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 d in the corneas of humans with diabetes and diabetic rats.

4 reased in proteinuric streptozotocin-induced diabetic rats.

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

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

7 costerone responses to hypoglycemic clamp in diabetic rats.

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

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

10 oxidative-nitrative stress in streptozotocin diabetic rats.

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

12 elations with reductions in visual acuity in diabetic rats.

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

14 Neurological deficit was greater in diabetic rats.

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

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

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

18 on, bone metabolism, and oxidative stress in diabetic rats.

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

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

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

22 2 expression was assessed in nondiabetic and diabetic rats.

23 as fibrous encapsulation in both normal and diabetic rats.

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

25 ameliorates insulin-induced hypoglycemia in diabetic rats.

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

27 corticosterone secretion to normal levels in diabetic rats.

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

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

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

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

32 ponding reduction in blood glucose levels in diabetic rats.

33 genotoxicity induced by streptozotocin (STZ) diabetic rats.

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

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

36 his resulted in restoration of euglycemia in diabetic rats.

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

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

39 ation were elevated in insulin resistant and diabetic rats.

40 comparable to the parent drugs in nonfasted diabetic rats.

41 d other parameters in streptozotocin-induced diabetic rats.

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

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

44 retinal vascular functions and thickness in diabetic rats.

45 A2a receptors are significantly increased in diabetic rats.

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

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

48 of synaptophysin and drebrin were reduced in diabetic rats.

49 and fibronectin overexpression in retinas of diabetic rats.

50 ote dendritic and synaptic reorganization in diabetic rats.

51 1, were quantified in streptozotocin-induced diabetic rats.

52 d intravitreally into streptozotocin-induced diabetic rats.

53 rong reinforcing effects of nicotine in male diabetic rats.

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

55 ter myocardial infarction to nondiabetic and diabetic rats.

56 pidly improves insulin sensitivity in type 2 diabetic rats.

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

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

59 urea, which are inhibited in heparin-treated diabetic rats.

60 and endothelial injury in the retinas of STZ-diabetic rats.

61 ry phenotype observed in the microvessels of diabetic rats.

62 ions in myocardial ketone body metabolism in diabetic rats.

63 the microvascular manifestations observed in diabetic rats.

64 cumulation and endothelial injury in the STZ-diabetic rats.

65 and their manifestations in microvessels of diabetic rats.

66 4 and retinoids were significantly lower in diabetic rats.

67 ings was evaluated in streptozotocin-induced diabetic rats.

68 734 and GSK2193874) resolve BRB breakdown in diabetic rats.

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

70 se levels between 91 and 443 mg/dL in type 1 diabetic rats.

71 promoted dermal wound healing in normal and diabetic rats.

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

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

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

75 Diazoxide also failed to suppress EGP in diabetic rats.

76 complex impacts BP and vascular function in diabetic rats.

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

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

79 ion, disrupting gastrointestinal function in diabetic rats.

80 direct stimulation of fibroblast activity in diabetic rats.

81 is mislocalized in cardiac mitochondria from diabetic rats.

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

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

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

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

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

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

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

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

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

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

92 VPL neurons from diabetic rats also display enhanced spontaneous activity

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

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

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

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

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

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

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

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

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

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

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

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

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

106 Streptozotocin-induced diabetic rats and mice were orally treated with PPARalph

107 Kidneys of diabetic rats and mice with unilateral ureteral obstruct

108 iber metrics were decreased significantly in diabetic rats and mice, which were partially prevented b

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

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

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

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

113 Diabetic rats and their non-diabetic littermates were ho

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

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

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

117 at diastolic blood pressure was increased in diabetic rats, and its diurnal variation was reduced.

118 Insulin reduced blood glucose in diabetic rats, and rescued the pressure natriuresis resp

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

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

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

122 nd changes in insulin biomarkers observed in diabetic rats are modulated via insulin.

