ライフサイエンスコーパス: IGT

1 IGT also was positively associated with other exposure m

2 IGT individuals also demonstrated higher IMT in right an

3 IGT is also a risk factor for NODAT.

4 IGT is also independently associated with traditional mi

5 IGT is more predictive of cardiovascular morbidity than

6 IGT(+) subjects have significantly reduced left ventricu

7 IGT, metabolic syndrome definitions, and IR markers all

8 IGT-associated increased cardiac DFA partitioning was di

9 63 vs. 7,453 +/- 469 microg/24 h, P < 0.001; IGT 16,871 +/- 2,113 vs. 10,133 +/- 1,488 microg/24 h, P

10 fractional uptake rates were measured in 15 IGT subjects (7 males/8 females) using the oral 14(R,S)-

11 es (<100, 100-119, 120-139 mg/dL), and in 21 IGT obese adolescents.

12 UNfemale -UNmale = 27.5%, P < 0.05), and 3) IGT progresses through both parental lineages (glucose t

13 abolism: 10% NODAT, 14% combined IGT/IFG, 9% IGT alone, and 18% IFG alone.

14 In 8 publications with information about IGT, estimates of RR ranged from 0.83 to 1.34.

15 WHO-IFG (1140 [10.2%]) and IGT (2245 [20.0%]) predicted greater conversion (7.5 per

16 tegories, while the highest NGT category and IGT group were similar.

17 IFG based on WHO criteria and IGT predict diabetes progression better than do the othe

18 All type 2 diabetes-and IGT-associated SNPs were in high linkage disequilibrium

19 s (n = 754), most of the type 2 diabetes-and IGT-associated SNPs were significantly associated with g

20 Impaired fasting glucose and IGT are associated with modest increases in the risk for

21 was found between the highest NGT group and IGT subjects.

22 Both IFG and IGT are risk factors for type 2 diabetes, and risk is ev

23 Whether IFG and IGT have comparable coronary heart disease (CHD) risk fa

24 rdiovascular disease associated with IFG and IGT is unclear.

25 Compared with NGT, subjects with IFG and IGT manifested a decrease in beta-cell glucose sensitivi

26 betes, and risk is even greater when IFG and IGT occur together.

27 etion was markedly decreased in both IFG and IGT, whereas second-phase insulin secretion was decrease

28 Five studies combined IFG and IGT, yielding a fixed-effects summary estimate of RR of

29 nct defects in beta-cell function in IFG and IGT.

30 on and insulin action in humans with IFG and IGT.

31 mportant role in the pathogenesis of IFG and IGT.

32 Partial pancreatectomy resulted in IFG and IGT.

33 ing a similar baseline prevalence of IFG and IGT.

34 k stratification of individuals with IFG and IGT.

35 ar in normoglycemic individuals (IS, IR, and IGT), whereas it was significantly decreased in normoten

36 6.1-6.9 mmol/l, 2hPG < or =7.8 mmol/l), and IGT (FPG <6.1 mmol/l, 2hPG 7.8-11.0 mmol/l), and from IF

37 sma glucagon levels in subjects with NGT and IGT but not T2DM.

38 Old mitochondria from subjects with NGT and IGT display mitochondrial dysfunction as manifested by r

39 ase secretion was similar across all NGT and IGT groups.

40 ) was suppressed within 15-30 min in NGT and IGT subjects and remained suppressed.

41 nce was observed between the highest NGT and IGT subjects.

42 eased twofold in obese subjects with NGT and IGT versus lean subjects with NGT (8.0 +/- 1.1 and 9.2 +

43 tochondria from older subjects (with NGT and IGT) displayed reduced ROS production versus the younger

44 Both NODAT and IGT confer a higher risk of developing cardiovascular di

45 e test (OGTT) to risk stratify for NODAT and IGT in renal transplant recipients and to relate cardiov

46 nificantly lower in patients with DM-SFN and IGT-SFN compared with iSFN at all biopsy sites (P = .001

47 ntitative association between OFC volume and IGT performance constitutes, to our knowledge, the first

48 In both IGT and diabetes, aPKC activation was markedly (70-80%)

49 ed in a significant increase in risk of both IGT and GDM [relative risk = 1.1 (95% CI: 1.02, 1.12) an

50 (transpaternal inheritance of LBW), or both (IGT).

