ライフサイエンスコーパス: FPG

1 FPG concentration and beta-cell function was measured wi

2 FPG concentrations at 28 gestational weeks (IQR: 22-32 w

3 of total diabetes (using the hemoglobin A1c, FPG, or 2-hour PG definition) was higher among non-Hispa

4 vel of 200 mg/dL or greater (hemoglobin A1c, FPG, or 2-hour PG definition).

5 justed prevalence (using the hemoglobin A1c, FPG, or 2-hour PG definitions for diabetes and prediabet

6 theless, 42% of subjects developing abnormal FPG did not develop abnormal 2hPG, and vice versa.

7 y these criteria, 43% progressed to abnormal FPG and 43% to abnormal 2hPG by 10 years of follow-up; a

8 By 10 years, 14% had progressed to abnormal FPG and 48% to abnormal 2hPG.

9 n subsidiary analyses, we defined "abnormal" FPG as > or =5.55 mmol/l and "diabetic" FPG as > or =6.1

10 ea, 8%, 42%, and 24%, respectively, achieved FPG levels of less than 7.8 mmol/L (140 mg/dL) and 9%, 2

11 s a hemoglobin A1c level of 5.7% to 6.4%, an FPG level of 100 mg/dL to 125 mg/dL, or a 2-hour PG leve

12 MD = 0.65; 95% CI 0.43 to 0.88; P <0.05) and FPG (MD = 9.04; 95% CI 2.17 to 15.9; P <0.05), but no si

13 6 mg/dL, and normal glucose as A1C <5.7% and FPG <100 mg/dL.

14 st important determinants of IA were age and FPG (R(2) = 0.519, P < 0.0001), and different FPG levels

15 amyloid severity was generated with age and FPG as required variables.

16 y 1.7 to 11.6 mm Hg per 10 years of age, and FPG increased by 0.8 to 20.4 mg/dL per 10 years of age i

17 The discrepancy between chromatographic and FPG-based approaches may reflect overestimation by HPLC

18 se more steeply in high-income countries and FPG in the Oceania countries, the Middle East, and the U

19 alysis determined effectiveness of HbA1c and FPG to discriminate between groups.

20 Levels of HbA1c and FPG were similar between the evolocumab and placebo grou

21 ata between ages 30 and 64 years for SBP and FPG, and between 30 and 54 years for TC.

22 f age-SBP relationship in older ages; TC and FPG age associations reversed in older ages, leading to

23 measured at baseline then every 24 weeks and FPG was measured at baseline, week 12, week 24, and ever

24 AGR was defined as FPG >/=6.1 mmol L(-)(1) (World Health Organization (WHO)

25 Diabetes was defined as FPG >6.9 mmol L(-)(1), or being on diabetes treatment.

26 tients randomized to metformin, 18% attained FPG levels of less than 7.8 mmol/L (140 mg/dL) and 13% a

27 Relations between FPG and offspring growth and obesity were assessed by li

28 d FPG or 2hPG, 22% progressed to diabetes by FPG whereas 17% progressed by 2hPG at 10 years.

29 years, 8% of these progressed to diabetes by FPG whereas 27% progressed by 2hPG.

30 according to fasting glucose concentration (FPG) as nondiabetic (FPG <110 mg/dl), impaired fasting g

31 istory of diabetes, and baseline covariates (FPG, BMI, education, smoking, and physical activity).

32 ifications: (1) normal by the new criterion (FPG concentration <6.1 mmol/L [110 mg/dL]); (2) impaired

33 paired fasting glucose by the new criterion (FPG concentration of 6.1-6.9 mmol/L [110-125 mg/dL]); (3

34 FG, FPG 110-125 mg/dl), and type 2 diabetes (FPG >126 mg/dl).

35 -11.0 mmol/l), and from IFG-IGT to diabetes (FPG > or =7.0 mmol/l or 2hPG > or =11.1 mmol/l).

36 ediabetic (FPG 5.6-6.9 mmol/L), or diabetic (FPG >/=7.0 mmol/L).

37 mal" FPG as > or =5.55 mmol/l and "diabetic" FPG as > or =6.1 mmol/l, making the baseline prevalence

38 PG (R(2) = 0.519, P < 0.0001), and different FPG levels were sensitive and specific to predict IA sev

39 acteristics of simple models of dysglycemia (FPG>/=100 mg/dL) identification were evaluated and optim

40 FI strengthened these associations.Elevated FPG before treatment indicates success with dietary weig

41 Two of the enzymes, FPG and NEIL1 known to cleave normal abasic sites (1) by

42 ng glucose both between and within families (FPG 4.1-18.5 mmol/l, IQ range 5.45-10.4), with a marked

43 tantially across populations, especially for FPG and TC.

