ライフサイエンスコーパス: prediabetic

1 T reg cells blocked diabetes development in prediabetic 13-wk-old NOD mice.

2 16-80years), there were 27 diabetics and 50 prediabetics (17 with impaired fasting glucose and 33 wi

3 = 248), we identified normoglycemic (48.7%), prediabetic (44.4%), and diabetic (6.9%) PLWH.

4 Experiments were performed in prediabetic 6-week-old ZDF rats in comparison with 12-we

5 ate this sexual dimorphism, we treated young prediabetic A(vy)/A mice transgenic for huIAPP (huIAPP-A

6 patients had a normal A1c (< 5.7%), 66 had a prediabetic A1c (5.7-6.4) and 29 had a diabetic A1c (> 6

7 Among the non-reported group, 56 had a prediabetic A1c and 3 had a diabetic A1c.

8 s of E2 in a nonobese model, we also treated prediabetic, ad libitum-fed and pair-fed Lean-huIAPP tra

9 reatic ductal epithelial cells isolated from prediabetic adult non-obese diabetic mice in long-term c

10 Injection of NOD mice at the prediabetic age and early hyperglycemic stage with beta-

11 henotyped individuals (174 normoglycemic, 79 prediabetic and 94 T2D).

12 ulature and insulin content of beta-cells in prediabetic and anti-CD3-treated NOD mice.

13 6J mice raised on high fat diet (HFD) become prediabetic and develop insulin resistance and sensory n

14 s, was significantly increased (P < 0.01) in prediabetic and diabetic islets.

15 nd aPKC activity diminished progressively in prediabetic and diabetic monkeys.

16 Of note, DeltaT2 of prediabetic and diabetic NOD mice injected with MN-Cy5.5

17 been shown to reestablish tolerance in both prediabetic and diabetic NOD mice.

18 es of HIP/PAP was determined in pancreata of prediabetic and diabetic NOD mice.

19 4 T cells can be detected in the pancreas of prediabetic and diabetic NOD mice.

20 Since prediabetic and diabetic patients are at high cardiovasc

21 ecific islet T cells were identified at both prediabetic and diabetic stages comprising two distinct

22 In prediabetic and diabetic ZDF islets, apoptosis measured

23 e (FAS) was fourfold and sevenfold higher in prediabetic and diabetic ZDF islets, respectively.

24 y acids (FFAs) in plasma are high (>1 mM) in prediabetic and diabetic ZDF rats; therefore, we culture

25 Treatment of prediabetic and new onset diabetic mice with imatinib (G

26 tment of some first-degree relatives and all prediabetic and new-onset (<1 year) T1D patients tested,

27 fatty acids was compared in islets of obese prediabetic and nonprediabetic Zucker diabetic fatty (ZD

28 a-cells and endothelial cells were tested in prediabetic and previously diabetic NOD mice treated wit

29 c control and be neuroprotective, we treated prediabetic and T2D mice with nicotinamide riboside (NR)

30 rce to enable further research into healthy, prediabetic and T2D states.

31 ent of skeletal muscle insulin resistance in prediabetic and type 2 diabetic monkeys.

32 mphocytes from only the type 1 diabetics and prediabetics and produced the proinflammatory cytokine I

33 yperinsulinemic clamps in nondiabetic, obese prediabetic, and diabetic monkeys.

34 lyzing plasma samples collected from normal, prediabetic, and diabetic subjects.

35 xpressed in vivo in the islet environment of prediabetic animals and type 1 diabetic patients, wherea

36 ly shift from people with IDDM to those with prediabetic autoimmunity to determine whether acute ente

37 mmune neuritis, and the inflamed pancreas of prediabetic BB rats.

38 Prediabetic BBDP and diabetes-resistant BB animals also

39 ansfer of purified CD4+CD25+ BBDR T cells to prediabetic BBDP rats prevented diabetes in 80% of recip

40 roup B: 78 individuals previously considered prediabetic but having FBGLs <100 mg/dL (HbA1c <5%) resu

41 d/or the establishment of mixed chimerism in prediabetic candidates may provide a benign and novel ap

42 s the most common criterion for exclusion of prediabetic candidates.

43 Animals exhibit prediabetic cardiomyopathy marked by diastolic dysfuncti

44 ed cellular pathways within the heart during prediabetic cardiomyopathy.

45 on is a cardiac-specific approach to improve prediabetic cardiomyopathy.

46 reduction of obesity and reversal of related prediabetic changes in patients.

