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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)-
12 UNfemale -UNmale = 27.5%, P < 0.05), and 3) IGT progresses through both parental lineages (glucose t
13 ontrols (123 +/- 46), relatives (85 +/- 46), IGT (83 +/- 48), and diabetes (65 +/- 31) (P < 0.001 con
14 ls (13.7 +/- 6.1), relatives (10.5 +/- 6.7), IGT (9.8 +/- 4.5), and diabetes (8.4 +/- 5.0) (P < 0.01
19 s (n = 754), most of the type 2 diabetes-and IGT-associated SNPs were significantly associated with g
25 Compared with NGT, subjects with IFG and IGT manifested a decrease in beta-cell glucose sensitivi
27 etion was markedly decreased in both IFG and IGT, whereas second-phase insulin secretion was decrease
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
38 Old mitochondria from subjects with NGT and IGT display mitochondrial dysfunction as manifested by r
41 eased twofold in obese subjects with NGT and IGT versus lean subjects with NGT (8.0 +/- 1.1 and 9.2 +
42 tochondria from older subjects (with NGT and IGT) displayed reduced ROS production versus the younger
44 e test (OGTT) to risk stratify for NODAT and IGT in renal transplant recipients and to relate cardiov
45 nificantly lower in patients with DM-SFN and IGT-SFN compared with iSFN at all biopsy sites (P = .001
46 ntitative association between OFC volume and IGT performance constitutes, to our knowledge, the first
48 ed in a significant increase in risk of both IGT and GDM [relative risk = 1.1 (95% CI: 1.02, 1.12) an
51 ol subjects and the combined type 2 diabetes/IGT case group showed strong association with rs7901695
55 time of transplantation with newly diagnosed IGT, we tested the dipeptidylpeptidase-4 inhibitor vilda
60 < 0.0001), but not with the transition from IGT to diabetes (hazard rate ratio 1.04 [0.90-1.20]; P =
61 warmth acted as a protective factor for good IGT performance (i.e., higher IGT score) among Val/Val h
62 Higher final glucose tolerance status (NGT > IGT > T2DM) was associated with improvements in insulin
71 (whole-body proteolysis) were higher in HIV+IGT at all insulin levels but declined in response to hy
73 ay, which may be further dysregulated in HIV+IGT, and support the notion that insulin signaling pathw
75 s with isolated postchallenge hyperglycemia (IGT) are more insulin resistant than individuals with is
78 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
80 n, n = 217; Hispanic-American, n = 193), IFG/IGT and diabetic subjects exhibited progressively increa
83 imilar to that in subjects with combined IFG/IGT and significantly higher than HOMA-IR in subjects wi
84 sistance, subjects with IGT and combined IFG/IGT had a significantly greater reduction in insulin sec
86 widely used screening test in detecting IFG/IGT or NODAT, fructosamine may be a more accurate diagno
90 0.001, ANOVA) in subjects with NFG/IGT, IFG/IGT, and IFG/diabetes but did not differ in subjects wit
91 0.001, ANOVA) in subjects with NFG/IGT, IFG/IGT, and IFG/diabetes but did not differ in subjects wit
