ライフサイエンスコーパス: fasting insulin

1 nce interval, 1.03-1.14 per 1-SD increase in fasting insulin).

2 esterol, triglycerides, fasting glucose, and fasting insulin.

3 m Hg for systolic blood pressure; and 7% for fasting insulin.

4 sessment of insulin resistance (HOMA-IR) and fasting insulin.

5 er than measures such as HOMA, which reflect fasting insulin.

6 waist circumference, waist to hip ratio and fasting insulin.

7 ociations with HbA1c (0.03%, -0.01 to 0.08), fasting insulin (0.00%, -0.06 to 0.07), and BMI (0.11 kg

8 [95% CI -0.01, 0.01]; p = 1.00; n = 46,186); fasting insulin (0.01 pmol/l [95% CI -0.00, 0.01,]; p =

9 lly lower circulating adiponectin and higher fasting insulin (0.02 SD; 95% CI -0.07 to 0.11; N = 29,7

10 s9939609 A allele was associated with higher fasting insulin (0.039 SD [95% CI 0.013-0.064]; P = 0.00

11 than that for HOMA (0.310 vs. 0.163) and for fasting insulin (0.171), adjusted for age, sex, ethnicit

12 ws' milk intake = 0.00 mmol/l; -0.03, 0.03); fasting insulin (0.8%; -3.2, 5.1); ISI (0) (-0.9%; -5.1,

13 2 +/- 0.075), Hb A1c (-0.052 +/- 0.015), and fasting insulin (-0.119 +/- 0.036) (all P </= 0.02 for c

14 = -0.01, +0.04; n trials = 99), but lowered fasting insulin (-1.1 pmol/L; -1.7, -0.5; n = 90).

15 tly lowered HbA1c (-0.11%; -0.17, -0.05) and fasting insulin (-1.6 pmol/L; -2.8, -0.4).

16 age-, sex-, and ethnicity-adjusted levels of fasting insulin (11.3 micro U/ml), homeostasis model ass

17 ely, showed significant decreasing trends in fasting insulin (11.7, 10.3, and 8.8 micro U/ml; P = 0.0

18 ply by 0.0555]; 95% CI, -3.78 to -0.72), and fasting insulin (-2.75 muIU/mL [to convert to picomoles

19 ciations with fasting blood glucose (FG) and fasting insulin, 2-h postload glucose (PG), 2-h postload

20 d pressure, 2-hour glucose, fasting glucose, fasting insulin, 2-hour insulin, insulin sensitivity, C-

21 8 +/- 4.8 vs. 16.2 +/- 5.8 pg/mL; P = 0.01), fasting insulin (20.9 +/- 10.6 vs. 9.7 +/- 6.6 mU/mL; P

22 ol/L, respectively; P for trend = 0.02), and fasting insulin (205 and 199 pmol/L, respectively; P for

23 ely after treatment were found for levels of fasting insulin (-6.37 IU/L; P = .02), total cholesterol

24 ared with 2.8 ng/mL for placebo; P < 0.001), fasting insulin (-6.5 compared with +1.2 muU/mL for plac

25 ting glucose was 5.29 mmol/L (SD 0.66), mean fasting insulin 71.29 pmol/L (47.72), and mean HOMA2-IR

26 glucose (-0.07 mmol/l; 95% CI: -0.19, 0.05); fasting insulin (8.0%; -8.7, 27.6); ISI(0) (-6.1%; -11.3

27 ; 95% confidence interval (CI) = 0.12-0.24), fasting insulin (8.5%; 95% CI = 5.9-11.1), interleukin-6

28 iglycerides (-19.1%; P-trend < 0.001), lower fasting insulin (-9.1%; P-trend = 0.002), and lower syst

29 ith a 0.31-SD (95% CI 0.26-0.35) increase in fasting insulin, a 0.34-SD (0.30-0.38) decrease in insul

30 The outcomes were blood pressure; fasting insulin, adiponectin, glucose, and apolipoprotei

31 on molecule-1, leptin, hemoglobin A(1c), and fasting insulin (adjusted odds ratio and 95% confidence

32 scan for quantitative trait loci influencing fasting insulin among 1,505 European Americans and 1,616

33 al racial groups; that lower S(I) and higher fasting insulin among African Americans compared with Eu

34 fined grains were positively associated with fasting insulin among women (P for trend = 0.002).

