ライフサイエンスコーパス: STZ

1 STZ diabetic hearts display increased physical interacti

2 STZ induced p38 mitogen-activated protein kinase (MAPK)

3 STZ metabolism was unaffected by PTGS deficiency.

4 STZ mitigated degranulation of RBL-2H3 (rat basophilic l

5 STZ rats showed stronger Rose Bengal staining, decreased

6 STZ uptake in the kidneys is to a large extent mediated

7 STZ-HFD feeding induced a much higher incidence of HCC i

8 STZ-induced diabetic mice exhibited distinct cardiac dys

9 STZ-induced hyperglycemia reduces visual function, affec

10 STZ-treated (8 weeks) mice exhibited increased urinary p

11 STZ-treated mice of short or long duration (</=4, >/=11

12 nd to reduce existing albuminuria in type 1 (STZ model) or type 2 (db/db model) diabetic mice.

13 , n = 6); 2) streptozotocin (STZ, n = 8); 3) STZ and melatonin (STZ+Mel, n = 8); 4) ligature (L, n =

14 zotocin-induced insulin deficiency (STZ), 3) STZ with antecedent recurrent (3 days) hypoglycemia ( ap

15 5) ligature and melatonin (L+Mel, n = 8); 6) STZ and ligature (STZ+L, n = 8); and 7) STZ, ligature, a

16 ; 6) STZ and ligature (STZ+L, n = 8); and 7) STZ, ligature, and melatonin (STZ+L+Mel, n = 8).

17 ronic glucose-lowering effect of leptin in a STZ-induced mouse model of poorly controlled T1D was ass

18 ic delivery of catalytic antioxidant ablates STZ-induced diabetes in mice.

19 mKL abolished STZ- and TNFalpha-induced inhibition of FAK and Akt phos

20 Additionally, STZ-injected wild-type (WT) diabetic mice displayed an a

21 is was not increased in monkeys administered STZ.

22 ta-cell regeneration in monkeys administered STZ.

23 ed 7 years) vervet monkeys were administered STZ (45-55 mg/kg, n = 7) or saline (n = 9).

24 STZ) or late intervention (weeks 8-15 after STZ).

25 enriched in the pancreas 10 to 15 days after STZ treatment.

26 , cold, and heat hypersensitivity 24 h after STZ.

27 d islets and were positive for insulin after STZ treatment.

28 e evaluated for beta-cell regeneration after STZ treatment.

29 At 1 week after STZ injection, animals with hyperglycemia with no eviden

30 aldehyde (CA) was administered 2 weeks after STZ injection and metabolic indices and renal structure

31 We observed that 4 weeks after STZ injections, the lack of HYAL1 1) prevents diabetes-i

32 w) as an early intervention (2-8 weeks after STZ) or late intervention (weeks 8-15 after STZ).

33 y ginger exerted a protective effect against STZ-induced diabetes by modulating antioxidant enzymes a

34 /PTGER4 agonists partially protected against STZ-induced diabetes and restored beta-cell function.

35 Analysis of the AMPAR-STZ binding interfaces suggests that electrostatic inter

36 y of PTGS-2 activity significantly amplified STZ effect, causing dramatic loss of insulin production

37 /d) and 5% (1.5 mg/eye/d) was assessed in an STZ-induced diabetic rat model by determining retinal le

38 tween the extracellular domains of AMPAR and STZ play an important role in modulating AMPAR function

39 thic painful conditions evaluated in CCI and STZ murine model.

40 ent in kidney and spleen between control and STZ treated mice.

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

42 is-NF-kappaB(EGFP) mice, ZF, ZDF(fa/fa), and STZ-induced diabetic rats.

43 ficult to distinguish between DN-related and STZ-induced nephropathy.

44 as increased 12- and 6.8-fold in the STZ and STZ+Ins groups, respectively, compared with the NONDIAB

45 However, as STZ injection alone results in mild kidney injury, the t

46 rberine administration at one time or before STZ-stimulation significantly (P<0.05) down-regulated th

47 Induction of diabetes by STZ in WT mice increased bladder weight and contractile

48 s induced in Nrf2(+/+) and Nrf2(-/-) mice by STZ injection.