51 glucose metabolism: 10% NODAT, 14% combined IGT/IFG, 9% IGT alone, and 18% IFG alone.

52 ol subjects and the combined type 2 diabetes/IGT case group showed strong association with rs7901695

53 , P = 0.09) and the combined type 2 diabetes/IGT trait (1.35, P = 0.07).

54 [1.27-2.50], P = 0.0008 for type 2 diabetes/IGT vs. NGT).

55 ated with type 2 diabetes or type 2 diabetes/IGT.

56 time of transplantation with newly diagnosed IGT, we tested the dipeptidylpeptidase-4 inhibitor vilda

57 ose load rather than fasting glycemia, i.e., IGT rather than IFG.

58 cose tolerance (n = 167 for NGT, n = 174 for IGT, and n = 159 for diabetes).

59 declining glucose tolerance, especially for IGT and new DM by OGTT compared with AIR.

60 Progression from IGT to diabetes was accompanied by a further increase in

61 < 0.0001), but not with the transition from IGT to diabetes (hazard rate ratio 1.04 [0.90-1.20]; P =

62 warmth acted as a protective factor for good IGT performance (i.e., higher IGT score) among Val/Val h

63 Higher final glucose tolerance status (NGT > IGT > T2DM) was associated with improvements in insulin

64 iteria for DM, and another 42.3% (11/26) had IGT.

65 Of 2,093 women, 65 (3%) had IGT and 118 (6%) had GDM.

66 eline 45% of the patients had NGT, 38.8% had IGT, and 15.8% had CFRD-No FH.

67 A total of 22.7% of women had IGT compared with 34.2% of men.

68 The BD and HC IGT performances were compared with the effects of chron

69 actor for good IGT performance (i.e., higher IGT score) among Val/Val homozygotes.

70 HIV+IGT had greater visceral adiposity, fasting serum interl

71 ts with normal glucose tolerance, and 21 HIV+IGT subjects.

72 (whole-body proteolysis) were higher in HIV+IGT at all insulin levels but declined in response to hy

73 ate during hyperinsulinemia was lower in HIV+IGT than the other two groups.

74 ay, which may be further dysregulated in HIV+IGT, and support the notion that insulin signaling pathw

75 Understanding how IGT genes modulate branch angles will provide insights i

76 definitions of intermediate hyperglycaemia: IGT (2 h plasma glucose >=7.8 mmol/L [>=140 mg/dL]); IFG

77 s with isolated postchallenge hyperglycemia (IGT) are more insulin resistant than individuals with is

78 Restricting to identifying IGT/NODAT using 2-hour oral glucose tolerance test (n =

79 more atherogenic in those with IGT or IFG + IGT.

80 mmol/l, 2hPG 7.8-11.0 mmol/l), and from IFG-IGT to diabetes (FPG > or =7.0 mmol/l or 2hPG > or =11.1

81 Of the 267 subjects who progressed to IFG-IGT, 216 had additional follow-up.

82 n, n = 217; Hispanic-American, n = 193), IFG/IGT and diabetic subjects exhibited progressively increa

83 NFG/IGT [n = 255], IFG/NGT [n = 59], and IFG/IGT [n = 102]) among nondiabetic subjects.

84 imilar to that in subjects with combined IFG/IGT and significantly higher than HOMA-IR in subjects wi

85 sistance, subjects with IGT and combined IFG/IGT had a significantly greater reduction in insulin sec

86 ts, while subjects with IGT and combined IFG/IGT had significantly reduced TGD.

87 widely used screening test in detecting IFG/IGT or NODAT, fructosamine may be a more accurate diagno

88 Forty (48%) recipients had IFG/IGT or NODAT.

89 sidered the gold standard in identifying IFG/IGT or NODAT.