44 In diabetic patients diagnosed by the former FPG criterion, HbA1c levels were normal in 18.6% (16.7%)

45 However, gestational FPG and prepregnancy obesity status interacted significa

46 e mothers, each unit increase in gestational FPG was associated with decreased offspring weight (B: -

47 e mothers, each unit increase in gestational FPG was associated with increased offspring weight (B: 0

48 1C (A1C) >/=6.5%, or fasting plasma glucose (FPG) >/=126 mg/dL, prediabetes as A1C 5.7%-<6.5% or FPG

49 f diabetes and had a fasting plasma glucose (FPG) <126 mg/dl at baseline.

50 rity correlated with fasting plasma glucose (FPG) (r = 0.662, P < 0.001) and HbA1c (r = 0.726, P < 0.

51 moglobin A1c (HbA1c)/fasting plasma glucose (FPG) alone fail to diagnose or miscategorize up to 40% o

52 ted higher levels of fasting plasma glucose (FPG) and blood hemoglobin A1c (HbA1c) than individuals o

53 ncertainties in mean fasting plasma glucose (FPG) and diabetes prevalence for adults aged 25 years an

54 ed concentrations of fasting plasma glucose (FPG) and fasting insulin (FI) as prognostic markers for

55 subjects and assayed fasting plasma glucose (FPG) and insulin sensitivities.

56 sion were changes in fasting plasma glucose (FPG) between biopsies (per 10 mg/dL increase; odds ratio

57 empagliflozin on the fasting plasma glucose (FPG) concentration and beta-cell function in subjects wi

58 wered the diagnostic fasting plasma glucose (FPG) concentration from 7.8 to 7.0 mmol/L (140 to 126 mg

59 ently attains target fasting plasma glucose (FPG) concentration of less than 7.8 mmol/L (140 mg/dL) o

60 d the association of fasting plasma glucose (FPG) concentrations during pregnancy with offspring grow

61 abetes diagnosis but fasting plasma glucose (FPG) has been useful for identifying patients with gluco

62 The sensitivity of fasting plasma glucose (FPG) in screening for new-onset diabetes after transplan

63 6.5% or greater or a fasting plasma glucose (FPG) level of 126 mg/dL or greater (hemoglobin A1c or FP

64 c)) and the level of fasting plasma glucose (FPG) maintained in pancreas transplant recipients?

65 l/mol) or greater or fasting plasma glucose (FPG) of 7.0 mmol/L or greater.

66 A fasting plasma glucose (FPG) test was used as the study outcome, signifying pote

67 Fasting plasma glucose (FPG) was measured from capillary blood using On-Call(R)

68 Gestational fasting plasma glucose (FPG) was positively associated with birth weight (B: 0.1

69 iated with increased fasting plasma glucose (FPG), A1C, fasting insulin, and insulin resistance by ho

70 al cholesterol (TC), fasting plasma glucose (FPG), and body mass index (BMI) on the risk of cardiovas

71 s of FINDRISC score, fasting plasma glucose (FPG), and HbA1c.

72 iation with HbA(1c), fasting plasma glucose (FPG), and mean fasting plasma glucose (mFPG) measured ov

73 d by measurements of fasting plasma glucose (FPG), intravenous glucose disappearance rate (KG), HbA1c

74 c (primary outcome), fasting plasma glucose (FPG), serum N(euro)-(carboxymethyl) lysine (CML), and pe

75 oglobin A1c (HbA1c), fasting plasma glucose (FPG), total cholesterol (TC), triglycerides (TG), and hi

76 pressure (SBP), and fasting plasma glucose (FPG), triglyceride, and high-density lipoprotein (HDL)-c

77 dy mass index (BMI), fasting plasma glucose (FPG), triglycerides (TG) and cholesterol levels.

78 holesterol (TC), and fasting plasma glucose (FPG).