35 Refined grains were associated with fasting insulin among women but not men.

36 and adiponectin in the NHS and HPFS and with fasting insulin and C-peptide levels in a nationally rep

37 Blood pressure and fasting insulin and cholesterol concentrations are highe

38 t may contain positional candidate genes for fasting insulin and fasting glucose (n = 1,604 subjects)

39 ught to gain insights into the regulation of fasting insulin and fasting glucose through the use of g

40 rs35929 modified the association of uMg with fasting insulin and fat mass in a general population.

41 ith smoking initiation, higher adiposity and fasting insulin and glucose but lower blood pressure and

42 Fasting insulin and glucose concentration were measured

43 i (QTLs) that contribute to the variation in fasting insulin and glucose concentrations are discrepan

44 ined with other endpoints (Matsuda index and fasting insulin and glucose concentrations).

45 Phylloquinone intake was not associated with fasting insulin and glucose concentrations, HOMA-IR, or

46 ith or without l-arginine, resulted in lower fasting insulin and glucose levels and enhanced rates of

47 have impaired glucose tolerance and elevated fasting insulin and glucose levels that are restored fol

48 nt levels, and a dose-dependent reduction of fasting insulin and glucose levels was observed.

49 s), percentage of body fat, waist-hip ratio, fasting insulin and glucose levels, and blood pressure.

50 Fasting insulin and glucose levels, weight, body composi

51 mass, left ventricular ejection fraction, or fasting insulin and glucose levels.

52 rcumference were measured regularly, as were fasting insulin and glucose levels.

53 Initiative (WHI) participants with available fasting insulin and glucose levels.

54 -analysis approach to test associations with fasting insulin and glucose on a genome-wide scale.

55 a prospective cohort study, body habitus and fasting insulin and glucose were measured at ages 9-10 a

56 ls of plasma lipids, C-reactive protein, and fasting insulin and glucose, among 8,773 adults in the N

57 (FM), systolic and diastolic blood pressure, fasting insulin and glucose, and homeostasis model asses

58 HFD increased fasting insulin and glucose, as well as glucose intolera

59 V risks included cholesterol, triglycerides, fasting insulin and glucose, body mass index (BMI), wais

60 m (ANS) dysfunction has been correlated with fasting insulin and glucose, independent of clinically d

61 n by demographic and anthropometric factors, fasting insulin and glucose.

62 ssment of insulin resistance (HOMA-IR) using fasting insulin and glucose.

63 res of glucose homeostasis: fasting glucose, fasting insulin and glycated hemoglobin (HbA1c) were stu

64 association was largely (79.9%) explained by fasting insulin and hemoglobin A(1c) levels; after furth

65 LC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1).

66 was significant genetic correlation between fasting insulin and HOMA-IR (rho(G) > 0.86, P < 0.05), a

67 not appreciably change the interactions for fasting insulin and HOMA-IR.

68 cose and HOMA-B and two loci associated with fasting insulin and HOMA-IR.

69 also associated with fasting plasma glucose, fasting insulin and HOMA-IR.