90 ssment-Insulin Resistance in identifying IFG/IGT were between 0.81 and 0.85.

91 0.001, ANOVA) in subjects with NFG/IGT, IFG/IGT, and IFG/diabetes but did not differ in subjects wit

92 0.001, ANOVA) in subjects with NFG/IGT, IFG/IGT, and IFG/diabetes but did not differ in subjects wit

93 DeltaG(30): NGT 157.7 +/- 9.7 pmol/mmol; IFG/IGT 100.4 +/- 5.4; diabetes 57.5 +/- 7.3; P < 0.001).

94 nce (HOMA: NGT 12.01 +/- 0.54 pmol/mmol; IFG/IGT 16.14 +/- 0.84; diabetes 26.99 +/- 2.62; P < 0.001)

95 it in beta-cell mass in the evolution of IFG/IGT and subsequently type 2 diabetes.

96 essment-Insulin Resistance in predicting IFG/IGT or NODAT were assessed using the area under the rece

97 In IGT individuals there is a relationship between macro- a

98 In IGT subjects, retinal BDF correlated with total:HDL (P =

99 hile plasma vWF was increased (P = 0.014) in IGT subjects compared to controls.

100 l RT also correlated with FMD (P = 0.017) in IGT but not NGT subjects.

101 antly diminished in IR (-56%), as well as in IGT and normotensive and hypertensive diabetic patients

102 NHGU is further blunted in IGT/GDM.

103 d that beta-cell function was compromised in IGT, DM2h, DMf, and DM, relative to NGT, by 13, 12, 59,

104 The lower ATIS and diminished adipose DI in IGT versus NGT is in line with the compromised glucose m

105 conserved C-terminal EAR-like motif found in IGT genes was required for these ectopic phenotypes.

106 nd 120 min postprandially was also higher in IGT versus control subjects (P < 0.001) in men (0.063 [0

107 ial DFA partitioning after 6 h was higher in IGT versus control subjects (P = 0.006) in both men (2.1

108 hase insulin secretion was decreased only in IGT.

109 tes to skeletal muscle insulin resistance in IGT and type 2 diabetes, rosiglitazone improves insulin-

110 tal muscles or liver is, however, similar in IGT(+) versus IGT(-).

111 us abdominal and visceral adipose tissues in IGT(+) directly associated with central obesity.

112 tprandial compared with control individuals (IGT(-)).

113 We investigated IGT performance in 20 patients with PD before STN surger

114 ite are -0.179, -0.164, and -0.198 for iSFN, IGT-SFN, and DM-SFN, respectively.

115 (10.4), and 61.6 (11.6) years for the iSFN, IGT-SFN, and DM-SFN groups, respectively.

116 and 13, 6, and 6 male patients in the iSFN, IGT-SFN, and DM-SFN groups, respectively.

117 IENFD loss over time in subjects with iSFN, IGT-SFN and DM-SFN as well as the spatiotemporal pattern

118 , 26.7, and 38.8 months for those with iSFN, IGT-SFN, and DM-SFN, respectively, and 32 months for hea

119 the prevalence of isolated IFG and isolated IGT, we conclude that female sex hormones may play an im

120 HRT users were more likely to have isolated IGT (2.2 [1.2-4.0]) after adjustment, but the prevalence

121 men, women were more likely to have isolated IGT (relative risk 1.8 [95% CI 1.3-2.5]) and less likely

122 creased insulin resistance) seen in isolated IGT identifies a subgroup of nondiabetic individuals who

123 ucose values among NGT (4.8 +/- 0.5 mmol/l), IGT (5.03 +/- 0.5 mmol/l), and group A (4.99 +/- 0.7 mmo

124 2-h glucose values (NGT 5.8 +/- 1.1 mmol/l, IGT 8.9 +/- 0.9 mmol/l, and group A 13.5 +/- 2.5 mmol/l)

125 Mechanistically, IGT in both F(1) and F(2) generations is linked to impai

126 e intolerance/gestational diabetes mellitus (IGT/GDM).