49 that cysteine residues that were oxidized by STZ were important for TRPA1 responsiveness to STZ.

50 The TRPA1-dependent sensory loss produced by STZ occurs before the onset of diabetes and may thus not

51 In this study, we combined STZ with whole-body hypoxia (10% O2) for quicker inducti

52 riptional networks containing 143 (Human-DBA STZ), 97 (Human-BKS db/db), and 162 (Human-BKS eNOS(-/-)

53 DBA/2J mice fed a high-fat Western diet (DBA/STZ/WD) and treated with the LXR agonist GW3965 and in L

54 aries and EPC dysfunction similar to the DBA/STZ/WD mice.

55 Compared with vehicle-treated DBA/STZ/WD mice, GW3965 treated mice showed fewer acellular

56 ) streptozotocin-induced insulin deficiency (STZ), 3) STZ with antecedent recurrent (3 days) hypoglyc

57 This was tested in diabetic STZ rats in a preventive and therapeutic treatment schem

58 er rats and streptozotocin-induced diabetic (STZ-D) rats and compared them with control rats.

59 control and streptozotocin-induced diabetic (STZ-D) rats.

60 ng in streptozotocin (STZ)-induced diabetic (STZ-diabetic) mice.

61 enesis using a streptozotocin-high fat diet (STZ-HFD) induced nonalcoholic steatohepatitis-hepatocell

62 ted that intraplantar injections of low dose STZ evoked acute polymodal hypersensitivities in mice.

63 Mice treated with low-dose STZ exhibited hyperglucagonemia, hyperglycemia, and gluc

64 man islets with catalytic antioxidant during STZ treatment protects from STZ-induced islet damage, an

65 PTGER4 in PTGER2(-/-) mice strongly enhanced STZ pathology.

66 elta-cell numbers doubled by Day 6 following STZ treatment.

67 and Pdx1(+)/somatostatin(+) cells following STZ treatment.

68 (+)/Insulin(-) cells were detected following STZ treatment, indicating the involvement of endocrine p

69 lpha-cells in each islet increased following STZ-mediated beta-cell destruction, peaked at Day 6, whi

70 d contraction was increased in bladders from STZ mice, and TLR4 inhibitor CLI-095 attenuated this inc

71 genous insulin levels, and rescued mice from STZ-induced diabetes.

72 TLR4KO mice were not protected from STZ-induced diabetes; however, despite levels of hypergl

73 antibiotics (Abx) were fully protected from STZ-induced T1D, which correlated with the abrogation of

74 tioxidant during STZ treatment protects from STZ-induced islet damage, and systemic delivery of catal

75 of nerve conduction velocity resulting from STZ-induced diabetes and corrected the STZ-induced diabe

76 mplicates the interpretation of results from STZ models of diabetic sensory neuropathy and strongly a

77 ults suggested that increasing the time from STZ diabetes induction to 3 and 5 months resulted in an

78 luding the well-known stress tolerance genes STZ, MYB51, and WRKY33.

79 HFD/STZ treatment induced a progressive myogenic tone augmen

80 odel (high-fat diet plus streptozotocin [HFD/STZ]) to induce a mild increase in blood glucose levels.

81 In STZ-diabetic mice, albuminuria, increased Src pTyr-416,

82 In STZ-DM rats, neither adrenalectomy-induced (ADX-induced)

83 Further, lack of the Glp-1r in STZ-treated Gcgr(-/-) mice elevated rates of endogenous

84 ng factor, and matrix metalloproteinase 2 in STZ-induced diabetic bone marrow supernatant and decreas

85 protective role of PTGS-2-derived PGE(2) in STZ-induced diabetes mediated by the receptor types PTGE

86 ivity of phosphorylated ERK1/2 (p-ERK1/2) in STZ-treated but not control rats.

87 ignal following acute AMPH administration in STZ-treated rats is reduced.

