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

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

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

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

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

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

9 6J mice raised on high fat diet (HFD) become prediabetic and develop insulin resistance and sensory n

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

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

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

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

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

15 4 T cells can be detected in the pancreas of prediabetic and diabetic NOD mice.

16 Since prediabetic and diabetic patients are at high cardiovasc

17 In prediabetic and diabetic ZDF islets, apoptosis measured

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

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

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

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

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

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

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

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

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

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

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

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

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

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

32 Prediabetic BBDP and diabetes-resistant BB animals also

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

53 xpression in skeletal muscle of diabetic and prediabetic humans.

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

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

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

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

58 We studied in prediabetic individuals from the Insulin Resistance Athe

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

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

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

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

63 Prediabetic individuals who were insulin resistant had h

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

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

66 For prediabetic individuals, lifestyle modification is the c

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

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

69 tly reduced progression rates to diabetes in prediabetic individuals.

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

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

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

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

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

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

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

77 Carefully screened prediabetic living kidney donors often revert to normal

78 Prediabetic macrophages treated with an MLL1 inhibitor d

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

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

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

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

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

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

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

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

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

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

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

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

91 Prediabetic mice receiving HOT-100% showed lower insulit

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

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

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

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

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

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

98 In DIO/prediabetic mice, metformin and rapamycin significantly

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

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

101 were detected within infiltrated islets from prediabetic mice.

102 n analog by daily subcutaneous injections to prediabetic mice.

103 dominant phenotype in the insulitis of young prediabetic mice.

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

105 ous glucagon-stimulated glucose excursion in prediabetic mice.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 Prediabetic NOD mice exhibit hyperglucagonemia, possibly

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

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

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

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

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

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

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

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

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

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

137 Prediabetic NOD mice were relatively glucose intolerant

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

139 Prediabetic NOD mice were used to determine the relation

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

161 Prediabetic nonobese diabetic (NOD) mice and control dia

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

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

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

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

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

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

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

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

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

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

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

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

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

175 tunity to study metabolic changes during the prediabetic period.

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

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

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

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

180 nterventions are only effective early in the prediabetic phase.

181 h17 are a distinct population throughout the prediabetic phase.

182 iabetes may not be representative of general prediabetic populations.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 elated with disease progression at the early prediabetic stage.

199 to attain normoglycemia in both diabetic and prediabetic stages.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

218 acteristic of reduced glucose control in the prediabetic state.

219 potential markers for progression within the prediabetic state.

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

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

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

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

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

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

226 Prediabetic subjects who were predominantly insulin resi

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

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

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

230 o increased adiposity and development of the prediabetic syndrome.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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