127 The PCOS women with high ZAG had fewer MetS, IGT and polycystic ovaries as compared with the low ZAG

128 The single-session mouse IGT measures dynamic risk-based decision making similar

129 e characterized a novel single-session mouse IGT using C57BL/6J mice (n = 44).

130 exhibited poor decision making in the mouse IGT.

131 C1 genes belong to a gene family (here named IGT for a shared conserved motif) found in all plant gen

132 tolerance categories (NFG/NGT [n = 654], NFG/IGT [n = 255], IFG/NGT [n = 59], and IFG/IGT [n = 102])

133 th isolated postchallenge hyperglycemia (NFG/IGT) had lower S(i) (means +/- SE: 2.10 +/- 0.04 vs. 2.5

134 uced (P < 0.001, ANOVA) in subjects with NFG/IGT, IFG/IGT, and IFG/diabetes but did not differ in sub

135 ower (P < 0.001, ANOVA) in subjects with NFG/IGT, IFG/IGT, and IFG/diabetes but did not differ in sub

136 A diagnosis of NODAT, IGT, and impaired fasting glucose (IFG) was based on Wor

137 - 0.02 L/min . m(2), P < 0.001), in nonobese IGT (0.62 +/- 0.02, P < 0.004), and in nonobese T2DM (0.

138 l glucose sensitivity; IFG subjects, but not IGT subjects, had decreased beta-cell rate sensitivity.

139 AT functioning in mice performing this novel IGT.

140 ognostic properties, with the combination of IGT or WHO-IFG showing the best, but still insufficient,

141 Early detection of IGT allows intensive diet and exercise modification, whi

142 When adjusted to age, the development of IGT in elderly individuals does not involve changes in m

143 nsitivity associated with the development of IGT.

144 The prevalence of IGT was elevated in the highest (vs. lowest) quartile of

145 lence of NODAT and ignores the prevalence of IGT.

146 The overall prevalences of IGT and GDM in the cohort were 2.6% and 5.2%, respective

147 Predicted probabilities of IGT and GDM were reduced by one-half with a 10% decrease

148 as associated with a 12% decrease in risk of IGT and a 9% decrease in risk of GDM.

149 n was used to calculate the relative risk of IGT and GDM, with adjustment for potential confounders.

150 onsuppressed glucagon120 had a lower risk of IGT in all cohorts (odds ratio 0.44-0.53, P < 0.01).

151 theses about the relation of diet to risk of IGT or GDM.

152 aseline prevalence of IFG similar to that of IGT.

153 the presenting symptom of either diabetes or IGT.

154 Most trials of treatment of IFG or IGT found no effects on all-cause or cardiovascular mort

155 Treatment of IFG or IGT was associated with delayed progression to diabetes.

156 consistently found that treatment of IFG or IGT was associated with delayed progression to diabetes.

157 ACZ885 in Atherosclerosis and Either T2DM or IGT Patients; NCT00995930).

158 Measured by [(1)(1)C]acetate with PET, IGT(+) subjects have a significant increase in myocardia

159 life events acted as a risk factor for poor IGT performance (i.e., high reward sensitivity) among Me

160 mpaired decision-making consistent with poor IGT performance of BD patients.

161 /- 67) (P < 0.001 controls versus relatives, IGT, and diabetes).

162 HB) is increasingly recognized as a reliable IGT and diabetes predictor, and can be measured using li

163 ration of only PM dilemmas increased women's IGT performance to the level of men.

164 duced in relatives (98 +/- 48, mean +/- SD), IGT (94 +/- 52), and diabetes (74 +/- 45) compared with

165 We recorded standard IGT performance measures and novel post-reward and post-

166 F than controls in the vmPFC on the standard IGT and greater activity in the cerebellum on both versi

167 users performed equally well on the standard IGT, but significantly worse than controls on the varian

168 viously documented glucose tolerance status (IGT or CF-related diabetes without fasting hyperglycemia

169 without adjustment for adult adiposity, T2D/IGT risk was lower per year later AAM (relative risk [RR

170 M is consistently associated with higher T2D/IGT risk, independent of adiposity.

171 ing mechanisms linking early menarche to T2D/IGT risk.