88 ults suggest that mobilopathy is apparent in STZ-diabetes but not in db/db mice.

89 These alterations may prime alpha cells in STZ-treated mice for more glucagon release per cell in r

90 geneic islets to achieve glycemic control in STZ-induced diabetic C57Bl/6 mice treated with or withou

91 ets required to achieve metabolic control in STZ-induced diabetic mice.

92 trated that reduction of the I(A) current in STZ-D DRG neurons is triggered by impaired [Ca(2+)](i) i

93 apoptotic and survival signaling detected in STZ-DM rats.

94 l ghrelin((6-13)) even prevented diabetes in STZ-treated rats and protected human circulating angioge

95 ry rates showed no systematic differences in STZ extractability between the two product types.

96 omotor responses to colorectal distention in STZ-D rats were normalized by administration of MAPK inh

97 romotor response to colorectal distention in STZ-D rats.

98 ted, plasma glucagon levels were elevated in STZ-DM rats, and although liraglutide treatment lowered

99 tivation of VMH GI neurons by low glucose in STZ rats after RH.

100 n significantly accelerated wound healing in STZ-induced diabetic mice.

101 Hyperglucagonemia in STZ-induced diabetes is thus likely due to increased glu

102 quirement to prevent severe hyperglycemia in STZ rats.

103 ired epinephrine response to hypoglycemia in STZ-diabetic animals.

104 serum expression of HMGB1 were increased in STZ compared with control mice.

105 TZ-induced diabetes but remained very low in STZ-diabetic Arg2(-/-) mice.

106 inin octapeptide were significantly lower in STZ-D rats compared with controls.

107 Measurements in STZ rats were compared to age-matched nondiabetic contro

108 beta-Cell formation was minimal in STZ-induced diabetes.

109 CRR and glucose sensing by VMH GI neurons in STZ rats.

110 Here, we show that diabetes prevention in STZ-treated Gcgr(-/-) animals requires remnant insulin a

111 The defective counterregulatory response in STZ-diabetic animals was restored to normal with either

112 genes expression ratio, compared to those in STZ-treatment alone group.

113 or 9 weeks in Ins2(Akita) mice or 6 weeks in STZ-induced diabetic DBA mice significantly attenuated a

114 Compared with nondiabetic mice, wounds in STZ-diabetic mice healed more slowly.

115 latonin (L+Mel, n = 8); 6) STZ and ligature (STZ+L, n = 8); and 7) STZ, ligature, and melatonin (STZ+

116 n = 8); and 7) STZ, ligature, and melatonin (STZ+L+Mel, n = 8).

117 ozotocin (STZ, n = 8); 3) STZ and melatonin (STZ+Mel, n = 8); 4) ligature (L, n = 6); 5) ligature and

118 th streptozotocin-induced diabetes mellitus (STZ-DM) were treated with either SST eye drops or vehicl

119 ycemia ( approximately 40-45 mg/dL, 90 min) (STZ+RH), and 4) insulin-treated STZ (STZ+Ins).

120 ghted marked lipid perturbations in MK2(+/+)-STZ mice, which encompass increased 1) circulating level

121 MK2(-/-)-STZ mice were also protected against all these diabetes-

122 While MK2(-/-)-STZ mice remained hyperglycemic, they showed improved IR

123 eventing inflammation-mediated damage in MLD-STZ and in preventing and reversing diabetes in NOD mice

124 employed a streptozotocin-induced rat model (STZ-DM) of uncontrolled insulin-deficient diabetes melli

125 erarin by employing an accelerated DN model, STZ-induced diabetes in the endothelial nitric oxide syn

126 ity, allowing for single low non-nephrotoxic STZ doses (70 mg/kg).

127 olfactory cerebral arteries; neither HFD nor STZ alone had an effect on blood glucose or resistance a

128 xynitrite, as a novel mechanism of action of STZ.

129 Western blot analysis of STZ-D DRG neurons revealed increases in phosphorylated M

130 on mass spectrometry, the initial bonding of STZ occurred by 1,2- and 1,4-nucleophilic additions of t

131 alpha cells of STZ-treated mice exhibited the following: 1) increased e

132 ned elevated plasma levels characteristic of STZ-DM.