70 n this analysis, HCV(+) subjects had greater fasting insulin and homeostasis model assessment (HOMA)

71 etween maternal protein intake and offspring fasting insulin and homeostasis model assessment of insu

72 73x10(-11) and Pinteraction=2.48x10(-11) for fasting insulin and homeostasis model assessment of insu

73 At the end of the trial, fasting insulin and homeostasis model assessment of insu

74 ein cholesterol, fasting and 2-hour glucose, fasting insulin and homeostatic model assessment of insu

75 s with plasma markers of insulin resistance (fasting insulin and homeostatic model of insulin resista

76 ns of plasma leptin, resistin, fed-state and fasting insulin and increased expression of adipogenic t

77 ion studies informative for fasting glucose, fasting insulin and indices of beta-cell function (HOMA-

78 f a CpG site within ABCG1 is associated with fasting insulin and merits further evaluation as a novel

79 atively associated with percent body fat and fasting insulin and positively correlated with IS and me

80 gher R(2), P<0.05) in predicting measures of fasting insulin and systolic and diastolic blood pressur

81 sitivity index was lower (P = 0.02), and the fasting insulin and the oral-glucose-tolerance test insu

82 Fasting insulin and triglycerides were significantly hig

83 increased diabetes risk, fasting glucose, or fasting insulin and, for diabetes, showed a trend toward

84 conditions: no intervention (ctl), overnight fasting, insulin and glucose (6 mU/g, 1 mg/g) under isof

85 GGT is associated with fasting insulin (and HOMA) to the same extent in all wom

86 th fasting glucose and HbA1c and of ALT with fasting insulin (and homeostasis model assessment of ins

87 and SES were independently related to S(I), fasting insulin, and AIR(g) after adjusting for confound

88 ist-to-height ratio to risk factors (lipids, fasting insulin, and blood pressures).

89 had normalized glucose tolerance, decreased fasting insulin, and decreased adiposity.

90 .3-0.7]) adjusted for ethnicity, age, waist, fasting insulin, and early insulin release (DeltaI(0-30)

91 associated with higher plasma CRP, ferritin, fasting insulin, and Hb A1c and lower adiponectin after

92 gn were used in which fasting blood glucose, fasting insulin, and HbA1c were outcomes and antibody cl

93 centrations of fasting glucose, 2-h glucose, fasting insulin, and HbA1c; 46 368 non-cases; study cons

94 t for baseline levels of C-reactive protein, fasting insulin, and hemoglobin A(1c) or exclusion of ca

95 active protein (CRP), ferritin, adiponectin, fasting insulin, and hemoglobin A1c (Hb A1c).

96 ines (leptin, adiponectin), fasting glucose, fasting insulin, and HOMA-IR values were measured at bas

97 dified genetic effects on changes in weight, fasting insulin, and homeostasis model assessment of ins

98 and increased triglycerides, 2-hour glucose, fasting insulin, and homeostatic model assessment of ins

99 A significant decrease in body weight, fasting insulin, and IGF-1 levels were observed in LAR(-

100 lycemia, improved glucose tolerance, reduced fasting insulin, and improved alpha-cell function.

101 increased fasting plasma glucose (FPG), A1C, fasting insulin, and insulin resistance by homeostasis m

102 Fasting blood glucose, fasting insulin, and insulin tolerance were all preserve

103 d pressure, hemoglobin A1c, fasting glucose, fasting insulin, and lipids at 3 months.

104 e insulin sensitive, as evidenced by reduced fasting insulin, and lower blood glucoses in response to

105 colorectal cancer studies directly measured fasting insulin, and none evaluated free IGF-I, or endog

106 es in weight, the insulinogenic index (IGR), fasting insulin, and proinsulin were predictive of diabe

107 The mean change in weight, fasting insulin, and proinsulin, but not IGR, differed b

108 ived measures of insulin sensitivity (S(I)), fasting insulin, and the acute insulin response to gluco

109 This meta-analysis suggests that early fasting insulin ascertainment in the general population

110 sociated SNP, rs4722551 near MIR148A, with a fasting insulin-associated SNP, rs4865796 in ARL15 (Pint

111 ed the interaction of triglyceride SNPs with fasting insulin-associated SNPs, individually and collec

112 ificantly and positively associated with log fasting insulin at follow-up (beta = 0.003, 95% CI 0.000

113 six previously unknown loci associated with fasting insulin at P < 5 x 10(-8) in combined discovery

114 d 19 common genetic variants associated with fasting insulin-based measures of IR.