172 teristic in boys or girls in relation to T2D/IGT.

173 The Iowa gambling task (IGT) is one of the most influential behavioral paradigms

174 le they took part in the Iowa Gambling Task (IGT), a monetary decision making task that strongly reli

175 ognition, especially the Iowa Gambling Task (IGT), and with schizophrenic psychopathology including t

176 be quantified using the Iowa Gambling Task (IGT), which requires choosing between advantageous and d

177 sion making, we used the Iowa Gambling task (IGT).

178 or placebo by using the Iowa Gambling Task (IGT).

179 The data suggest that IGT genes are ancient, and play conserved roles in deter

180 modified criteria were used, suggesting that IGT is phenotypically different from IFG and is associat

181 The IGT family also includes TAC1 and LAZY1, which are known

182 The IGT requires subjects to choose among four card decks (t

183 We assessed the IGT performance of 16 BD subjects (7 female) and 17 heal

184 effect on diabetes risk may occur before the IGT-to-diabetes transition.

185 Imaging studies have shown that, during the IGT, men increase activity in the right dorsolateral pre

186 OG volume, the better the performance in the IGT (r = 0.541, P = 0.005), and the larger the left hemi

187 hough CHD risk factors were increased in the IGT group, the incidence of CHD events was not significa

188 However, performance in the IGT relies on a complex set of cognitive subprocesses, i

189 ics showed poorer performance than HC in the IGT, performance was not correlated with OFC volume.

190 At the retinal arterial level, the IGT subjects showed higher baseline diameter fluctuation

191 in the standard and a variant version of the IGT as well as a control task.

192 (rCBF) in the vmPFC on both versions of the IGT compared to the control task.

193 eward-concurrent cues to a rat analog of the IGT precipitates a hypodopaminergic state, characterized

194 ty in the cerebellum on both versions of the IGT.

195 Preoperative performance on the IGT was significantly impaired compared to after surgery

196 e present study, men and women performed the IGT during PM, MI, or control deliberations.

197 ic learning (cerebellum) when performing the IGT.

198 ps underwent cognitive evaluations using the IGT, Wisconsin Card Sorting Test, and Trail Making Test

199 oss diverse plant phyla, and fall within the IGT gene family.

200 Failure to increase insulin secretion led to IGT, and a decrease in insulin secretion led to overt di

201 se subjects with impaired glucose tolerance (IGT(+)) display significant increase in fractional myoca

202 Both impaired glucose tolerance (IGT) (as defined by the 1985 World Health Organization c

203 r development of impaired glucose tolerance (IGT) (hazard rate ratio 1.15 [1.07-1.23]; P < 0.0001), b

204 betes (n = 137), impaired glucose tolerance (IGT) (n = 139), and normal glucose tolerance (n = 342) f

205 type 2 diabetes/impaired glucose tolerance (IGT) (n = 293) with those of control subjects with norma

206 We identified impaired glucose tolerance (IGT) and gestational diabetes mellitus (GDM) during preg

207 quartiles) with impaired glucose tolerance (IGT) and gestational diabetes mellitus (GDM), and we use

208 ubjects with IFG/impaired glucose tolerance (IGT) and IFG/diabetes but did not differ in subjects wit

209 characterized by impaired glucose tolerance (IGT) and insulin resistance with respect to glucose meta

210 e the results to impaired glucose tolerance (IGT) and normal glucose tolerance (NGT) subjects, beta-c

211 pathogenesis of impaired glucose tolerance (IGT) and type 2 diabetes.

212 sk of developing impaired glucose tolerance (IGT) and type 2 diabetes.

213 lucose (IFG) and impaired glucose tolerance (IGT) from published prospective observational studies.

