ライフサイエンスコーパス: STZ

1 STZ diabetic hearts display increased physical interacti

2 STZ metabolism was unaffected by PTGS deficiency.

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

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

5 STZ-induced diabetic mice exhibited distinct cardiac dys

6 STZ-induced hyperglycemia reduces visual function, affec

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

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

9 STZ-treated rats also displayed a decrease in pIRS-2 and

10 STZ-treated rats also displayed a decrease in plasma ins

11 STZ-treated rats displayed an increase in glucose levels

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 egulation in two models: SS hypertension and STZ-induced type 1 diabetes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 Platelets from STZ-induced diabetic mice exhibited increased activation

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

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

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

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

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

67 /kg) by oral gavage daily starting 2 wk from STZ injection.

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

69 HFD/STZ treatment induced a progressive myogenic tone augmen

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

71 the MAVS pathway was protective against ICVI-STZ-induced cognitive pathology.

72 We found that muMT mice and ICVI-STZ mice induced hippocampal ERV activation, as shown by

73 entricular injection of streptozotocin (ICVI-STZ).

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

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

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

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

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

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

80 s and myofiber area were decreased 20-30% in STZ-Diabetes mice due to increased ubiquitin-proteasome

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 quirement to prevent severe hyperglycemia in STZ rats.

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

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

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

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

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

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

102 n ubiquitin-mediated proteolysis pathways in STZ-Diabetes, including regulation of Fbxo32 (Atrogin1),

103 ation/autophagy were completely prevented in STZ FoxO-TKO mice.

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

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

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

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

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

109 gs using the in vivo streptozotocin-induced (STZ) diabetic rat model and ex-vivo cultured osteocytes

110 addition, NF-kappaB activation following LD-STZ treatment was validated using immunofluorescence and

111 ivation induced by low-dose streptozocin (LD-STZ) treatment in the immunocompetent SKH1 mouse model o

112 We showed that LD-STZ-treated SKH1 mice had significantly higher (2-3 time

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

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

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

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

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

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

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

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

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

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

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

124 nhibition of FOXM1 in diabetic mouse models (STZ-induced and db/db) results in delayed wound healing

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

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

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

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

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

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

131 ned elevated plasma levels characteristic of STZ-DM.

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

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

134 in Sprague-Dawley rats via a single dose of STZ (70 mg/kg) resulted in elevated maximum glucose and

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

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

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

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

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

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

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

146 BEZ treatment of STZ mice significantly suppressed the hepatic expression

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

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

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

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

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

152 Furthermore, treatments of STZ-rats with the hypouricemic drugs allopurinol (50 mg/

153 iabetic neuropathy should replace the use of STZ.

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

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

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

157 ventral tegmental area (VTA) of vehicle- or STZ-treated rats that received sham surgery or an insuli

158 The present study included vehicle- or STZ-treated rats that received sham surgery or insulin p

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

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

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

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

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

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

165 ous of streptozotocin-induced diabetic rats (STZ-rats) analyzed at 8 weeks of hyperglycemia.

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

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

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

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

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

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

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

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

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

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

176 with the diabetogenic agent streptozotocin (STZ).

177 lomerulosclerosis (FSGS) and streptozotocin (STZ)-induced diabetic glomerulosclerosis.

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

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

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

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

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

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

184 ouse model of DPN induced by streptozotocin (STZ) injection.

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

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 ets isolated from mice given streptozotocin (STZ) to induce T1DM in concert with induction of GLUT3.

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

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

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

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

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

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

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

206 of functional beta-cells in streptozotocin (STZ)-induced diabetic mice.

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

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

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

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

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

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

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

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

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

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

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

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

219 intraperitoneal injection of streptozotocin (STZ) (35 mg/kg) resulted in hyperglycemia, activation of

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

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

222 involving administration of streptozotocin (STZ), which produces hypoinsulinemia in rats.

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

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

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

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

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

228 intraperitoneal injection of streptozotocin (STZ).

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

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

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

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

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

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

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

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

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 type 1 DM, mice treated with streptozotocin (STZ) showed a similar increase in susceptibility to AF.

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

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

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

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

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

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

247 n these M-FoxO-TKO mice with streptozotocin (STZ).

248 were rendered diabetic with streptozotocin (STZ).

249 d diabetic by treatment with streptozotocin (STZ).

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

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

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

253 0 min) (STZ+RH), and 4) insulin-treated STZ (STZ+Ins).

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

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

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

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

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 on of endothelial NF-kappaB signaling in the STZ model reduced the WD-induced increase in leukocyte a

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

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

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

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

269 4 weeks, the highest ABL was observed in the STZ+L group, and the difference was significant (P <0.05

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

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

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

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

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

275 e accumulation and endothelial injury in the STZ-diabetic rat model but that the combination of high

276 e accumulation and endothelial injury in the STZ-diabetic rats.

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

278 Importantly, all of the STZ-induced changes in behavior and insulin biomarkers w

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

280 4-fold in the STZ+RH group compared with the STZ group.

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

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

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

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

285 Z were important for TRPA1 responsiveness to STZ.

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

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

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

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

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

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

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

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

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

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

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