ライフサイエンスコーパス: IFG

1 IFG (100 to 125 mg/dl) or insulin resistance (by homeost

2 IFG correlated with RT specifically on salient non-targe

3 IFG effects on GCase stability and substrate levels were

4 IFG inhibits GCase with K(i) approximately 30 nM for wil

5 IFG treatment did not alter the GS and GC accumulation s

6 14% combined IGT/IFG, 9% IGT alone, and 18% IFG alone.

7 For CVD, only the 1997 IFG definition yielded significantly greater odds of CVD

8 1.0 to 3.0, p = 0.048), whereas for the 1997 IFG definition, the OR for CHD in women was 2.2 (95% CI

9 risk factors, and CHD compared with the 1997 IFG definition.

10 risk factors, and CHD with the 1997 and 2003 IFG definition was compared.

11 Individuals identified with the 2003 IFG definition did not have an increase in known CHD whe

12 For the 2003 IFG definition, the OR for CHD among women was 1.7 (95%

13 o 1.31], women: 1.30 [95% CI: 1.10 to 1.54]; IFG 100: men: 1.23 [95% CI: 1.06 to 1.42], women: 1.16 [

14 Overall, 12.5% had diabetes and 7.8% IFG.

15 In 8 publications with information about IFG (100 to 125 mg/dl) (IFG 100), estimates of RR ranged

16 In 18 publications with information about IFG (110 to 125 mg/dl) (IFG 110), estimates of RR ranged

17 nts free of CVD, categorized by the 1997 ADA IFG definition (fasting plasma glucose 110 to 125 mg/dl;

18 Although IFG fully inhibits GlcCerase in the lysosome in an in si

19 Although IFG is viewed as increasing CHD risk, this association i

20 tional connectivity between the amygdala and IFG, OFC, and vmPFC.

21 ation use or fasting glucose>/=126 mg/dL and IFG as fasting glucose 100-125 mg/dL.

22 ith reference to models of dmPFC, dlPFC, and IFG functioning.

23 competition in MTG, left angular gyrus, and IFG.

24 ith IFG/impaired glucose tolerance (IGT) and IFG/diabetes but did not differ in subjects with IFG/nor

25 NOVA) in subjects with NFG/IGT, IFG/IGT, and IFG/diabetes but did not differ in subjects with NFG/NGT

26 NOVA) in subjects with NFG/IGT, IFG/IGT, and IFG/diabetes but did not differ in subjects with NFG/NGT

27 d influences from right TPJ to right IPS and IFG (inferior frontal gyrus).

28 arietal regions, including IPS, FEF, MFG and IFG, in addition to regions in visual cortex.

29 did not differ in subjects with NFG/NGT and IFG/NGT.

30 lead first to hepatic insulin resistance and IFG and then to extrahepatic insulin resistance, hypergl

31 archical organization of the pre-SMA-STN and IFG-STN pathways, since interruption of pre-SMA function

32 ism of branched-chain amino acids in T2D and IFG.

33 We conclude that left TPJ and IFG form a sensory-driven network that integrates contex

34 ions, we applied cTBS over the left anterior IFG (aIFG) or posterior IFG (pIFG) to test the anatomic

35 between IFG and incident DM and also between IFG and incident CV events.

36 s was used to assess the association between IFG and incident DM and also between IFG and incident CV

37 The associations between IFG, incident type 2 diabetes mellitus (T2DM), and cardi

38 and glucose disposal did not differ between IFG and NFG subjects, implying hepatic and extrahepatic

39 ity between the right amygdala and bilateral IFG, OFC, vmPFC, anterior cingulate cortex, and frontopo

40 hat the TD group had greater mPFC, bilateral IFG, and left superior temporal pole activity than the A

41 Both IFG and IGT are risk factors for type 2 diabetes, and ri

42 lin secretion was markedly decreased in both IFG and IGT, whereas second-phase insulin secretion was

43 In women, both IFG definitions were associated with increased CHD risk,

44 lung and spleen involvement was enhanced by IFG treatment.

45 nk between cerebral correlates of cognitive (IFG) and emotional ("fear network") processing during sy

46 n resistance, subjects with IGT and combined IFG/IGT had a significantly greater reduction in insulin

47 bjects, while subjects with IGT and combined IFG/IGT had significantly reduced TGD.