47 om 227 newly diagnosed diabetic children; 68 prediabetic children who were prospectively followed to

48 oassay in children newly diagnosed with T1D, prediabetic children, and high-risk children with multip

49 14% of patients with Gitelman syndrome were prediabetic, compared with 5% of heterozygous carriers a

50 rtitioning in liver and adipose tissues is a prediabetic condition in obese adolescents.

51 ) mice had abnormal islets and a more severe prediabetic condition than Pdx1(+/-) mice.

52 st had at least 1 clinical risk factor for a prediabetic condition.

53 HGD and HBD induced similar obesity metrics, prediabetic conditions, enterocyte injury, altered serum

54 Under prediabetic conditions, SIRT3 was decreased in wound mac

55 ity complex (pMHC) class II chimera (DEF) to prediabetic double-transgenic mice prevents the onset of

56 in resistance, and diabetes complications in prediabetic DT/HF mice.

57 gh doses of IL-2 rapidly precipitated T1D in prediabetic female and male mice and increased myeloid c

58 To test this hypothesis, unconditioned, prediabetic female NOD mice were given a single injectio

59 rnover in B cells from young, but not older, prediabetic female NOD mice.

60 ell proliferative responses were observed in prediabetic female NOD splenocytes only to the aa 755-77

61 L2 blockade rapidly precipitated diabetes in prediabetic female nonobese diabetic (NOD) mice regardle

62 In 70-90-day-old normoglycemic (prediabetic) female NOD TLR4(+/+) and NOD TLR4(-/-) mice

63 egorized as normoglycemic (FPG <5.6 mmol/L), prediabetic (FPG 5.6-6.9 mmol/L), or diabetic (FPG >/=7.

64 has any effect on beta cells of healthy and prediabetic/glucose-intolerant obese mice remains unknow

65 The differences in CHD risk factors among prediabetic groups may have clinical implications for sc

66 Among non-diabetic and prediabetic groups, men have significantly higher serum

67 significantly delays diabetes development in prediabetic hCD20 transgenic NOD mice.

68 Among 41 islet cell Ag-positive prediabetic human subjects, 36.5% showed PBMC-proliferat

69 xpression in skeletal muscle of diabetic and prediabetic humans.

70 ine prediabetic patients, 43% (3/7) remained prediabetic in both groups, and 29% (2/7) of teprotumuma

71 cts of air Pollution Exposure on healthy and prediabetic individuals (SCOPE)] conducted in Beijing be

72 artitioning of dietary fatty acids occurs in prediabetic individuals and is associated with early imp

73 mmunoprecipitated with sera from a subset of prediabetic individuals and newly diagnosed type 1 diabe

74 for the design of suitable interventions in prediabetic individuals at risk to develop type 1 diabet

75 nical insulin-dependent diabetes mellitus in prediabetic individuals at risk.

76 We studied in prediabetic individuals from the Insulin Resistance Athe

77 In SHOPUS, prediabetic individuals lost a mean of 6.04 kg (95% CI:

78 Glucose management for diabetic and prediabetic individuals often fail to reduce or improve

79 h linear mixed models.In the DiOGenes trial, prediabetic individuals regained a mean of 5.83 kg (95%

80 rapid onset of disease, and in 6/44 (14%) of prediabetic individuals up to several years before clini

81 shown an increased proinflammatory state in prediabetic individuals who are predominantly insulin re

82 Prediabetic individuals who were insulin resistant had h

83 nance (NMR) lipoprotein particle measures in prediabetic individuals, considering potentially modifyi

84 hown a range of lipoprotein abnormalities in prediabetic individuals, including compositional changes

85 For prediabetic individuals, lifestyle modification is the c

86 d weight loss improves insulin resistance in prediabetic individuals, postprandial hyperinsulinemia i

87 shown demonstrable benefit for high-risk and prediabetic individuals, we aimed to determine whether t

88 e metabolism and insulin secretion in obese, prediabetic individuals.

89 plementation on glucose metabolism in obese, prediabetic individuals.

90 tly reduced progression rates to diabetes in prediabetic individuals.

91 peutic agent that may be used chronically in prediabetic individuals.

92 lly to induce full tolerance toward GAD65 in prediabetic individuals.

93 mitochondrial function are activated in the prediabetic, insulin-resistant stage.

94 pancreatic lymph nodes and pancreas at late prediabetic intervals.

95 nd functional stability of Foxp3(+) Tregs in prediabetic islets and maintenance of T1D protection.