115 a = -0.0097, P = 0.006), insulin resistance (fasting insulin beta = -0.1467, P = 0.010; homeostasis m

116 e (beta +/- SE: -2.33 +/- 0.86%; P = 0.006), fasting insulin (beta +/- SE: -8.76 +/- 4.13%; P = 0.03)

117 he top loci associated with type 2 diabetes, fasting insulin, beta-cell function by homeostasis model

118 This was followed by an improvement of fasting insulin, blood glucose, body weight, and glucose

119 olesterol but also with lower triglycerides, fasting insulin, blood pressure, and incident diabetes i

120 Changes in fasting plasma glucose, fasting insulin, blood pressure, and total, LDL, and HDL

121 L cholesterol, fasting blood glucose, HbA1c, fasting insulin, bodyweight, waist-to-hip ratio, BMI, an

122 Fasting insulin, C-peptide, and triglyceride levels sign

123 For example fasting insulin changed by 0% per doubling of AMH (95%CI

124 LF = -0.44 +/- 0.19 mmol/L; P < 0.001), and fasting insulin concentration (PY = -1.76 +/- 1.01 mU/mL

125 g plasma glucose concentration 83 mg/dL, and fasting insulin concentration 37 pmol/L) were used.

126 Hypercarnitinemia in the presence of a fasting insulin concentration had no effect on either of

127 The fasting insulin concentration is considered a reasonable

128 A higher fasting insulin concentration or hyperinsulinemia was si

129 Loci influencing fasting insulin concentration showed association with li

130 African ADM having a lower S(I) and a higher fasting insulin concentration.

131 ol/L (95% CI: 0.035, 0.063-ln-pmol/L) higher fasting insulin concentration.

132 eatment; P = 0.004) and appeared to decrease fasting insulin concentrations (change: -2.2 muU/mL afte

133 ears of age were also associated with raised fasting insulin concentrations (P<0.001 for both).

134 ociated with both higher fasting glucose and fasting insulin concentrations after adjustment for pote

135 tions were positively associated with higher fasting insulin concentrations and HOMA-BCF even after a

136 at the participants in the upper one-half of fasting insulin concentrations averaged only 57% of the

137 Fasting insulin concentrations decreased by an average o

138 Fasting insulin concentrations did not mediate the effec

139 n of the highest with the lowest quantile of fasting insulin concentrations showed a pooled RR (95% C

140 who had been breastfed had marginally lower fasting insulin concentrations than did those who were f

141 At the highest doses of sirolimus, fasting insulin concentrations were high and did not inc

142 The mean (SD) fasting insulin concentrations were significantly (P = 0

143 mmarize the literature on the association of fasting insulin concentrations with risk of hypertension

144 onal adjustment for systolic blood pressure, fasting insulin concentrations, diabetes, and antihypert

145 ing time control experiments, with sustained fasting insulin concentrations, the arterial baroreflex-

146 ose and leucine kinetics were measured under fasting insulin conditions and during euglycemic hyperin

147 rol (HDL-C), triglycerides, fasting glucose, fasting insulin, CRP, PDFG-AB, and systolic and diastoli

148 Fasting insulin decreased (P = 0.03), and both fasting (

149 baseline with alternate-day fasting, whereas fasting insulin decreased 57 +/- 4% (P < 0.001).

150 es to the fatty acid burden that accompanies fasting, insulin deficiency, and overnutrition, response

151 The association of processed meat and fasting insulin did not reach statistical significance a

152 ifference 10.3, 95% CI 8.9 to 11.8 mmHg) and fasting insulin (% difference 145%, 95%CI 124 to 168%).

