戻る
「早戻しボタン」を押すと検索画面に戻ります。

今後説明を表示しない

[OK]

コーパス検索結果 (left1)

通し番号をクリックするとPubMedの該当ページを表示します
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 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
15 abolism: 10% NODAT, 14% combined IGT/IFG, 9% IGT alone, and 18% IFG alone.
16     In 8 publications with information about IGT, estimates of RR ranged from 0.83 to 1.34.
17 tegories, while the highest NGT category and IGT group were similar.
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 on and insulin action in humans with IFG and IGT.
30 mportant role in the pathogenesis of IFG and IGT.
31   Partial pancreatectomy resulted in IFG and IGT.
32 ing a similar baseline prevalence of IFG and IGT.
33 k stratification of individuals with IFG and IGT.
34 nct defects in beta-cell function in 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 nce was observed between the highest NGT and IGT subjects.
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
43                               Both NODAT and IGT confer a higher risk of developing cardiovascular di
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
47                                      In both IGT and diabetes, aPKC activation was markedly (70-80%)
48 ed in a significant increase in risk of both IGT and GDM [relative risk = 1.1 (95% CI: 1.02, 1.12) an
49 (transpaternal inheritance of LBW), or both (IGT).
50  glucose metabolism: 10% NODAT, 14% combined IGT/IFG, 9% IGT alone, and 18% IFG alone.
51 ol subjects and the combined type 2 diabetes/IGT case group showed strong association with rs7901695
52 , P = 0.09) and the combined type 2 diabetes/IGT trait (1.35, P = 0.07).
53  [1.27-2.50], P = 0.0008 for type 2 diabetes/IGT vs. NGT).
54 ated with type 2 diabetes or type 2 diabetes/IGT.
55 time of transplantation with newly diagnosed IGT, we tested the dipeptidylpeptidase-4 inhibitor vilda
56 ose load rather than fasting glycemia, i.e., IGT rather than IFG.
57 cose tolerance (n = 167 for NGT, n = 174 for IGT, and n = 159 for diabetes).
58  declining glucose tolerance, especially for IGT and new DM by OGTT compared with AIR.
59                             Progression from IGT to diabetes was accompanied by a further increase in
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 &gt; IGT > T2DM) was associated with improvements in insulin
63 iteria for DM, and another 42.3% (11/26) had IGT.
64                  Of 2,093 women, 65 (3%) had IGT and 118 (6%) had GDM.
65 eline 45% of the patients had NGT, 38.8% had IGT, and 15.8% had CFRD-No FH.
66                A total of 22.7% of women had IGT compared with 34.2% of men.
67                                The BD and HC IGT performances were compared with the effects of chron
68 actor for good IGT performance (i.e., higher IGT score) among Val/Val homozygotes.
69                                          HIV+IGT had greater visceral adiposity, fasting serum interl
70 ts with normal glucose tolerance, and 21 HIV+IGT subjects.
71  (whole-body proteolysis) were higher in HIV+IGT at all insulin levels but declined in response to hy
72 ate during hyperinsulinemia was lower in HIV+IGT than the other two groups.
73 ay, which may be further dysregulated in HIV+IGT, and support the notion that insulin signaling pathw
74                            Understanding how IGT genes modulate branch angles will provide insights i
75 s with isolated postchallenge hyperglycemia (IGT) are more insulin resistant than individuals with is
76                   Restricting to identifying IGT/NODAT using 2-hour oral glucose tolerance test (n =
77  more atherogenic in those with IGT or IFG + IGT.
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
79    Of the 267 subjects who progressed to IFG-IGT, 216 had additional follow-up.
80 n, n = 217; Hispanic-American, n = 193), IFG/IGT and diabetic subjects exhibited progressively increa
81  IFG/NGT (n = 11), NFG/IGT (n = 98), and IFG/IGT (n = 18).
82 NFG/IGT [n = 255], IFG/NGT [n = 59], and IFG/IGT [n = 102]) among nondiabetic subjects.
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
85 ts, while subjects with IGT and combined IFG/IGT had significantly reduced TGD.
86  widely used screening test in detecting IFG/IGT or NODAT, fructosamine may be a more accurate diagno
87               Forty (48%) recipients had IFG/IGT or NODAT.
88 sidered the gold standard in identifying IFG/IGT or NODAT.
89 ssment-Insulin Resistance in identifying IFG/IGT were between 0.81 and 0.85.
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)
94 it in beta-cell mass in the evolution of IFG/IGT and subsequently type 2 diabetes.
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
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  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)
126                             Mechanistically, IGT in both F(1) and F(2) generations is linked to impai
127 e intolerance/gestational diabetes mellitus (IGT/GDM).