96 consequence of high plasma FFA levels or if prediabetic islets have an increased lipogenic capacity

97 nd diabetic ZDF rats; therefore, we cultured prediabetic islets in 1 mM FFA.

98 ty of T cell scanning for cognate antigen in prediabetic islets.

99 lonal expansion of Valpha5(+) transcripts in prediabetic LEW.1WR1 islets, suggesting that rat Valpha5

100 Carefully screened prediabetic living kidney donors often revert to normal

101 Prediabetic macrophages treated with an MLL1 inhibitor d

102 ur findings suggest a potential link between prediabetic markers, in particular impaired glucose tole

103 developing schizophrenia, is associated with prediabetic markers, or developing diabetes, to determin

104 ht or obese (body mass index, 28-40 kg/m(2)) prediabetic men and women (ages, 45-70 y) from October 2

105 and energy metabolism in overweight or obese prediabetic men and women.

106 tose diet (HFHFD), which induces obesity and prediabetic metabolic changes, to study the onset of per

107 othelial function in the obese condition the prediabetic metabolic syndrome is caused by TNF-alpha ov

108 trol and Zucker obese fatty (ZOF, a model of prediabetic metabolic syndrome) rats.

109 Young (5- to 6-week-old) prediabetic mice and aged (23- to 24-week-old) diabetic

110 with an inhibition of disease progression in prediabetic mice and prolonged survival of syngeneic isl

111 ant paradigm shift, effector Th40 cells from prediabetic mice are Foxp3(+).

112 ral administration of heat-killed (HK) BF to prediabetic mice caused enhanced immune regulation and s

113 Late wound macrophages from prediabetic mice demonstrated an increase in MLL1, H3K4m

114 Of note, early wound macrophages from prediabetic mice displayed similarly decreased MLL1, H3K

115 Indeed, supplementation with FcsFNDC4 in prediabetic mice improved glucose tolerance and inflamma

116 g numbers in the lymphoid organs, whether in prediabetic mice of any age or in animals with recent-on

117 Prediabetic mice receiving HOT-100% showed lower insulit

118 th inhibit pancreatic tumor growth in obese, prediabetic mice through shared and distinct mechanisms.

119 evelopment of autoimmune disease, we exposed prediabetic mice to various viral infections.

120 in NOD.scid recipients, but Th40 cells from prediabetic mice transfer diabetes very slowly.

121 and the development of hepatic steatosis in prediabetic mice while protecting against sensory neurop

122 We document here that infection of prediabetic mice with a virus expressing an H-2Kb-restri

123 erinsulinemic yet glucose-tolerant mice, and prediabetic mice with impaired glucose tolerance and red

124 +) IL-10(+) peripheral regulatory T cells in prediabetic mice, and liposome administration at the ons

125 In DIO/prediabetic mice, metformin and rapamycin significantly

126 recipients of T cells from diabetic, but not prediabetic mice, whereas 10F.9G2 was effective in both

127 ted inflamed islets soon after infusion into prediabetic mice, which was quickly followed by a select

128 were detected within infiltrated islets from prediabetic mice.

129 n analog by daily subcutaneous injections to prediabetic mice.

130 dominant phenotype in the insulitis of young prediabetic mice.

131 echanisms is already present in the liver of prediabetic mice.

132 ous glucagon-stimulated glucose excursion in prediabetic mice.

133 s (APC) to the T cells was not detectable in prediabetic mice.

134 number at the peritoneum of diabetic but not prediabetic mice.

135 In HHTg prediabetic model, skeletal muscle insulin resistance de

136 Clinical studies have shown that prediabetic MODY subjects have normal insulin sensitivit

137 others, 43% (105 of 246) in the offspring of prediabetic mothers (i.e., women who were not diabetic a

138 ated UAE in the offspring of nondiabetic and prediabetic mothers were similar (odds ratio of 0.94; 95

139 es (95% CI 1.7-8.4) that of the offspring of prediabetic mothers; the odds of elevated UAE in the off

140 with aPKCs, PKB activation was diminished in prediabetic muscle but, differently from aPKCs, seemed t

141 stigate the mechanisms of these phenomena in prediabetic Ncb5or(-/-) mice and find that, despite incr

142 trophic factor, exendin-4 (Ex-4), during the prediabetic neonatal period dramatically prevents the de

143 innate responsiveness, we compared cDCs from prediabetic NOD and control C57BL/6 (B6) mice stimulated

144 However, splenocytes from prediabetic NOD donors did transfer IDDM to NOD-scid.bet

145 In contrast, splenocytes from young prediabetic NOD donors only transferred IDDM to class I+

146 y decreased T1D transfer by splenocytes from prediabetic NOD donors was observed in Il-2rgamma(null)-

147 i-insulin B:9-23 T cell clones isolated from prediabetic NOD islets have a conserved Valpha-segment/J

148 e diabetes antigen IGRP (NRP-V7-reactive) in prediabetic NOD mice and compared them to others that sh

149 specific CD8(+) T cells were also present in prediabetic NOD mice and contribute to IDDM.