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

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

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

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

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

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

129 f IL-6, TNFalpha, and MMP-9 were elevated in diabetic rats both 2 and 3 weeks post-surgery.

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

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

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

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

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

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

136 ied a >130-fold increase in MPs in plasma of diabetic rats compared to normal rats, the majority of w

137 a >130-fold increase in MPs in the plasma of diabetic rats compared to normal rats.

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 cantly altered neurotrophic factor levels in diabetic rat corneas, which were partially restored by f

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 In diabetic rats, depletion of EZH2 decreased histone 3 lys

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

148 However, the diabetic rats exhibited decreased intensity and delayed

149 Likewise, 5-month diabetic rats exhibited increased permeability of FITC-a

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

151 Diabetic rats exhibited significantly reduced visual fun

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

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

154 r endothelial injury in streptozotocin (STZ)-diabetic rats fed a laboratory Western diet (WD).

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 Likewise, compared with control, the diabetic rat heart developed pronounced fibrosis and a d

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

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

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

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

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

168 nal microvessels from streptozotocin-induced diabetic rats in poor glycemia for four months, followed

169 otes ketoacidosis in both healthy and type 2 diabetic rats in the setting of insulinopenia through in

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

171 In retinas of diabetic rats, increased LOX-PP level, decreased AKT pho

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 ing the in vivo streptozotocin-induced (STZ) diabetic rat model and ex-vivo cultured osteocytes from

184 cumulation and endothelial injury in the STZ-diabetic rat model but that the combination of high leve

185 1.5 mg/eye/d) was assessed in an STZ-induced diabetic rat model by determining retinal leukostasis an

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

187 rculating MPs using a streptozotocin-induced diabetic rat model with well-characterized microvascular

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

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

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

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

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

193 Using a diabetic rat model, we identified a >130-fold increase i

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

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

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

197 vement of insulin resistance, using a type 2 diabetic rat model.

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

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

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

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

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

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

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

205 Diabetic rats of both sexes exhibit a reduction in cardi

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

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

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

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

210 after VEGF-induced vascular permeability in diabetic rats or in animals intravitreally injected with

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

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

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

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

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

216 For comparison, some diabetic rats received eye drops containing NTX in steri

217 Diabetic rats received twice daily applications of a sin

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

219 ersed dry eye relative to values measured in diabetic rats receiving vehicle.

220 therapy rescued the natriuretic response in diabetic rats, restoring normal downregulation of tubula

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

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

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

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

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

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

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

228 Diabetic rats showed significantly increased plasma 1-de

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

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

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

232 serum and vitreous of streptozotocin-induced diabetic rats (STZ-rats) analyzed at 8 weeks of hypergly

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

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

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

236 mpared with age- and duration-matched type 1 diabetic rats (T1D) (60 mg/kg streptozotocin).

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

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

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

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

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

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

243 Finally, in the renal glomeruli of diabetic rats, the acetylation of S6 kinase was signific

244 In diabetic rats, the administration of the stabilized co-f

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

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

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

248 In diabetic rats, the production of [5-(13)C]glutamate was

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

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

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

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

253 insulin concentrations in the blood of live diabetic rats to resolve inter-animal differences in the

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

255 Streptozotocin diabetic rats treated daily with heparin showed similar

256 Diabetic rats treated with periocularly administered cel

257 Diabetic rats treated with SSTR2a needed little or no gl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 Diabetic rats were fed daily with human lactobacilli eng

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

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

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

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

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

280 otocin-induced T1DM rats and age-matched non-diabetic rats were subjected to daily uniaxial ulnar loa

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

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

283 However, when diabetic rats were treated with vitamin K1 (5 mg/kg, sc,

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

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

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

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

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

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

290 Treatment of diabetic rats with A717 significantly attenuated overexp

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

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

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

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

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

296 Treatment of diabetic rats with RCS scavengers normalized spontaneous

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

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

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

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