92 DeltaG(30): NGT 157.7 +/- 9.7 pmol/mmol; IFG/IGT 100.4 +/- 5.4; diabetes 57.5 +/- 7.3; P < 0.001).
93 nce (HOMA: NGT 12.01 +/- 0.54 pmol/mmol; IFG/IGT 16.14 +/- 0.84; diabetes 26.99 +/- 2.62; P < 0.001)
95 essment-Insulin Resistance in predicting IFG/IGT or NODAT were assessed using the area under the rece
96 (NGT; 2-h glucose <7.8 mmol/l) or impaired (IGT; 2-h glucose 7.8-11.1 mmol/l) glucose tolerance: NFG
101 antly diminished in IR (-56%), as well as in IGT and normotensive and hypertensive diabetic patients
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
109 tes to skeletal muscle insulin resistance in IGT and type 2 diabetes, rosiglitazone improves insulin-
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 Pima Indians with isolated IFG and isolated IGT show similar impairments in insulin action, but thos
120 the prevalence of isolated IFG and isolated IGT, we conclude that female sex hormones may play an im
121 HRT users were more likely to have isolated IGT (2.2 [1.2-4.0]) after adjustment, but the prevalence
122 men, women were more likely to have isolated IGT (relative risk 1.8 [95% CI 1.3-2.5]) and less likely
123 creased insulin resistance) seen in isolated IGT identifies a subgroup of nondiabetic individuals who
124 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
125 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)
128 The PCOS women with high ZAG had fewer MetS, IGT and polycystic ovaries as compared with the low ZAG
132 C1 genes belong to a gene family (here named IGT for a shared conserved motif) found in all plant gen
134 tolerance categories (NFG/NGT [n = 654], NFG/IGT [n = 255], IFG/NGT [n = 59], and IFG/IGT [n = 102])
135 th isolated postchallenge hyperglycemia (NFG/IGT) had lower S(i) (means +/- SE: 2.10 +/- 0.04 vs. 2.5
136 uced (P < 0.001, ANOVA) in subjects with NFG/IGT, IFG/IGT, and IFG/diabetes but did not differ in sub
137 ower (P < 0.001, ANOVA) in subjects with NFG/IGT, IFG/IGT, and IFG/diabetes but did not differ in sub
138 ion discrimination across subjects with NGT, IGT, and type 2 diabetes than measurements derived from
140 l glucose sensitivity; IFG subjects, but not IGT subjects, had decreased beta-cell rate sensitivity.
143 When adjusted to age, the development of IGT in elderly individuals does not involve changes in m
150 n was used to calculate the relative risk of IGT and GDM, with adjustment for potential confounders.
151 onsuppressed glucagon120 had a lower risk of IGT in all cohorts (odds ratio 0.44-0.53, P < 0.01).
157 consistently found that treatment of IFG or IGT was associated with delayed progression to diabetes.
160 life events acted as a risk factor for poor IGT performance (i.e., high reward sensitivity) among Me
162 /- 31) (P < 0.001 controls versus relatives, IGT, and diabetes) as were the responses in the brachial
165 HB) is increasingly recognized as a reliable IGT and diabetes predictor, and can be measured using li
167 duced in relatives (98 +/- 48, mean +/- SD), IGT (94 +/- 52), and diabetes (74 +/- 45) compared with
169 F than controls in the vmPFC on the standard IGT and greater activity in the cerebellum on both versi
170 users performed equally well on the standard IGT, but significantly worse than controls on the varian
171 viously documented glucose tolerance status (IGT or CF-related diabetes without fasting hyperglycemia
173 le they took part in the Iowa Gambling Task (IGT), a monetary decision making task that strongly reli
174 ognition, especially the Iowa Gambling Task (IGT), and with schizophrenic psychopathology including t
175 be quantified using the Iowa Gambling Task (IGT), which requires choosing between advantageous and d
179 modified criteria were used, suggesting that IGT is phenotypically different from IFG and is associat
184 Imaging studies have shown that, during the IGT, men increase activity in the right dorsolateral pre
185 OG volume, the better the performance in the IGT (r = 0.541, P = 0.005), and the larger the left hemi
186 betic group, sICAM levels were higher in the IGT and diabetic groups, while sVCAM concentrations were
187 hough CHD risk factors were increased in the IGT group, the incidence of CHD events was not significa
189 ics showed poorer performance than HC in the IGT, performance was not correlated with OFC volume.
197 ps underwent cognitive evaluations using the IGT, Wisconsin Card Sorting Test, and Trail Making Test
199 ed during the transition from NGT (11.7%) to IGT (7.3%) to diabetes (6.5%) (P < 0.05 for trend).
200 Failure to increase insulin secretion led to IGT, and a decrease in insulin secretion led to overt di
201 m glucose tolerance deteriorated from NGT to IGT (+4.2%) to diabetes (+2.6%) over 5.1 +/- 1.4 years (
202 se subjects with impaired glucose tolerance (IGT(+)) display significant increase in fractional myoca
203 so in those with impaired glucose tolerance (IGT) (+2.7%, P < 0.01) compared with subjects with NGT.