150 Autoantibodies against P4Hb were detected in prediabetic NOD mice and in early human type 1 diabetes

151 ay explain the hyperglucagonemia observed in prediabetic NOD mice and may contribute to the pathogene

152 ng that the inflamed islets of Langerhans in prediabetic NOD mice are under peripheral immune surveil

153 hepatocytes arrests beta-cell destruction in prediabetic NOD mice by generating InsB9-23-specific Fox

154 The draining pancreatic lymph nodes of prediabetic NOD mice contained CD4 T cells that recogniz

155 We conclude that beta-cells of prediabetic NOD mice display dysfunction and overt ER st

156 Importantly, prediabetic NOD mice displayed increased frequencies of

157 Prediabetic NOD mice exhibit hyperglucagonemia, possibly

158 d CD8(+) Teffs were isolated from spleens of prediabetic NOD mice for comparison with similar cells f

159 T cell responses spontaneously developed in prediabetic NOD mice for their reactivity to the EXO, an

160 In prediabetic NOD mice immunized with PLP48-70, PD-L2 bloc

161 vated B cells, but not control B cells, into prediabetic NOD mice inhibited spontaneous Th1 autoimmun

162 to search for changes in miRNA expression in prediabetic NOD mice islets.

163 Finally, T cells from prediabetic NOD mice respond spontaneously to these pept

164 of isogenic c-Rel-competent Treg cells from prediabetic NOD mice reversed the accelerated diabetes d

165 ve CD4(+) T cells from the BDC2.5 mouse into prediabetic NOD mice to mimic a physiological precursor

166 The T cells from prediabetic NOD mice treated with an agonistic anti-CTLA

167 Furthermore, DeltaT2 of the pancreata of prediabetic NOD mice was significantly higher than that

168 Prediabetic NOD mice were relatively glucose intolerant

169 When prediabetic NOD mice were treated with 2-deoxyglucose to

170 Prediabetic NOD mice were used to determine the relation

171 Infection of prediabetic NOD mice with Coxsackie virus B3 or lymphocy

172 Treatment of prediabetic NOD mice with islet beta cell Ag-pulsed CD86

173 Treatment of prediabetic NOD mice with low-dose beta-glucan resulted

174 In this study, we treated prediabetic NOD mice with low-dose mouse IL-2/CD25 over

175 any CVB strain may be able to induce T1D in prediabetic NOD mice, T1D onset is linked both to the vi

176 mined whether such abnormalities occurred in prediabetic NOD mice-the prototypic model for human type

177 ti-CD3 monoclonal antibody (mAb)-treated and prediabetic NOD mice.

178 reactive CD4(+) T cells in the pancreases of prediabetic NOD mice.

179 d the onset of diabetes when administered to prediabetic NOD mice.

180 cell population in the islet infiltrates of prediabetic NOD mice.

181 (+)CD4(+) T-cells, are essentially normal in prediabetic NOD mice.

182 eters to provide a global view of T-cells in prediabetic NOD mice.

183 of SLC was also observed in the pancreas of prediabetic NOD mice.

184 CD4+CD25+ T cells, which control diabetes in prediabetic NOD mice.

185 eptides or with medium before injection into prediabetic NOD mice.

186 a-cell destruction and abrogate insulitis in prediabetic NOD mice.

187 with T1D-resistant mice or different ages of prediabetic NOD mice.

188 ased in hyperglycemic NOD mice compared with prediabetic NOD mice.

189 D27(+)CD44(lo) subsets, infiltrate islets of prediabetic NOD mice.

190 ransplantation of IDO-expressing islets from prediabetic NOD mouse donors into NODscid recipient mice

191 athogenic CD4+ T cells is much higher in the prediabetic NOD pancreas than in these other organs.

192 wasting when infused into either diabetic or prediabetic NOD recipients.