128 The PCOS women with high ZAG had fewer MetS, IGT and polycystic ovaries as compared with the low ZAG
129                     The single-session mouse IGT measures dynamic risk-based decision making similar
130 e characterized a novel single-session mouse IGT using C57BL/6J mice (n = 44).
131  exhibited poor decision making in the mouse IGT.
132 C1 genes belong to a gene family (here named IGT for a shared conserved motif) found in all plant gen
133 ce: NFG/NGT (n = 307), IFG/NGT (n = 11), NFG/IGT (n = 98), and IFG/IGT (n = 18).
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
139                        A diagnosis of NODAT, IGT, and impaired fasting glucose (IFG) was based on Wor
140 l glucose sensitivity; IFG subjects, but not IGT subjects, had decreased beta-cell rate sensitivity.
141 AT functioning in mice performing this novel IGT.
142                           Early detection of IGT allows intensive diet and exercise modification, whi
143     When adjusted to age, the development of IGT in elderly individuals does not involve changes in m
144 nsitivity associated with the development of IGT.
145                            The prevalence of IGT was elevated in the highest (vs. lowest) quartile of
146 lence of NODAT and ignores the prevalence of IGT.
147                   The overall prevalences of IGT and GDM in the cohort were 2.6% and 5.2%, respective
148                   Predicted probabilities of IGT and GDM were reduced by one-half with a 10% decrease
149 as associated with a 12% decrease in risk of IGT and a 9% decrease in risk of GDM.
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).
152 theses about the relation of diet to risk of IGT or GDM.
153 aseline prevalence of IFG similar to that of IGT.
154 the presenting symptom of either diabetes or IGT.
155           Most trials of treatment of IFG or IGT found no effects on all-cause or cardiovascular mort
156                          Treatment of IFG or IGT was associated with delayed progression to diabetes.
157  consistently found that treatment of IFG or IGT was associated with delayed progression to diabetes.
158 ACZ885 in Atherosclerosis and Either T2DM or IGT Patients; NCT00995930).
159       Measured by [(1)(1)C]acetate with PET, IGT(+) subjects have a significant increase in myocardia
160  life events acted as a risk factor for poor IGT performance (i.e., high reward sensitivity) among Me
161 mpaired decision-making consistent with poor IGT performance of BD patients.
162 /- 31) (P < 0.001 controls versus relatives, IGT, and diabetes) as were the responses in the brachial
163 /- 67) (P < 0.001 controls versus relatives, IGT, and diabetes).
164 /- 5.0) (P < 0.01 controls versus relatives, IGT, and diabetes).
165 HB) is increasingly recognized as a reliable IGT and diabetes predictor, and can be measured using li
166 ration of only PM dilemmas increased women's IGT performance to the level of men.
167 duced in relatives (98 +/- 48, mean +/- SD), IGT (94 +/- 52), and diabetes (74 +/- 45) compared with
168                         We recorded standard IGT performance measures and novel post-reward and post-
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
172                      The Iowa gambling task (IGT) is one of the most influential behavioral paradigms
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
176 sion making, we used the Iowa Gambling task (IGT).
177  or placebo by using the Iowa Gambling Task (IGT).
178                        The data suggest that IGT genes are ancient, and play conserved roles in deter
179 modified criteria were used, suggesting that IGT is phenotypically different from IFG and is associat
180                                          The IGT family also includes TAC1 and LAZY1, which are known
181                                          The IGT requires subjects to choose among four card decks (t
182                              We assessed the IGT performance of 16 BD subjects (7 female) and 17 heal
183 effect on diabetes risk may occur before the IGT-to-diabetes transition.
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
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 ty in the cerebellum on both versions of the IGT.
194              Preoperative performance on the IGT was significantly impaired compared to after surgery
195 e present study, men and women performed the IGT during PM, MI, or control deliberations.
196 ic learning (cerebellum) when performing the IGT.
197 ps underwent cognitive evaluations using the IGT, Wisconsin Card Sorting Test, and Trail Making Test
198 oss diverse plant phyla, and fall within the IGT gene family.
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.
204             Both impaired glucose tolerance (IGT) (as defined by the 1985 World Health Organization c
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
214 sk of developing impaired glucose tolerance (IGT) and type 2 diabetes.
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