133 Diabetogenicity of STZ in PTGER1(-/-), PTGER2(-/-), PTGER3(-/-), and PTGER4

134 ntraperitoneal injection of a single dose of STZ (60 mg/kg).

135 In animals given a single high dose of STZ causing severe and rapid development of hyperglycemi

136 following a single diabetes-inducing dose of STZ in mice.

137 idney damage was induced with a high dose of STZ.

138 Longer duration of STZ-diabetes (>/=20 weeks) induced impairment of G-CSF-

139 athological alterations in the glomerulus of STZ-Nrf2(+/+) mice.

140 8-9 weeks old were treated with 30 mg/kg of STZ.

141 lleviating diabetic insults in the livers of STZ-NIC diabetic rats.

142 Although alpha-cell mass of STZ-treated mice remained unchanged, total pancreatic gl

143 rovides novel insights into the mechanism of STZ toxicity in kidneys and suggests a more efficient re

144 t of its interaction with LDLR in a model of STZ-induced diabetes.

145 elicit action potentiation in NG neurons of STZ-D rats compared with controls.

146 ished in the colon projecting DRG neurons of STZ-D rats.

147 e significantly down-regulated in retinas of STZ-rats and in human diabetic retinas (postmortem) comp

148 d a significant reduction in the severity of STZ-induced diabetes; only 13% of the STZ-treated RhoB-n

149 BEZ treatment of STZ mice significantly suppressed the hepatic expression

150 s finding, in a separate study, treatment of STZ-DM rats with a glucagon-neutralizing antibody was su

151 ive therapeutical impact in the treatment of STZ-induced diabetic rats, producing normalization of fa

152 Treatment of STZ-rats with the GHRH agonist, MR-409, prevented retina

153 Phlorizin treatment of STZ-treated mice lowered blood glucose concentrations an

154 t was completely blocked by pre-treatment of STZ-treated rats with the D(2) receptor antagonist raclo

155 iabetic neuropathy should replace the use of STZ.

156 reased significantly after 6 and 18 weeks of STZ-induced diabetes but remained very low in STZ-diabet

157 lood flow in wild-type mice after 6 weeks of STZ-induced diabetes, an effect significantly attenuated

158 reducing albuminuria after 6 and 18 weeks of STZ-induced diabetes.

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

160 red kidney protection in Ins2(Akita) mice or STZ-induced diabetic renal injury.

161 Furthermore, pancreatic STZ uptake was increased, hereby decreasing the threshol

162 on and delayed ERG responses by 1 month post-STZ.

163 In 1 week post-STZ-treated and 6- and 12-week-old Akita mice, urinary p

164 i.p. for 7 days) administration 4 weeks post-STZ injection (paradigm A) reversed the diabetes-induced

165 cataracts did not develop until 6 weeks post-STZ.

166 attenuated beta-cell apoptosis and prevented STZ-induced diabetes.

167 Streptozotocin-induced diabetic rats (STZ-rats) were treated with 15 mug/kg GHRH agonist, MR-4

168 Compared with the normal control rats, STZ rats had reduced body weight, and body length, but m

169 se the Sglt inhibitor phlorizin could reduce STZ uptake in the kidneys.

170 response study revealed that leptin reverses STZ-induced diabetes in a dose-dependent manner.

171 xiliary proteins, TARP gamma2, or stargazin (STZ).

172 nctions and complications in a streptozocin (STZ)-induced rat model of type I diabetes mellitus (DM)

173 Streptozotocin (STZ) is widely used as diabetogenic agent in animal mode

174 Streptozotocin (STZ)-induced diabetes is the most commonly used animal m

175 ated control (NL, n = 6); 2) streptozotocin (STZ, n = 8); 3) STZ and melatonin (STZ+Mel, n = 8); 4) l

176 tage-gated ion channels in a streptozotocin (STZ)-induced diabetes model that lead to increased gluca

177 islet cell composition in a streptozotocin (STZ)-induced diabetes mouse model in detail.