193 es, and that pancreatic lymph nodes from the prediabetic NOD, but not from the resistant mice, were a

194 Studies in prediabetic non-insulin-treated patients will likely be

195 Prediabetic nonobese diabetic (NOD) mice and control dia

196 gh population in the islets of Langerhans of prediabetic nonobese diabetic (NOD) mice that is extreme

197 f islet beta cell-reactive autoantibodies in prediabetic nonobese diabetic (NOD) mice, we abrogated t

198 and examined the effects on autoimmunity in prediabetic nonobese diabetic (NOD) mice.

199 y diseases, including in the pancreas of the prediabetic nonobese diabetic (NOD) mouse.

200 Islets from prediabetic obese mice show significantly higher CypD-de

201 ts analogs yield therapeutic effects against prediabetic or diabetic disorders regardless of obesity.

202 Here we show, by adoptive transfers, that prediabetic or diabetic NOD splenocytes upon encounterin

203 he IgA-Biome profiles between normoglycemic, prediabetic, or diabetic samples distinct from that of t

204 Here we show that RAE-1 is present in prediabetic pancreas islets of NOD mice and that autorea

205 s unresponsive to leptin, that CNTF improves prediabetic parameters in these models, and that CNTF ac

206 glitazone reduced progression to diabetes in prediabetic patients by 60%.

207 of new-onset patients and 80% (56 of 70) of prediabetic patients compared with our current fluid pha

208 The identification and treatment of prediabetic patients may significantly delay the onset o

209 pathogenicity of autoreactive lymphocytes in prediabetic patients of genetically diverse backgrounds.

210 Among baseline prediabetic patients, 43% (3/7) remained prediabetic in

211 The samples represented the prediabetic period and ranged from the age of 3 months t

212 During this prediabetic period, there is a chronic decline in beta-c

213 onal analysis of islets harvested during the prediabetic period.

214 tunity to study metabolic changes during the prediabetic period.

215 was most effective during a clearly defined prediabetic phase and prevented up to 100% of diabetes b

216 that beta-cell loss occurs early during the prediabetic phase has recently been challenged.

217 the disease are usually identifiable in the prediabetic phase of impaired glucose tolerance, early i

218 l of T1D, administration of ML351 during the prediabetic phase prevented dysglycemia, reduced beta-ce

219 nterventions are only effective early in the prediabetic phase.

220 h17 are a distinct population throughout the prediabetic phase.

221 iabetes may not be representative of general prediabetic populations.

222 Older age (p < 0.01) and HbA1c in the prediabetic range or higher (p = 0.01) were associated w

223 In a prediabetic rat model, we hypothesized that stimulating

224 In contrast, prediabetic rats expressing the same level of wild-type

225 s in FFA concentrations, the islets of obese prediabetic rats have a higher lipogenic capacity than c

226 is inhibition directly improved cognition in prediabetic rats without alteration in insulin sensitivi

227 d cognitive decline and brain pathologies in prediabetic rats.

228 Furthermore, protection of prediabetic recipients was autoantigen specific and did

229 et leads to acceleration of disease onset in prediabetic recipients.

230 onset type 1 diabetes and 60-65% (n = 42) of prediabetic relatives of patients with type 1 diabetes.

231 CML was increased in ICA(+) and prediabetic schoolchildren and in diabetic and nondiabet

232 precipitation assays using new-onset T1D and prediabetic sera.

233 We show that prediabetic serum hyperinsulinemia is reflected in the c

234 everse diabetes with clinical restoration of prediabetic serum levels of IL-10.

235 pid species being upregulated already in the prediabetic stage associated with the loss of beta-cells

236 of gluconeogenic genes was suppressed at the prediabetic stage but not at the onset of diabetes; and

237 i-NKG2D monoclonal antibody (mAb) during the prediabetic stage completely prevented disease by impair

238 on of IL-15 signaling with anti-CD122 at the prediabetic stage delayed diabetes development.

239 Peripheral CB1R blockade initiated in the prediabetic stage prevented these changes or reversed th

240 This alteration is already apparent in the prediabetic stage to a somewhat lower level, hinting at

241 pression was increased in islet cells in the prediabetic stage, and inhibition of IL-15 signaling wit

242 emia when given to hyperglycemic mice at the prediabetic stage.

243 fic therapeutics for intervention during the prediabetic stage.

244 c disease from the outset, actually from the prediabetic stage.

245 elated with disease progression at the early prediabetic stage.

246 to attain normoglycemia in both diabetic and prediabetic stages.