221 A) metabolism in impaired glucose tolerance (IGT) is different in men and women.
222 alent in men and impaired glucose tolerance (IGT) more prevalent in women.
223 lucose (IFG) and impaired glucose tolerance (IGT) often coexist and as such represent a potent risk f
224 ic patients have impaired glucose tolerance (IGT) or diabetes mellitus (DM).
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
227                  Impaired glucose tolerance (IGT) serves as a marker for the state of insulin resista
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
230 obese youth with impaired glucose tolerance (IGT) versus normal glucose tolerance (NGT).
231 ose (IFG) and/or impaired glucose tolerance (IGT) was found in 36% (n = 191).
232 in 427 subjects; impaired glucose tolerance (IGT) was found in 87 subjects, and diabetes was found by
233 sive obesity and impaired glucose tolerance (IGT) with aging.
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
236 fasting glucose, impaired glucose tolerance (IGT), and NODAT.
237  mellitus (GDM), impaired glucose tolerance (IGT), and normal glucose tolerance.
238 ntolerance (IR), impaired glucose tolerance (IGT), and normotensive and hypertensive type 2 diabetes
239 bjects with NGT, impaired glucose tolerance (IGT), and T2DM.
240 ulin resistance, impaired glucose tolerance (IGT), and type 2 diabetes are largely unknown.
241 g glucose (IFG), impaired glucose tolerance (IGT), and type 2 diabetes is not well defined.
242 tolerance (NGT), impaired glucose tolerance (IGT), and type 2 diabetes, using acute insulin response
243 s, subjects with impaired glucose tolerance (IGT), and type 2 diabetic subjects.
244 tolerance (NGT), impaired glucose tolerance (IGT), or CFRD without fasting hyperglycemia (CFRD-No FH)
245 tolerance (NGT), impaired glucose tolerance (IGT), or T2DM.
246 lucose (IFG), or impaired glucose tolerance (IGT), potentially resulting in improved outcomes.
247 in subjects with impaired glucose tolerance (IGT).
248 e development of 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 glucose (IFG) or impaired glucose tolerance (IGT).
253 betes (n = 137), impaired glucose tolerance (IGT; n = 139), and normal glucose tolerance (NGT; n = 34
254  (NGT; n = 190), impaired glucose tolerance (IGT; n = 209), and diabetes (n = 230)].
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 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
266 lutants during pregnancy was associated with IGT but not GDM.
267 ity in women, whereas it was associated with IGT per se in men.
268  and reduced neuronal reuptake compared with IGT subjects (by 46%; P = 0.04).
269                             Individuals with IGT demonstrated higher BP values (P < 0.001), fasting t
270 viduals with NGT, and older individuals with IGT.
271 nished insulin secretion in individuals with IGT.
272 ysregulated in HIV-infected individuals with IGT.
273 ac DFA partitioning nevertheless occurs with IGT both in men and women.
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 (
276                                Patients with IGT are at significantly increased risk for death and mo
277 B activation was diminished in patients with IGT but not significantly in diabetic patients.
278                                Patients with IGT-associated neuropathy may represent an attractive ta
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.
282                                Subjects with IGT and early-stage, asymptomatic type 2 diabetic patien
283                                Subjects with IGT and IFG have different metabolic characteristics.
284 ubjects with NGT compared with subjects with IGT and subjects diagnosed by 2-h OGTT criteria alone.
285 were not restored to normal in subjects with IGT and T2DM.
286  ROS generation, whether older subjects with IGT have a further worsening of mitochondrial function (
287           We hypothesized that subjects with IGT may be more insulin resistant and have higher levels
288 icantly higher than HOMA-IR in subjects with IGT or NGT.
289 er subjects with NGT and older subjects with IGT versus younger subjects.
290  (ISOCAL) on DFA metabolism in subjects with IGT.
291 associated with weight loss in subjects with IGT.
292 ), and in women, it was higher in those with IGT (7,453 +/- 469 vs. 10,133 +/- 1,488 microg/24 h, P <
293 n insulin-resistant cohorts, both those with IGT and those with T2D.
294 significantly more atherogenic in those with IGT or IFG + IGT.
295 DI was approximately 43% lower in youth with IGT and correlated positively with glucose DI.
296 , betaCGS was 30 and 65% lower in youth with IGT and T2D, respectively; rate sensitivity was 40% lowe
297                  We conclude that youth with IGT manifest a global decline in insulin sensitivity, in
298                                   Youth with IGT or T2D had 32 and 38% reduced incretin effect compar
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

WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。
 
Page Top