178 irmed in diabetic mice after streptozotocin (STZ) injection.

179 with the diabetogenic agent streptozotocin (STZ).

180 phenotype of nondiabetic and streptozotocin (STZ)-induced diabetic homozygous PKC-alpha/beta double-k

181 t mitochondria from Sham and streptozotocin (STZ)-induced type 1 diabetic (T1DM) guinea pigs (GPs).

182 In both streptozotocin (STZ)-treated mice and cells in culture exposed to hyperg

183 and genotoxicity induced by streptozotocin (STZ) diabetic rats.

184 were chemically destroyed by streptozotocin (STZ) in Gcgr(-/-):Glp-1r(-/-) mice and in Glp-1r(-/-) an

185 s: diabetic group induced by streptozotocin (STZ) injection or normoglycemic controls injected with c

186 ce were rendered diabetic by streptozotocin (STZ) injections.

187 ) mice were made diabetic by streptozotocin (STZ) treatment, and bladder contractile function and TLR

188 icient mice by five low-dose streptozotocin (STZ) injections.

189 esponse to multiple low-dose streptozotocin (STZ), hep-tg animals developed less severe hyperglycemia

190 sferred to multiple low-dose streptozotocin (STZ)-induced T1DM.

191 sucrose-challenged low-dosed streptozotocin (STZ)-induced diabetic rats and db/db mice.

192 We show here that during streptozotocin (STZ)-induced T1D, the nucleotide-binding oligomerization

193 Wistar rats received either streptozotocin (STZ) to induce uDM (STZ-DM) or vehicle and remained nond

194 Klotho (KL(+/-)) exacerbated streptozotocin (STZ)-induced diabetes (a model of T1DM), including hyper

195 ere protected from high-fat/ streptozotocin (STZ)-induced hyperglycemia that was accompanied by incre

196 t develop diabetes following streptozotocin (STZ)-mediated ablation of insulin-producing beta-cells.

197 r observations were made for streptozotocin (STZ)-treated and db(+)/db(-) mouse models.

198 toring Ca(2+) sensitivity in streptozotocin (STZ) diabetic cardiac muscles.

199 val and prevents diabetes in streptozotocin (STZ) treated rats.

200 (attempted regeneration) in streptozotocin (STZ)-induced diabetes in adult nonhuman primates.

201 e cutaneous wound healing in streptozotocin (STZ)-induced diabetic (STZ-diabetic) mice.

202 d atherosclerotic lesions in streptozotocin (STZ)-induced diabetic ApoE(-/-) mice.

203 etic Ins2(Akita) mice and in streptozotocin (STZ)-induced diabetic Dilute Brown Agouti (DBA) and argi

204 ced BK-beta(1) expression in streptozotocin (STZ)-induced diabetic mouse arteries and in human corona

205 butes to neuropathic pain in streptozotocin (STZ)-induced diabetic rats, we analyzed dendritic spine

206 ptokinetic tracking (OKT) in streptozotocin (STZ)-induced diabetic rats.

207 , reduces diabetic injury in streptozotocin (STZ)-induced diabetic rodent models.

208 ) E(2) signaling pathways in streptozotocin (STZ)-induced type 1 diabetes.

209 Studies were performed in streptozotocin (STZ)-injected DBA/2J mice fed a high-fat Western diet (D

210 Experimental DR in streptozotocin (STZ)-injected rodents is described as an inflammatory di

211 se/Akt pathway and increased streptozotocin (STZ)-induced apoptosis; conversely, overexpression of SH

212 used multiple low-dose (MLD) streptozotocin (STZ) injections and the NOD mouse model to investigate t

213 sity and a nicotinamide (NA)-streptozotocin (STZ)-HFD-induced model of mild type 2 diabetes.

214 stance and nicotinamide (NA)-streptozotocin (STZ)-HFD-induced type 2 diabetes.

215 els of diabetic nephropathy: streptozotocin (STZ)-treated, OVE26, and Akita mice.