79 from NGT to abnormal fasting plasma glucose (FPG; > or =6.1 mmol/l), abnormal 2-h plasma glucose (2hP

80 inition of diabetes (fasting plasma glucose [FPG] > or = 126 mg/dl on two occasions, or a casual plas

81 sting hyperglycemia (fasting plasma glucose [FPG] 5.5-9.2 mmol/l, interquartile [IQ] range 6.6-7.4),

82 = 56 +/- 2.2 years, fasting plasma glucose [FPG] = 8.4 +/- 1.3 mmol/L, HbA(1c) = 7.5 +/- 0.54%) with

83 NA with formamidopyrimidine DNA glycosylase (FPG) to convert 8-oxo-7,8-dihydroguanine (8-oxoGua) to a

84 G) and formamido-pyrimidine-DNA glycosylase (FPG), 3'-5' exonucleases, and enzymes with template-inde

85 se in formamidopyrimidine DNA N-glycosylase (FPG)-sensitive cleavage sites in mitochondrial DNA, comp

86 g the failure of fatty partial liver grafts (FPG) remain unknown.

87 progression rates, a fast progression group (FPG) and slow progression group, as evidenced by differe

88 that significantly reduces levels of HbA1c, FPG, and CML, and improves periodontal therapy outcome i

89 For 1 mmol/L higher FPG, RRs in this age group were 1.18 (1.08-1.29) for IHD

90 h impaired FPG should, at minimum, have home FPG testing.

91 t patients are monitored for PTDM by 12-hour FPG levels drawn for clinic visits.

92 lasma glucose (2hPG; > or =7.8 mmol/l), IFG (FPG 6.1-6.9 mmol/l, 2hPG < or =7.8 mmol/l), and IGT (FPG

93 <110 mg/dl), impaired fasting glucose (IFG, FPG 110-125 mg/dl), and type 2 diabetes (FPG >126 mg/dl)

94 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 IFG-IGT

95 ollow-up; among subjects developing impaired FPG or 2hPG, 22% progressed to diabetes by FPG whereas 1

96 ll renal transplant recipients with impaired FPG should, at minimum, have home FPG testing.

97 incorporation was 25% in LPG but only 5% in FPG, and graft weight increased by 64% in LPG while rema

98 ) was inversely related with the increase in FPG concentration (r=-36, r=0.001), whereas DeltaC-pep[A

99 g) was associated with stepwise increases in FPG and insulin and reduced hepatic insulin sensitivity.

100 o dideoxynucleoside analogs and increases in FPG are related with HS progression.

101 d NADH dehydrogenase-3 decreased markedly in FPG, and these effects were blocked by N-(1-naphtyl)ethy

102 rosine adducts) increased more profoundly in FPG than in lean partial grafts (LPG).

103 d by 64% in LPG while remaining unchanged in FPG.

104 illary blood glucose [CapBG] >/=11.1 mmol/L, FPG >/=7.0 mmol/L, 2-hr plasma glucose >/=11.1 mmol/L, o

105 Likewise, FPG and CML levels were significantly reduced in the pro

106 and a known bifunctional glycosylase/lyase (FPG), the results of which were used in comparison with

107 ned free of insulin treatment and maintained FPG <126 mg/dl and HbA1c levels <6.5%.

108 At birth, maternal FPG during pregnancy was significantly associated with o

109 At 7 y, higher maternal FPG concentrations were significantly associated with in

110 with gestational diabetes mellitus, maternal FPG concentrations during pregnancy were significantly a

111 Mean FPG and diabetes prevalence in 2008 were also high in so

112 Mean FPG in 2008 was lowest in sub-Saharan Africa, east and s

113 Bayesian hierarchical model to estimate mean FPG and its uncertainty by age, country, and year, accou

114 a had the largest rise, and the highest mean FPG (6.09 mmol/L, 5.73-6.49 for men; 6.08 mmol/L, 5.72-6

115 We recorded almost no change in mean FPG in east and southeast Asia and central and eastern E

116 In 2008, global age-standardised mean FPG was 5.50 mmol/L (95% uncertainty interval 5.37-5.63)

117 ]); (3) diabetes diagnosed solely by the new FPG concentration criterion of 7.0 through 7.7 mmol/L (1

118 Among diabetic patients diagnosed by the new FPG criterion only, HbA1c levels were normal in 60.9% (5

119 glucose concentration (FPG) as nondiabetic (FPG <110 mg/dl), impaired fasting glucose (IFG, FPG 110-

120 Among subjects with normal FPG concentrations, HbA1c levels in the NHANES III (and

121 ticipants were categorized as normoglycemic (FPG <5.6 mmol/L), prediabetic (FPG 5.6-6.9 mmol/L), or d

122 On the basis of FPG before treatment, participants were categorized as n

123 The median concentration of FPG-sensitive sites, measured with the comet assay, was

124 The detection of FPG- and endo III-sensitive DNA lesions revealed the pre

125 Modifications of the dietary effects of FPG and FI before treatment were examined with linear mi

126 lycosylation but with moderate elevations of FPG concentrations (6.1-7.7 mmol/L [110-139 mg/dL]) shou

127 e synthase (iNOS) plays a role in failure of FPG.