153 ess (% difference 6.0%, 95%CI 1.5 to 10.7%), fasting insulin (% difference 31%, 95%CI 22 to 40%), tri

154 ic women, i.e., in the highest fourth of the fasting insulin distribution, were similar to those obta

155 Secondary outcomes included fasting insulin, fasting plasma glucose, 2-hour plasma g

156 signed to shed light on the genetic basis of fasting insulin (FI) and IR in 927 non-diabetic African

157 of MARV with analysis of triglycerides (TG), fasting insulin (FI) and waist-to-hip ratio (WHR) in 4,7

158 trations of fasting plasma glucose (FPG) and fasting insulin (FI) as prognostic markers for successfu

159 loci that influence fasting glucose (FG) and fasting insulin (FI) levels, as identified by genome-wid

160 Fasting insulin for the entire group was significantly l

161 liver disease measures; and serum levels of fasting insulin, glucose, and cholesterol in C57BL/6 mal

162 me body weight as chow fed control mice, the fasting insulin, glucose, and hepatic triglyceride level

163 We measured fasting insulin, glucose, and lipid levels, erythrocyte

164 AMH, fasting insulin, glucose, HDLc, LDLc, triglycerides and

165 d measures of anthropometry, blood pressure, fasting insulin, glucose, lipids, and NAFLD by ultrasoun

166 ficantly interacted with the diabetes GRS on fasting insulin, glycated hemoglobin (HbA1c), the homeos

167 erol <40 mg/dl, blood pressure >130/80 mmHg, fasting insulin > or =100 pmol/liter, or impaired glucos

168 ng glucose (100-125 vs. <90 mg/dL), elevated fasting insulin (>15-20 and >20 vs. <10 muU/mL), and low

169 2-h glucose, A1C, BMI, waist circumference, fasting insulin, HDL cholesterol, triglycerides, and blo

170 ysteine, plasma markers of glycemic control (fasting insulin, hemoglobin A1c, C-peptide, and leptin),

171 We assessed the progress in fasting insulin, homeostasis model assessment of insulin

172 Insulin-related variables included fasting insulin, Homeostasis Model Assessment, C-peptide

173 in sensitivity phenotype associations (i.e., fasting insulin, homeostasis model assessment-insulin re

174 The decrease in fasting insulin, homeostatic model assessment of insulin

175 tomography scanning to measure VAT and serum fasting insulin, IGF-I, and IGFBP-3 measurements.

176 ated with 25.8% (95% CI: 1.0%, 58.4%) higher fasting insulin in adult life, 29.6% (5.1%, 58.4%) highe

177 sociated with higher IGF2BP2 levels and with fasting insulin in an independent genetic meta-analysis

178 cript levels were positively associated with fasting insulin in both the FHS and RS.

179 ected a quantitative trait locus influencing fasting insulin in female subjects (logarithm of odds [L

180 riants within Tpcn2 that are associated with fasting insulin in humans.

181 nteraction and conducted linkage analysis of fasting insulin in Hypertension Genetic Epidemiology Net

182 rongest linkage was found for the changes in fasting insulin in response to exercise training with a

183 nd LEPR K109R polymorphisms on the change in fasting insulin in whites (P = 0.010).

184 ociation with 30' Deltainsulin (OGTT 30' min fasting insulin) in an interaction with percentage of bo

185 t)) exhibited glucose intolerance, decreased fasting insulin, increased fasting glucagon levels, and

186 me spent sedentary predicts higher levels of fasting insulin independent of the amount of time spent

187 cerns were validated, including elevated non-fasting insulin (insulin resistance), and elevated angio

188 orrelations (range 0.32-0.52, P < 0.05) with fasting insulin, insulin 2 h after oral glucose challeng

189 The changes in fasting glucose, fasting insulin, insulin resistance (homeostasis model a

190 LF, but not VAT, was correlated with fasting insulin, insulin-stimulated glucose disposal, an

191 Upon fasting, insulin is lowered to remove ARF1 and kinesin f

192 nce (OR per 1 SD, 1.4; 95% CI, 1.0-2.0), and fasting insulin level (OR per 1 SD, 1.6; 95% CI, 1.2-2.1

193 ings suggest that 2 biomarkers of longevity (fasting insulin level and body temperature) are decrease

194 ne spillover (r = -0.47; P = 0.008), whereas fasting insulin level related to neuronal norepinephrine

195 igher genetically determined log-transformed fasting insulin level was associated with higher CHD ris

196 ndex were positively associated and baseline fasting insulin level was inversely associated with 5-ye

197 nt of insulin resistance (HOMA-IR) index, or fasting insulin level, within the lowest quartile (q1)]

198 was associated with significant increases in fasting insulin level.

