contents in diabetic rats was prevented by the combination treatment

259 Impaired RDD in diabetic rats was rapidly normalized by spinal delivery

260 staining in the glomeruli of heparin-treated diabetic rats was very high at week 1 and decreased to n

261 opathic pain in streptozotocin (STZ)-induced diabetic rats, we analyzed dendritic spine morphology an

262 lly, retinas of streptozotocin (STZ)-induced diabetic rats were analyzed to determine if diabetes alt

263 Control and diabetic rats were assessed across 12 weeks of hyperglyc

264 Streptozotocin-diabetic rats were assigned to two groups-treated with t

265 etinas of control and streptozotocin-induced diabetic rats were determined by mass spectrometry.

266 Diabetic rats were fed daily with human lactobacilli eng

267 Control and type 2 diabetic rats were housed for 3 weeks in normoxia or 11%

268 betes and miRNAs differentially expressed in diabetic rats were identified and compared with controls

269 Non-diabetic and diabetic rats were intranasally treated with saline, iso

270 h oil on streptozotocin-nicotinamide induced diabetic rats were investigated.

271 Streptozotocin-induced diabetic rats were maintained in poor glycemic control (

272 muscle of control and streptozotocin-induced diabetic rats were measured by liquid chromatography/tan

273 Acute and multi-dose studies in normal and diabetic rats were performed to assess the ability of da

274 The diabetic rats were then treated with miR-133a mimic or s

275 d further with a second VEH, and STZ-treated diabetic rats were treated either with the second VEH or

276 To test this, diabetic rats were treated intravitreally with A717, a s

277 In the present study, streptozotocin diabetic rats were treated with an orally administered c

278 The STZ-induced diabetic rats were treated with BRI (1 mg/kg/d) or vehic

279 Diabetic rats were treated with insulin, candesartan (AR

280 Control and streptozotocin (STZ)-diabetic rats were treated with or without the PARP inhi

281 Both normal and diabetic rats were used in the current study to investig

282 High-fat/low-dose streptozotocin diabetic rats were used to examine diabetes-induced chan

283 ontrolled SA release on bone regeneration in diabetic rats where enhanced inflammation is expected.

284 cked the development of tactile allodynia in diabetic rats, whereas relatively minor effects were obs

285 ation properties were enhanced in BMECs from diabetic rats, which also expressed high levels of basal

286 ted proteins were observed in the retinas of diabetic rats, which were significantly changed with DPP

287 n were inactive in lowering blood glucose in diabetic rats, while synthetic L-DKP insulin was fully a

288 Treatment of diabetic rats with a PPAR-alpha agonist induced hepatic

289 Treatment of diabetic rats with A717 significantly attenuated overexp

290 We found that the diabetic rats with an impairment of spatial learning and

291 Treating diabetic rats with dapsone, an agent known to inhibit ne

292 Here, we immunized streptozotocin-induced diabetic rats with KLH to assess the capacity of the eli

293 control rats, diabetic rats, insulin-treated diabetic rats with moderate or mild hyperglycemia, and d

294 ibitor elicits direct tubular effects in non-diabetic rats with normal renal functions.

295 Treatment of diabetic rats with RCS scavengers normalized spontaneous

296 od flow rate is reduced significantly in the diabetic rat, with a substantial decrease of flow throug

297 e transplanted into the liver of a recipient diabetic rat, with resulting local hyperinsulinism that

298 glycemic control after s.c. implantation in diabetic rats, with reproducible dosing controlled by th

299 ificantly different from those obtained from diabetic rats without any supplementation.

300 was identified after calorie restriction in diabetic rats (ZDF-CR).