48 Five studies combined IFG and IGT, yielding a fixed-effects summary estimate o

49 as similar to that in subjects with combined IFG/IGT and significantly higher than HOMA-IR in subject

50 y estimates for men and women were detected (IFG 110: men: 1.17 [95% CI: 1.05 to 1.31], women: 1.30 [

51 and widely used screening test in detecting IFG/IGT or NODAT, fructosamine may be a more accurate di

52 rom a 64-contact grid overlying more distant IFG sites.

53 th information about IFG (100 to 125 mg/dl) (IFG 100), estimates of RR ranged from 0.87 to 1.40.

54 th information about IFG (110 to 125 mg/dl) (IFG 110), estimates of RR ranged from 0.65 to 2.50.

55 Dysregulatory IFG dynamics were associated with weaker reciprocal exci

56 was not affected by empagliflozin in either IFG or NFG.

57 interruption of pre-SMA function can enhance IFG-STN connectivity and improve control over inappropri

58 regions relevant to cognitive control (esp. IFG/AI and the dorsal anterior cingulate cortex) were st

59 tion at baseline and follow-up examinations; IFG was defined as no T2DM and fasting glucose 100 to 12

60 e was the strongest predictive biomarker for IFG after glucose (odds ratio [OR] 1.65 [95% CI 1.39-1.9

61 g odds ratio and 95% confidence interval for IFG based on a fully adjusted model: isoleucine 2.29 (1.

62 fies girls who are at greater risk of future IFG and T2DM.

63 und, and notably, the stability of the GCase-IFG complex is pH sensitive.

64 ith development of impaired fasting glucose (IFG) after atenolol treatment.

65 -two subjects with impaired fasting glucose (IFG) and 28 subjects with normal fasting glucose (NFG) i

66 n in subjects with impaired fasting glucose (IFG) and compare the results to impaired glucose toleran

67 se associated with impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) from published

68 Impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) often coexist

69 the development of impaired fasting glucose (IFG) and type 2 diabetes (T2DM) at age 18-19 y could pro

70 n in subjects with impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT).

71 ve of diabetes and impaired fasting glucose (IFG) in a large HBV-infected multiethnic cohort.

72 with diabetes and impaired fasting glucose (IFG) in Fukuoka, Japanese subjects (n = 1108) and age-,

73 Impaired fasting glucose (IFG) is more prevalent in men and impaired glucose toler

74 tion definition of impaired fasting glucose (IFG) on prevalence of IFG, coronary heart disease (CHD)

75 entified as either impaired fasting glucose (IFG) or impaired glucose tolerance (IGT).

76 determine whether impaired fasting glucose (IFG) predicts cardiovascular disease (CVD) events.

77 of NODAT, IGT, and impaired fasting glucose (IFG) was based on World Health Organization guidelines.

78 y assessed whether impaired fasting glucose (IFG), insulin resistance, and waist-to-hip ratio (WHR) h

79 ptomatic diabetes, impaired fasting glucose (IFG), or impaired glucose tolerance (IGT), potentially r

80 iovascular risk of impaired fasting glucose (IFG).

81 he pathogenesis of impaired fasting glucose (IFG).

82 and is preceded by impaired fasting glucose (IFG).

83 n in subjects with impaired fasting glucose (IFG).

84 7 with predonation impaired fasting glucose (IFG).

85 e participants had impaired fasting glucose (IFG; i.e., 100-125 mg/dL FBG) at first visit.

86 ower threshold for impaired fasting glucose [IFG]) and early-onset coronary artery disease (CAD).

87 2 individuals with impaired fasting glucose [IFG], and 1,897 control subjects) from TwinsUK.

88 he bilateral anterior interior frontal gyri (IFG), left posterior IFG, SMG, and posterior cingulate c

89 vity, with the right inferior frontal gyrus (IFG) a critical region for executive function.

90 to the left, while the infero-frontal gyrus (IFG) activation was to the right.

91 icate that the right inferior frontal gyrus (IFG) and both left and right insula were more activated

92 d network, including inferior frontal gyrus (IFG) and inferior parietal cortex (IPC).

93 ive responses in the inferior frontal gyrus (IFG) and IPL (supramarginal) regions revealed differenti

94 rly between the left inferior frontal gyrus (IFG) and left subcortical regions (including the amygdal

95 yrus (MTG), and left inferior frontal gyrus (IFG) and of semantic competition in MTG, left angular gy

96 onal symmetry of the inferior frontal gyrus (IFG) and superior temporal gyrus (STG), the sensory and

97 rain areas including inferior frontal gyrus (IFG) and temporo-parietal junction (TPJ) were employed i

98 g network, the right inferior frontal gyrus (IFG) and the primary motor cortex (M1), using electocort

99 ) which includes the inferior frontal gyrus (IFG) and the somotosensory related cortex (SRC).