216 intraperitoneal injection of streptozotocin (STZ) (n = 10); group 2 (G2): rats were not exposed to ST

217 was induced by injection of streptozotocin (STZ), and retinal blood flow rate was measured under ane

218 Thus, in a rat model of streptozotocin (STZ)-induced chronic type 1 diabetes mellitus (T1DM), an

219 ally reduced the severity of streptozotocin (STZ)-induced diabetes in nonobese diabetic severe combin

220 endothelial cells (RECs) of streptozotocin (STZ)-induced diabetic rats 3 months after the onset of d

221 ns within the bone marrow of streptozotocin (STZ)-induced diabetic rats following treatments that pre

222 In a rat model of streptozotocin (STZ)-induced T1D, GHRH receptor expression was found to

223 intraperitoneal injection of streptozotocin (STZ).

224 injections of a low dose of streptozotocin (STZ).

225 tive rats by an injection of streptozotocin (STZ-SS).

226 Dawley rats as well as RH or streptozotocin (STZ)-diabetic rats received bilateral VMH microinjection

227 Age-matched control or streptozotocin (STZ)-induced diabetic, and db/db mice with lean-controls

228 by high fat diet (HFD) plus streptozotocin (STZ) in C57BL/6J mice for 13 weeks starting from 4 weeks

229 a-cell survival and prevents streptozotocin (STZ)- and obesity-induced diabetes.

230 tion in the experimental rat streptozotocin (STZ) model of diabetic retinopathy (DR).

231 the diabetic BB rat and the streptozotocin (STZ)-induced diabetic rat, and compared them with nondia

232 The streptozotocin (STZ)-induced murine model of type 1 diabetes, in combina

233 by administration of PP2 to streptozotocin (STZ)-induced diabetic DBA2/J mice.

234 cells or the beta cell toxin streptozotocin (STZ).

235 lopathy and albuminuria upon streptozotocin (STZ)-induced hyperglycemia.

236 Diabetes was induced using streptozotocin (STZ) in human apoE3 (E3) or human apoE4 (E4) mice defici

237 ro experimental models using streptozotocin (STZ)-treated primary pancreatic islet cells from ICR mic

238 es was induced in mice using streptozotocin (STZ).

239 were rendered diabetic with streptozotocin (STZ) for 1, 3, or 5 months' duration.

240 star rats were injected with streptozotocin (STZ) two days after birth using 45 and 90 mg/kg, respect

241 Four beagle dogs with streptozotocin (STZ)-induced diabetes and four healthy dogs were include

242 e study in C57Bl/6 mice with streptozotocin (STZ)-induced diabetes to determine a leptin dose insuffi

243 sulin tolerance in mice with streptozotocin (STZ)-induced diabetes, an insulin-deficient mouse model

244 se (DIO) mice, and rats with streptozotocin (STZ)-induced diabetes.

245 Trx) in the VMH of rats with streptozotocin (STZ)-induced type 1 diabetes.

246 were rendered diabetic with streptozotocin (STZ).

247 d diabetic by treatment with streptozotocin (STZ).

248 /-), and RhoB(-/-) mice with streptozotocin (STZ).

249 ut (KO) mice with or without streptozotocin (STZ)-induced diabetes.

250 ing mouse models of chronic (streptozotocin [STZ]-induced diabetes) and acute (ischemia-reperfusion [

251 fatty (ZDF(fa/fa)) rats and streptozotosin (STZ) induced diabetic Sprague-Dawley rats, after two mon

252 0 min) (STZ+RH), and 4) insulin-treated STZ (STZ+Ins).