128 This study confirms the inadequacy of FPG screening for NODAT in the first 6 weeks after trans

129 The slope of increase of FPG with age over 10 years was also greater in Alzheimer

130 The mean slope of FPG over 10 years in each case was also compared between

131 liver regeneration, and improved survival of FPG.

132 and 5.5-fold higher after transplantation of FPG than LPG.

133 suggested that the effect of the Q allele on FPG and HOMA-IR was stronger in those with a higher BMI

134 =126 mg/dL, prediabetes as A1C 5.7%-<6.5% or FPG 100-<126 mg/dL, and normal glucose as A1C <5.7% and

135 total diabetes (using the hemoglobin A1c or FPG definition) increased from 9.8% (95% CI, 8.9%-10.6%)

136 l of 126 mg/dL or greater (hemoglobin A1c or FPG definition) or (2) additionally including 2-hour pla

137 total diabetes (using the hemoglobin A1c or FPG definition) was 12.3% (95% CI, 10.8%-14.1%); among t

138 s diagnosed with diabetes using HbA1c and/or FPG diagnostic criteria.

139 diabetes (HbA1c 5.7-6.4% [39-46 mmol/mol] or FPG 5.6-6.9 mmol/L) at baseline.

140 Overnight FPG are inadequate for diagnosis of PTDM.

141 ormoglycemic (FPG <5.6 mmol/L), prediabetic (FPG 5.6-6.9 mmol/L), or diabetic (FPG >/=7.0 mmol/L).

142 ; and (4) diabetes diagnosed by the previous FPG concentration criterion of 7.8 mmol/L (140 mg/dL) or

143 All rats that received FPG died, whereas all those receiving LPG survived.

144 with SBP (r = 0.30 and 0.19, respectively), FPG (r = 0.25 and 0.22, respectively), triglycerides (r

145 with SBP (r = 0.22 and 0.22, respectively), FPG (r = 0.22 and 0.25, respectively), triglycerides (r

146 diposity are positively associated with SBP, FPG, and triglycerides and inversely associated with HDL

147 2 and the major allele of the rs1887922 SNP (FPG P < 0.001, mFPG P < 0.003, HbA(1c) P < 0.025).

148 gnoses were made based on prelunch or supper FPG >200 mg/dl.

149 We cross-tabulated FPG concentrations (<6.1 mmol/L [110 mg/dL], 6.1-6.9 mmo

150 e with GCK mutations as having diabetes than FPG >/=7 mmol/l (68% vs. 48%, p = 0.0009).

151 The FPG concentration decreased only in subjects with IFG fr

152 The FPG concentration remained unchanged (95 +/- 2 to 94 +/-

153 I has an intercalation motif observed in the FPG DNA glycosylase family of repair enzymes.

154 id not eliminate the severe phenotype in the FPG facial nucleus, suggesting that the FPG phenotype is

155 the FPG facial nucleus, suggesting that the FPG phenotype is the result of a more severe or accelera

156 isease-associated gene expression within the FPG facial motor nucleus confirmed the presence of a mor

157 sed by self-report, diabetes medication use, FPG >or=126 mg/dl, and/or plasma glucose >or=200 mg/dl a

158 Clinic visit FPG levels did not differ between PTDM and non-PTDM pati

159 moglobin) that contained individuals in whom FPG concentrations, 2-hour glucose concentrations using

160 0.013), 4% with HbA1c (P<0.001), and 0% with FPG (P<0.001; n=26).

161 c versus 20% with OGTT (P=0.600) and 2% with FPG (P=0.059; n=50), whereas, at 12 months, NODAT was fo

162 A1c versus 6% with OGTT (P=1.00) and 2% with FPG (P=0.618; n=51).

163 aC-pep[AUC]15-120 positively correlated with FPG concentration (r=0.29, r<0.05).

164 abetes should not be diagnosed in those with FPG concentrations less than 7.8 mmol/L (140 mg/dL) unle

165 The finding that women with FPG 110 to 125 mg/dl had similar CHD risk compared with

166 ol subjects (n = 11, age = 54 +/- 1.8 years, FPG = 4.8 +/- 0.2 mmol/L) using resting-state functional