247 metabolic syndrome can be considered to be a prediabetic state and contributes greatly to increased m

248 COVID-19 could be asymptomatic of a diabetic/prediabetic state and therefore would not be expected to

249 data suggest that atherogenic changes in the prediabetic state are mainly seen in insulin-resistant s

250 own whether these atherogenic changes in the prediabetic state are predominantly due to insulin resis

251 sensitivity and secretion that lead to this prediabetic state are unknown.

252 served a complete set of events leading to a prediabetic state in HCV-transgenic mice, providing a va

253 models to help practitioners screen for the prediabetic state in hope of providing earlier opportuni

254 and testosterone may constitute part of the prediabetic state in men along with previously reported

255 n's PC growth inhibition in the context of a prediabetic state is unknown.

256 etabolic neuropathophysiology underlying the prediabetic state may confer susceptibility to the adver

257 minate the root causes of disparities in the prediabetic state offer the potential to reduce the trem

258 hanges in traditional CV risk factors in the prediabetic state were mainly seen in insulin-resistant

259 ly address the problem of disparities in the prediabetic state will require greater interdisciplinary

260 office practice: bullying, screening for the prediabetic state, and pediatric oral health.

261 During insulin resistance in the prediabetic state, increased insulin biosynthesis can ov

262 Type 2 DM, but not a prediabetic state, increases the risk of generalized per

263 t with an active inflammatory process in the prediabetic state, which is unrelated to coincident EV i

264 potential markers for progression within the prediabetic state.

265 glucose responses in the range typical of a prediabetic state.

266 ed with deficiency of muscle function in the prediabetic state.

267 lycemia induced by insulin resistance in the prediabetic state.

268 ic phenotypes can be unmasked by OGTT in the prediabetic state.

269 acteristic of reduced glucose control in the prediabetic state.

270 ntrol studies with biochemical assessment of prediabetic states in patients with first-episode psycho

271 at type 2 diabetes mellitus (T2DM) and other prediabetic states of insulin resistance could contribut

272 We hypothesised that biochemical measures of prediabetic states would be more common in antipsychotic

273 s with recent-onset type 1 diabetes and from prediabetic subjects at high risk for disease.

274 ious lipoprotein abnormalities were found in prediabetic subjects compared with subjects who stayed n

275 ese results provide additional evidence that prediabetic subjects may be at an increased risk of hear

276 Forty-nine prediabetic subjects were included in a randomized cross

277 ndardization Program [DASP] workshop) and 70 prediabetic subjects who were followed to diabetes were

278 Prediabetic subjects who were predominantly insulin resi

279 identify better (for intensive intervention) prediabetic subjects who would ultimately require lifelo

280 By contrast, prediabetic subjects with a predominant defect in first-

281 of inflammatory proteins compared with both prediabetic subjects with decreased insulin secretion as

282 did not impair glucose metabolism in obese, prediabetic subjects.

283 o increased adiposity and development of the prediabetic syndrome.

284 e in preventing progression to overt IDDM in prediabetic tg mice with ongoing islet infiltration.

285 omal genomic scan to identify loci linked to prediabetic traits in Pima Indians, a population with a

286 olic impact of this intervention in 2-mo-old prediabetic University of California, Davis type 2 diabe

287 In mice made prediabetic via diet-induced obesity, IND was no longer

288 Prediabetic wild-type or transgenic BDC2.5 NOD mice were

289 glucose metabolism, in obese mice and obese, prediabetic women.

290 In cultured prediabetic ZDF islets, FFA induced a fourfold greater r

291 The beta-cell mass in 5- to 7-week-old prediabetic ZDF rats (4.3 +/- 0.06 mg) was similar to ag

292 Whereas prediabetic ZDF rats had a fourfold elevation in islet f

293 nicotinamide or aminoguanidine treatment of prediabetic ZDF rats prevented the iNOS expression in is

294 was partially prevented in vivo by treating prediabetic ZDF rats with L-cycloserine for 2 weeks.

295 vity in normal islets and in islets of obese prediabetic ZDF rats; in the latter, this correlated wit

296 he fat-laden, dysfunctional islets of obese, prediabetic Zucker diabetic fatty (fa/fa) rats with muta

297 tivity in pancreatic islet extracts from the prediabetic Zucker diabetic fatty (ZDF) rat between 5-6

298 cid-induced suppression of insulin output in prediabetic Zucker diabetic fatty (ZDF) rats is mediated

299 clude that the antidiabetic effect of TGZ in prediabetic Zucker Diabetic Fatty rats involves preventi

300 of beta cells from lipoapoptosis, we treated prediabetic Zucker Diabetic Fatty rats with 200 mg/kg pe