100 tal cortex (IPC) and inferior frontal gyrus (IFG) are jointly activated by duration and numerosity di

101 We focused on the inferior frontal gyrus (IFG) as our ROI, as recent studies have demonstrated bot

102 hildren in the right inferior frontal gyrus (IFG) as well as in bilateral temporal regions.

103 ivation at the right inferior frontal gyrus (IFG) during both tasks.

104 cortex (dlPFC), and inferior frontal gyrus (IFG) have all been implicated in resolving decision conf

105 (cTBS) over the left inferior frontal gyrus (IFG) in healthy volunteers, then used functional MRI to

106 cortex (OFC) and the inferior frontal gyrus (IFG) in subjects performing this task.

107 The inferior frontal gyrus (IFG) is a key cortical hub in the circuits of emotion an

108 tectonically diverse inferior frontal gyrus (IFG) of humans is known to be critically involved in a w

109 irror neurons in the inferior frontal gyrus (IFG) of humans, we used a repetition suppression paradig

110 area located in the inferior frontal gyrus (IFG) of the human brain, has been identified as one of s

111 sed activity in left inferior frontal gyrus (IFG) of the prefrontal cortex.

112 ested that the right inferior frontal gyrus (IFG) plays a critical role in manual response inhibition

113 r area (pre-SMA) and inferior frontal gyrus (IFG) to the subthalamic nucleus (STN) are thought to sup

114 paired when the left inferior frontal gyrus (IFG) was driven at beta (18.7 Hz) compared to stimulatio

115 s-fcMRI)] with right inferior frontal gyrus (IFG), an anterior component of the ventral network.

116 erior cingulate, the inferior frontal gyrus (IFG), and ventral and lateral temporal lobes bilaterally

117 networks [bilateral inferior frontal gyrus (IFG), bilateral medial prefrontal cortex (mPFC), and bil

118 The inferior frontal gyrus (IFG), orbitofrontal cortex (OFC), and ventromedial PFC (

119 observed in the left inferior frontal gyrus (IFG), posterior superior temporal gyrus (STG), and infer

120 ignatures within the inferior frontal gyrus (IFG), which our prior work has linked to impaired feedba

121 unction in the right inferior frontal gyrus (IFG)-one node in a corticothalamic inhibitory control (I

122 + > CS-) in the left inferior frontal gyrus (IFG).

123 guage regions in the inferior frontal gyrus (IFG).

124 guage area, the left inferior frontal gyrus (IFG).

125 l junction (TPJ) and inferior frontal gyrus (IFG).

126 tal gyrus (MFG), and inferior frontal gyrus (IFG).

127 es, 840 (12.7%) had T2DM and 940 (13.8%) had IFG at the baseline examination.

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

129 One-third of the population has IFG with the 2003 definition, yet many of these individu

130 Having IFG was not independently associated with an increased s

131 onic features as cortical areas in the human IFG, suggesting structural homology.

132 d is evidence of mirror neurons in the human IFG.

133 cts in insulin/insulin-like growth factor I (IFG-I) intracellular signaling processes.

134 considered the gold standard in identifying IFG/IGT or NODAT.

135 Assessment-Insulin Resistance in identifying IFG/IGT were between 0.81 and 0.85.

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

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

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

139 In IFG subjects, the defect in beta-cell glucose sensitivit

140 lucose disposal remained lower (P < 0.01) in IFG than in NFG subjects.

141 ower (P < 0.05) and EGP higher (P < 0.05) in IFG than in NFG subjects.

142 Unlike these regions, however, activity in IFG was not modulated by reductions in the relative valu

143 The islet anatomy in IFG and type 2 diabetes reveals an approximately 50 and

144 -Cell mass is approximately 50% deficient in IFG and approximately 65% deficient in type 2 diabetes.

145 te distinct defects in beta-cell function in IFG and IGT.

146 eased (P < 0.05) rates of gluconeogenesis in IFG.

147 tance contribute to fasting hyperglycemia in IFG with the former being due at least in part to impair

148 ctivity and protein levels were increased in IFG-treated mice.