253 tion of the model sulfonamide sulfathiazole (STZ) and the stronger nucleophile para-ethoxyaniline was

254 In wild type mice, systemic STZ treatment (180 mg/kg) evoked a loss of cold and mech

255 s, our study provides the first insight that STZ treatment sensitizes release mechanisms of alpha cel

256 Mass spectrometry studies revealed that STZ oxidizes TRPA1 cysteines to disulfides and sulfenic

257 Collectively, these results suggest that STZ mediates its anti-itch effects by boosting the antip

258 from STZ-induced diabetes and corrected the STZ-induced diabetes-associated increase of immunoreacti

259 block was increased 12- and 6.8-fold in the STZ and STZ+Ins groups, respectively, compared with the

260 STZ+RH group, 6.2-fold less than that in the STZ group (31%).

261 .6%, 7.8-fold less than the incidence in the STZ group (44%).

262 gher glucose infusion rate than those in the STZ group, consistent with the blunted epinephrine respo

263 gfa expression increased in podocytes in the STZ model of diabetes.

264 tina was found to be almost 3x faster in the STZ rats (P < 0.01).

265 ound to decrease by approximately 33% in the STZ rats compared to controls (P < 0.001) as assessed by

266 he STZ+L+Mel group compared with that in the STZ+L group (P <0.05).

267 + osteoclast numbers were the highest in the STZ+L group, and melatonin significantly decreased osteo

268 4 weeks, the highest ABL was observed in the STZ+L group, and the difference was significant (P <0.05

269 melatonin significantly decreased ABL in the STZ+L+Mel group compared with that in the STZ+L group (P

270 AB group, yet this decreased 5.4-fold in the STZ+RH group compared with the STZ group.

271 d nadirs of severe hypoglycemia, rats in the STZ+RH group required a 1.7-fold higher glucose infusion

272 Incidence of third-degree heart block in the STZ+RH group was 5.6%, 7.8-fold less than the incidence

273 ity due to severe hypoglycemia was 5% in the STZ+RH group, 6.2-fold less than that in the STZ group (

274 enhanced basal TRPC channel activity in the STZ-SS rats, and increased response to Ang II; total cal

275 ity of STZ-induced diabetes; only 13% of the STZ-treated RhoB-null animals became hyperglycemic, as o

276 As opposed to the STZ-induced model of DR, in diabetic NGRs, most leukocyt

277 4-fold in the STZ+RH group compared with the STZ group.

278 emia similar to those of WT STZ mice, TLR4KO STZ mice were protected from diabetes-induced bladder hy

279 10); group 2 (G2): rats were not exposed to STZ (n = 10).

280 fied when mice of both sexes were exposed to STZ-HFD.

281 To investigate the mechanism leading to STZ-induced nephropathy, kidney damage was induced with

282 Z were important for TRPA1 responsiveness to STZ.

283 rthermore, PKO mice were more susceptible to STZ-induced beta-cell destruction, insulin deficiency, a

284 Notably, when Abx-treated STZ-injected WT mice received the NOD2 ligand muramyl di

285 dL, 90 min) (STZ+RH), and 4) insulin-treated STZ (STZ+Ins).

286 thelialization compared with vehicle-treated STZ-diabetic mice.

287 Treating STZ-HFD male mice with 2% cholestyramine led to signific

288 Treating STZ-induced diabetic animals with the RCS scavenger, pyr

289 d either streptozotocin (STZ) to induce uDM (STZ-DM) or vehicle and remained nondiabetic.

290 convincing advantages over the commonly used STZ-induced T1D.

291 DM was induced via STZ injection in Sprague-Dawley rats.

292 In vitro, STZ activated TRPA1 in isolated sensory neurons, TRPA1 c

293 ained similar to wild-type controls, whereas STZ-associated increases in alpha-cell number and serum

294 on and reduced vascular leakage in mice with STZ-induced diabetes.

295 DBA/2J mice with STZ-induced hyperglycemia were treated with the selectiv

296 xogenous insulin administration in rats with STZ-induced diabetes.

297 c status of mice treated simultaneously with STZ and simvastatin, we conclude that the effect of stat

298 Furthermore, incubation of tyrosine with STZ resulted in formation of dityrosine, suggesting form

299 lammatory cytokines in dogs with and without STZ-induced diabetes; however, chronic hyperglycemia see

300 vels of hyperglycemia similar to those of WT STZ mice, TLR4KO STZ mice were protected from diabetes-i