205 r development of impaired glucose tolerance (IGT) (hazard rate ratio 1.15 [1.07-1.23]; P < 0.0001), b
206 betes (n = 137), impaired glucose tolerance (IGT) (n = 139), and normal glucose tolerance (n = 342) f
207 type 2 diabetes/impaired glucose tolerance (IGT) (n = 293) with those of control subjects with norma
208 with those with impaired glucose tolerance (IGT) (World Health Organization criteria), remain to be
209 We identified impaired glucose tolerance (IGT) and gestational diabetes mellitus (GDM) during preg
210 quartiles) with impaired glucose tolerance (IGT) and gestational diabetes mellitus (GDM), and we use
211 ubjects with IFG/impaired glucose tolerance (IGT) and IFG/diabetes but did not differ in subjects wit
212 characterized by impaired glucose tolerance (IGT) and insulin resistance with respect to glucose meta
213 e the results to impaired glucose tolerance (IGT) and normal glucose tolerance (NGT) subjects, beta-c
215 oup 2) to induce impaired glucose tolerance (IGT) for comparison with normal subjects (group 1).
216 lucose (IFG) and impaired glucose tolerance (IGT) from published prospective observational studies.
217 Subjects with impaired glucose tolerance (IGT) have increased myocardial partitioning of dietary f
218 lucose (IFG) and impaired glucose tolerance (IGT) identify individuals at high risk for progression t
219 nflammation, and impaired glucose tolerance (IGT) in the prediction of DM and to determine whether va
220 ince diabetes or impaired glucose tolerance (IGT) is common in CF, we hypothesized that their protein
223 lucose (IFG) and impaired glucose tolerance (IGT) often coexist and as such represent a potent risk f
225 articipants with impaired glucose tolerance (IGT) or diet-controlled type 2 diabetes had EF measured
226 individuals with impaired glucose tolerance (IGT) or frank diabetes based on the rarely utilized oral
228 es (T2DM) in 441 impaired glucose tolerance (IGT) subjects who participated in the ACT NOW Study and
229 progression from impaired glucose tolerance (IGT) to diabetes and responses to preventive interventio
232 in 427 subjects; impaired glucose tolerance (IGT) was found in 87 subjects, and diabetes was found by
234 articipants with impaired glucose tolerance (IGT), 11 with T2D, and 8 healthy control subjects were s
235 nt patients with impaired glucose tolerance (IGT), a risk factor for the development of NODAT and an
238 ntolerance (IR), impaired glucose tolerance (IGT), and normotensive and hypertensive type 2 diabetes
242 tolerance (NGT), impaired glucose tolerance (IGT), and type 2 diabetes, using acute insulin response
244 tolerance (NGT), impaired glucose tolerance (IGT), or CFRD without fasting hyperglycemia (CFRD-No FH)
253 betes (n = 137), impaired glucose tolerance (IGT; n = 139), and normal glucose tolerance (NGT; n = 34
256 [NGT], n = 712; impaired glucose tolerance [IGT], n = 353; newly diagnosed diabetes by 2-h glucose f
258 anelles through intracellular gene transfer (IGT) or between species by horizontal gene transfer (HGT
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 d sex-matched white European adults (30 with IGT and 30 with normal glucose tolerance [NGT]) were rec
265 nate (PFHxS) were positively associated with IGT (137 cases) [OR per log10-unit increase=1.99 (95% CI
274 ne are of potential benefit in patients with IGT after renal transplantation in addition to lifestyle
275 D1 expression was increased in patients with IGT and correlated with glucose levels across the OGTT (
279 t (N), normal pregnant (P), or pregnant with IGT/GDM (pregnant dogs fed a high-fat and -fructose diet
280 everity of insulin resistance, subjects with IGT and combined IFG/IGT had a significantly greater red
281 ucose-tolerant subjects, while subjects with IGT and combined IFG/IGT had significantly reduced TGD.
284 ubjects with NGT compared with subjects with IGT and subjects diagnosed by 2-h OGTT criteria alone.
286 ROS generation, whether older subjects with IGT have a further worsening of mitochondrial function (
292 ), and in women, it was higher in those with IGT (7,453 +/- 469 vs. 10,133 +/- 1,488 microg/24 h, P <
296 , betaCGS was 30 and 65% lower in youth with IGT and T2D, respectively; rate sensitivity was 40% lowe
299 Despite similar percent body fat, youth with IGT versus NGT had higher GlyRa, lower ATIS at baseline
300 secretion was higher in men with and without IGT (normal 13,743 +/- 863 vs. 7,453 +/- 469 microg/24 h
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