149 ted portal insulin concentrations present in IFG subjects after an overnight fast (approximately 80 p

150 insulin concentrations typically present in IFG subjects within 30 min of eating, extrahepatic (but

151 Partial pancreatectomy resulted in IFG and IGT.

152 isposition) index increased significantly in IFG, but not in subjects with normal glucose tolerance.

153 vs. 5.91+/-11 mg/g, P=0.29) were similar in IFG and normal glucose donors.

154 EGP was comparably suppressed in IFG and NFG groups during prandial insulin infusion, ind

155 Isofagomine (IFG) is an acid beta-glucosidase (GCase) active site inh

156 h the pharmacological chaperone isofagomine (IFG) at pH 7.5.

157 , we report that the iminosugar isofagomine (IFG), an active-site inhibitor, increases GlcCerase acti

158 erformed with mice treated with isofagomine (IFG), a pharmacologic chaperone for GCase.

159 I 1.3-2.5]) and less likely to have isolated IFG (0.5 [0.3-0.7]) adjusted for ethnicity, age, waist,

160 of sex and HRT on the prevalence of isolated IFG and isolated IGT, we conclude that female sex hormon

161 entially normal in individuals with isolated IFG.

162 intervention groups: tDCS(anodal) over left IFG, IPC, or sham.

163 only when tDCS(anodal) was applied over left IFG.

164 revealed increased connectivity of the left IFG and additional major hubs overlapping with the langu

165 n this system, particularly between the left IFG and left pallidum, putamen, and insular cortex, is a

166 Functional connectivity between the left IFG and the right IFG and right inferior parietal lobule

167 s of the functional connectivity of the left IFG and used graph theory to study its local functional

168 d with reduced neural activation in the left IFG during speech production.

169 Significant activation in the left IFG in conjunction with other cortical and subcortical b

170 ng-state functional connectivity of the left IFG in participants with BD and in those at increased ge

171 unpredictable, phasic disruption of the left IFG selectively disrupts control of responses to high-co

172 In BD, the left IFG was functionally dysconnected from a network of regi

173 n beta frequency for stimulation of the left IFG, demonstrating an intimate causal relationship betwe

174 , a sustained oscillatory "echo" in the left IFG, which outlasted the stimulation period by approxima

175 to high-PI probes, was specific to the left IFG.

176 r been ruled out, however, is that this left IFG effect may merely reflect sensitivity to such nonspe

177 dorsal anterior cingulate cortex and to left IFG and dorsolateral prefrontal cortex.

178 ta indicate that there is significantly less IFG, lower insulin levels, and insulin resistance, but h

179 nnections within and between the three major IFG subgyri: the pars orbitalis, pars triangularis, and

180 arietal attentional network, the IPS and MFG/IFG appear to be most heavily involved in attentive cue

181 The right middle/inferior frontal gyrus (MFG/IFG), which is included in the FPCN, showed greater conn

182 left intraparietal sulcus (IPS) and left MFG/IFG.

183 e DAN, as well as the left IPL and right MFG/IFG of the VAN.

184 ted with increased CHD risk, whereas neither IFG definition identified men at increased short-term ri

185 Nevertheless, IFG was activated only by unexpected shifts of attention

186 en avenues to primary prevention of obesity, IFG, and T2DM in children.

187 The majority (57.8%) of IFG donors had reverted to normal fasting glucose at a m

188 Administration of IFG (30 mg/kg/day) to the mice homozygous for GCase muta

189 e were 5 incident cases of T2DM, 37 cases of IFG, and 597 noncases.

190 an Diabetes Association (ADA) definitions of IFG to predict CVD.

191 change in body mass index and development of IFG and T2DM together were assessed.

192 sible pre-teen predictors for development of IFG, T2DM, and changes in body mass index at age 18-19 y

193 notype data available for the development of IFG.

194 lanine hydroxylase (PAH) with development of IFG.

195 A major effect of IFG is to facilitate the folding and transport of newly

196 The effect of IFG on GCase function was investigated in GCase mutant f

197 60) AA genotype had the highest incidence of IFG (P for trend=0.0003).

198 (95% CI: 10%, 58%, p = 0.003) higher odds of IFG, respectively.

199 lay an important role in the pathogenesis of IFG and IGT.

200 0001), WHR (p < 0.0001), and the presence of IFG (p = 0.04), but not BMI (p = 0.24), were independent

201 70S GlcCerase synthesized in the presence of IFG exhibits a shift in pH optimum from 6.4 to 5.2 and a

202 The prevalence of IFG increased from 8% to 35% with the 2003 criterion.

203 The prevalence of IFG, CHD risk factors, and CHD with the 1997 and 2003 IF

204 aired fasting glucose (IFG) on prevalence of IFG, coronary heart disease (CHD) risk factors, and CHD

205 rmal fasting glucose, a higher proportion of IFG donors had developed DM (15.56% vs. 2.2%, P=0.06).