214 Subjects with impaired glucose tolerance (IGT) have increased myocardial partitioning of dietary f

215 lucose (IFG) and impaired glucose tolerance (IGT) identify individuals at high risk for progression t

216 nflammation, and impaired glucose tolerance (IGT) in the prediction of DM and to determine whether va

217 ince diabetes or impaired glucose tolerance (IGT) is common in CF, we hypothesized that their protein

218 A) metabolism in impaired glucose tolerance (IGT) is different in men and women.

219 alent in men and impaired glucose tolerance (IGT) more prevalent in women.

220 lucose (IFG) and impaired glucose tolerance (IGT) often coexist and as such represent a potent risk f

221 ic patients have impaired glucose tolerance (IGT) or diabetes mellitus (DM).

222 articipants with impaired glucose tolerance (IGT) or diet-controlled type 2 diabetes had EF measured

223 individuals with impaired glucose tolerance (IGT) or frank diabetes based on the rarely utilized oral

224 Impaired glucose tolerance (IGT) serves as a marker for the state of insulin resista

225 es (T2DM) in 441 impaired glucose tolerance (IGT) subjects who participated in the ACT NOW Study and

226 progression from impaired glucose tolerance (IGT) to diabetes and responses to preventive interventio

227 obese youth with impaired glucose tolerance (IGT) versus normal glucose tolerance (NGT).

228 ose (IFG) and/or impaired glucose tolerance (IGT) was found in 36% (n = 191).

229 in 427 subjects; impaired glucose tolerance (IGT) was found in 87 subjects, and diabetes was found by

230 sive obesity and impaired glucose tolerance (IGT) with aging.

231 articipants with impaired glucose tolerance (IGT), 11 with T2D, and 8 healthy control subjects were s

232 nt patients with impaired glucose tolerance (IGT), a risk factor for the development of NODAT and an

233 fasting glucose, impaired glucose tolerance (IGT), and NODAT.

234 mellitus (GDM), impaired glucose tolerance (IGT), and normal glucose tolerance.

235 ntolerance (IR), impaired glucose tolerance (IGT), and normotensive and hypertensive type 2 diabetes

236 bjects with NGT, impaired glucose tolerance (IGT), and T2DM.

237 ulin resistance, impaired glucose tolerance (IGT), and type 2 diabetes are largely unknown.

238 g glucose (IFG), impaired glucose tolerance (IGT), and type 2 diabetes is not well defined.

239 tolerance (NGT), impaired glucose tolerance (IGT), and type 2 diabetes, using acute insulin response

240 s, subjects with impaired glucose tolerance (IGT), and type 2 diabetic subjects.

241 tolerance (NGT), impaired glucose tolerance (IGT), or CFRD without fasting hyperglycemia (CFRD-No FH)

242 tolerance (NGT), impaired glucose tolerance (IGT), or T2DM.

243 lucose (IFG), or impaired glucose tolerance (IGT), potentially resulting in improved outcomes.

244 iabetes (T2D) or impaired glucose tolerance (IGT), with and without adjustment for adiposity, and to

245 glucose (IFG) or impaired glucose tolerance (IGT).

246 n in people with impaired glucose tolerance (IGT).

247 e development of impaired glucose tolerance (IGT).

248 in subjects with impaired glucose tolerance (IGT).

249 the diagnosis of impaired glucose tolerance (IGT).

250 ose (IFG) and/or impaired glucose tolerance (IGT).

251 arly diabetes or impaired glucose tolerance (IGT).

252 betes (n = 137), impaired glucose tolerance (IGT; n = 139), and normal glucose tolerance (NGT; n = 34

253 (NGT; n = 190), impaired glucose tolerance (IGT; n = 209), and diabetes (n = 230)].

254 e [NGT], 57 with impaired glucose tolerance [IGT], and 207 with type 2 diabetes mellitus [T2DM]), div

255 e [NGT], 48 with impaired glucose tolerance [IGT], and 34 with type 2 diabetes [T2D]).