206 r individuals with the pre-diabetes state of IFG do not exhibit abnormal proximal thoracic distensibi

207 Most trials of treatment of IFG or IGT found no effects on all-cause or cardiovascul

208 Treatment of IFG or IGT was associated with delayed progression to di

209 trials consistently found that treatment of IFG or IGT was associated with delayed progression to di

210 The combined prevalence of diabetes or IFG was highest among blacks (36.7%) and those either bo

211 t did not differ in subjects with NFG/NGT or IFG/NGT.

212 h above-median HOMA-IR, above-median WHR, or IFG had a higher LV mass-to-volume ratio (p < 0.05 for a

213 interior frontal gyri (IFG), left posterior IFG, SMG, and posterior cingulate cortices (PCC).

214 er the left anterior IFG (aIFG) or posterior IFG (pIFG) to test the anatomic specificity of the effec

215 ngs suggest that the right ventral posterior IFG may play a more general role in response inhibition

216 showed that the bilateral ventral posterior IFG, anterior insula, inferior frontal junction (IFJ), m

217 x total caloric intake interaction predicted IFG and T2DM at age 18-19 y.

218 Assessment-Insulin Resistance in predicting IFG/IGT or NODAT were assessed using the area under the

219 hin the prefrontal-central networks (i.e., r-IFG/M1 and/or r-preSMA/M1) is realized in rapid, periodi

220 ctivation of right inferior frontal gyrus (r-IFG) and right presupplementary motor area (r-preSMA) is

221 tivity in the beta frequency band in a right IFG/basal ganglia network, with downstream effects on M1

222 Furthermore, cingulate and right IFG volume increases were more pronounced in the MAA tha

223 aneous bilinguals between the left and right IFG, as well as between the inferior frontal gyrus and b

224 connectivity relative to controls from right IFG to dorsal anterior cingulate cortex and to left IFG

225 ne-induced change in connectivity from right IFG to dorsolateral prefrontal cortex was proportional t

226 For each patient, there was a greater right IFG response in the beta frequency band ( approximately

227 dren used a network that was primarily right IFG and bilateral pSTS, suggesting reduced use of social

228 level-dependent (BOLD) response in the right IFG (F1,78 = 14.87) and thalamus (F1,78 = 14.97) (P < .0

229 udy 2, greater IC-BOLD response in the right IFG (t23 = -2.49; beta = -0.47; P = .02), and weaker cor

230 nectivity between the left IFG and the right IFG and right inferior parietal lobule was also signific

231 propose that specialized areas in the right IFG and the left and right insula are multisensory opera

232 Our results show that TMS of the right IFG impairs categorical duration discrimination, whereas

233 These results indicate that the right IFG is specifically involved at the categorical decision

234 In addition, the right IFG response occurred 100-250 ms after the stop signal,

235 xetine increased connectivity from the right IFG to the dorsal anterior cingulate.

236 unctional connectivity seeded from the right IFG to the dorsolateral prefrontal cortex (DLPFC) and an

237 tasks, with a congruency effect in the right IFG.

238 a decrease in beta-cell glucose sensitivity; IFG subjects, but not IGT subjects, had decreased beta-c

239 In conclusion, this T2D-IFG biomarker study has surveyed the broadest panel of n

240 001) compared with subjects not having T2DM (IFG plus normal fasting glucose).

241 Pre-teen IFG, insulin resistance (and insulin), and rapidly incre

242 These results indicate that IFG stabilizes GCase in tissues and serum and can reduce

243 The results showed that IFG prevalence in Japanese men (15.9%) and women (7.4%)

244 To determine whether the IPC and the IFG are involved in response conflict (or facilitation)

245 ocial communication information, just as the IFG is specialized to process and integrate speech and g

246 ctions and their neural underpinnings at the IFG.

247 onstrated increased connectivity between the IFG and regions of the "fear network" (amygdalae, insula

248 ciprocal excitatory connectivity between the IFG and the vmPFC.

249 d coefficients of determination for both the IFG (r(2) = 0.261, p < 0.001) and the STG (r(2) = 0.142,

250 has not been well studied after changing the IFG criterion, especially in a clinical practice setting

251 ected prefrontal-limbic model comprising the IFG, vmPFC, and amygdala.