256 [NGT], n = 712; impaired glucose tolerance [IGT], n = 353; newly diagnosed diabetes by 2-h glucose f

257 cose intolerant (impaired glucose tolerance [IGT]; n = 17) or treatment-naive T2D (n = 17).

258 anelles through intracellular gene transfer (IGT) or between species by horizontal gene transfer (HGT

259 ificantly worse than controls on the variant IGT.

260 liver is, however, similar in IGT(+) versus IGT(-).

261 en functionally relocated to the nucleus via IGT.

262 gnancy (F(0)) programs reduced birth weight, IGT, and obesity in both first- and second-generation of

263 ifty-two participants (25 with iSFN, 13 with IGT-SFN, and 14 with DM-SFN) and 10 healthy controls wer

264 ese youth (n = 91) and adults (n = 132) with IGT or recently diagnosed type 2 diabetes were randomize

265 d sex-matched white European adults (30 with IGT and 30 with normal glucose tolerance [NGT]) were rec

266 nate (PFHxS) were positively associated with IGT (137 cases) [OR per log10-unit increase=1.99 (95% CI

267 lutants during pregnancy was associated with IGT but not GDM.

268 ity in women, whereas it was associated with IGT per se in men.

269 and reduced neuronal reuptake compared with IGT subjects (by 46%; P = 0.04).

270 Individuals with IGT demonstrated higher BP values (P < 0.001), fasting t

271 viduals with NGT, and older individuals with IGT.

272 nished insulin secretion in individuals with IGT.

273 ysregulated in HIV-infected individuals with IGT.

274 ac DFA partitioning nevertheless occurs with IGT both in men and women.

275 ne are of potential benefit in patients with IGT after renal transplantation in addition to lifestyle

276 D1 expression was increased in patients with IGT and correlated with glucose levels across the OGTT (

277 Patients with IGT are at significantly increased risk for death and mo

278 B activation was diminished in patients with IGT but not significantly in diabetic patients.

279 Patients with IGT-associated neuropathy may represent an attractive ta

280 t (N), normal pregnant (P), or pregnant with IGT/GDM (pregnant dogs fed a high-fat and -fructose diet

281 everity of insulin resistance, subjects with IGT and combined IFG/IGT had a significantly greater red

282 ucose-tolerant subjects, while subjects with IGT and combined IFG/IGT had significantly reduced TGD.

283 Subjects with IGT and early-stage, asymptomatic type 2 diabetic patien

284 Subjects with IGT and IFG have different metabolic characteristics.

285 ubjects with NGT compared with subjects with IGT and subjects diagnosed by 2-h OGTT criteria alone.

286 were not restored to normal in subjects with IGT and T2DM.

287 ROS generation, whether older subjects with IGT have a further worsening of mitochondrial function (

288 We hypothesized that subjects with IGT may be more insulin resistant and have higher levels

289 icantly higher than HOMA-IR in subjects with IGT or NGT.

290 er subjects with NGT and older subjects with IGT versus younger subjects.

291 (ISOCAL) on DFA metabolism in subjects with IGT.

292 associated with weight loss in subjects with IGT.

293 ), and in women, it was higher in those with IGT (7,453 +/- 469 vs. 10,133 +/- 1,488 microg/24 h, P <

294 n insulin-resistant cohorts, both those with IGT and those with T2D.

295 significantly more atherogenic in those with IGT or IFG + IGT.

296 DI was approximately 43% lower in youth with IGT and correlated positively with glucose DI.

297 , betaCGS was 30 and 65% lower in youth with IGT and T2D, respectively; rate sensitivity was 40% lowe

298 We conclude that youth with IGT manifest a global decline in insulin sensitivity, in

299 Youth with IGT or T2D had 32 and 38% reduced incretin effect compar

300 Despite similar percent body fat, youth with IGT versus NGT had higher GlyRa, lower ATIS at baseline

301 secretion was higher in men with and without IGT (normal 13,743 +/- 863 vs. 7,453 +/- 469 microg/24 h