252 Lowering the threshold to define the IFG component (from 110 to 100 mg/dl) and the value of t

253 ific promoter and is also homozygous for the IFG-responsive V394L GCase.

254 Here we show that in the IFG, responses were suppressed both when an executed act

255 Specifically, neural activity in the IFG, SRC, and STS were related to cognitive empathy.

256 an association between the trajectory of the IFG and language outcomes at 4 years of age (chi(2) = 10

257 Here, we show that portions of the IFG as well as other cortical and subcortical regions in

258 Functional dysconnectivity of the IFG from regions involved in emotional regulation may re

259 ent to examine whether the activation of the IFG is dependent on the type of visuo-motor associations

260 de causal evidence for a pivotal role of the IFG-STN pathway during action control.

261 enhanced activation and connectivity of the IFG-STN pathway.

262 solely on the functional connectivity of the IFG.

263 ipolar electrical stimuli to one site on the IFG while recording the electrical response evoked by th

264 three prefrontal-limbic regions, wherein the IFG provides evaluation of stimulus meaning, which then

265 he level of albumin excretion in 45 of these IFG donors to 45 matched controls with normal predonatio

266 eral prefrontal cortex (VLPFC) (analogous to IFG) is not, contributing instead to higher order proces

267 ling found an excitatory pathway from TPJ to IFG to FEF, suggesting that this was the pathway by whic

268 rong rs-fcMRI among themselves, not with TPJ/IFG, defining a distinct network that may retrieve/activ

269 task-related activation in the left ventral IFG, an area specifically implicated in semantic retriev

270 In 8-week IFG-treated mice, the accumulated glucosylceramide and g

271 pe 2 diabetes, and risk is even greater when IFG and IGT occur together.

272 with normal fasting glucose (NFG), 845 with IFG, and 414 with diabetes, all aged 45 to 85 years and

273 R for cardiovascular disease associated with IFG and IGT is unclear.

274 line AA levels were strongly associated with IFG development.

275 Factors associated with IFG were obesity (OR, 4.13) and hypertension (OR, 3.27),

276 metabolites were found to be associated with IFG.

277 secretion and insulin action in humans with IFG and IGT.

278 Individuals with IFG were more likely to be older and hypertensive, with

279 t age 2 months (nondiabetic), 5 months (with IFG), and 10 months (with diabetes) to prospectively exa

280 s of any retinopathy among participants with IFG and type 2 diabetes were 9.4% and 32.4%, respectivel

281 importance of intervention for persons with IFG to reduce their incidence of T2DM.

282 e disposal were measured in 31 subjects with IFG and 28 subjects with normal fasting glucose (NFG) af

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

284 ransport with empagliflozin in subjects with IFG and NFG produces comparable glucosuria but lowers th

285 +/- 4 g glucosuria on day 2 in subjects with IFG and NFG, respectively, and the glucosuria was mainta

286 oncentration decreased only in subjects with IFG from 110 +/- 2 to 103 +/- 3 mg/dL (P < 0.01) after 1

287 Subjects with IFG had TGD similar to normal glucose-tolerant subjects,

288 asting glucose (NFG) and eight subjects with IFG received empagliflozin (25 mg/day) for 2 weeks.

289 tide were higher (P < 0.05) in subjects with IFG than in those with NFG, whereas endogenous glucose p

290 HOMA-IR in subjects with IFG was similar to that in subjects with combined IFG/IG

291 ves beta-cell function only in subjects with IFG.

292 tion in insulin secretion than subjects with IFG.

293 ced beta-cell function only in subjects with IFG.

294 stion was lower (P < 0.001) in subjects with IFG/impaired glucose tolerance (IGT) and IFG/diabetes bu

295 diabetes but did not differ in subjects with IFG/normal glucose tolerance (NGT) or NFG/NGT.

296 ic stiffness was not increased in those with IFG compared with those with NFG (1.90 +/- 0.05 versus 1

297 /- 0.81 g, P < 0.0009) but not in those with IFG in comparison with NFG (145.2 +/- 1.03 versus 145.8

298 ason, an opportunity may exist in those with IFG to prevent LV hypertrophy and abnormal aortic stiffn

299 Fibroblasts treated with IFG at muM concentrations showed enhancement of WT and m

300 Age 9-10 y IFG and HOMA-IR (or insulin), 10-y change in HOMA-IR (or