199 mes stronger association in those with lower fasting insulin levels (<80 pmol/L: beta=-0.013, p=1.6x1

200 A 3-fold increase in serum fasting insulin levels (p < 0.002) and a 55% increase in

201 le rs16872779 (intronic) was associated with fasting insulin levels (p=0.0097).

202 h fasting glucose (R = 0.325, p = 0.001) and fasting insulin levels (rho = 0.217, p = 0.033).

203 f triglyceride-raising alleles had increased fasting insulin levels (SD 0.00 per weighted allele [95%

204 d with insulin resistance phenotypes (higher fasting insulin levels adjusted for BMI, lower HDL chole

205 glucose and 433 transcripts associated with fasting insulin levels after adjusting for age, sex, tec

206 Patients with heart failure (HF) have higher fasting insulin levels and a higher prevalence of insuli

207 cose utilization, with a concomitant rise in fasting insulin levels and HOMA1-%B scores.

208 Fasting insulin levels and homeostasis model assessment

209 LF/P or LF/C rats (P <0.001) as measured by fasting insulin levels and homeostasis model assessment

210 h of pancreatic islets with mildly increased fasting insulin levels and hypoglycemia.

211 The association between fasting insulin levels and incident HF was similar for H

212 nucleotide polymorphisms and haplotypes with fasting insulin levels and insulin secretion in the MACA

213 ciation of the T at-risk allele with reduced fasting insulin levels and insulin secretion index (home

214 of rs6759676 was also associated with lower fasting insulin levels and lower HOMA insulin resistance

215 7BL/6J Slc30a8 knockout (KO) mice had normal fasting insulin levels and no change in glucose-stimulat

216 locity at baseline were associated both with fasting insulin levels and with HF; however, additional

217 -53% relative to body weight), and 60% lower fasting insulin levels compared with littermate controls

218 Median fasting insulin levels decreased with pioglitazone and i

219 , waist circumference (P = 0.03), and higher fasting insulin levels in girls (P = 0.02).

220 type 2 diabetes or raise fasting glucose or fasting insulin levels in nondiabetic individuals.

221 tly associated with significantly lower mean fasting insulin levels throughout the range of observed

222 Fasting insulin levels were determined.

223 Fasting insulin levels were not associated with risk of

224 Fasting insulin levels were positively associated with t

225 At 6 months, fasting insulin levels were significantly reduced from b

226 mosome 19 T2dm2 quantitative trait locus for fasting insulin levels, acting via impaired insulin secr

227 se production (EGP), despite an elevation in fasting insulin levels, and impaired suppression of EGP

228 Mice fed a HFD displayed increased fasting insulin levels, hepatosteatosis and major change

229 Thus, SINKO mice had lower fasting insulin levels, improved glucose tolerance and i

230 sulin sensitivity, associated with decreased fasting insulin levels, increased recruitment of the glu

231 between puberty timing and body mass index, fasting insulin levels, lipid levels, type 2 diabetes an

232 0a8 KO mice had reduced ( approximately 20%) fasting insulin levels, though this was not associated w

233 etes mellitus-2 locus (T2dm2), which affects fasting insulin levels, to distal chromosome 19 in a lep

234 ance, which almost perfectly correlated with fasting insulin levels, was also not associated with ris

235 4+ T-cell numbers correlated positively with fasting insulin levels.

236 iets improved lipid-related risk factors and fasting insulin levels.

237 dual component of the metabolic syndrome and fasting insulin levels.

238 b mice from beta-cell apoptosis and improves fasting insulin levels.

239 hysical activity, caloric intake, and BMI to fasting insulin levels.

240 n normal blood glucose levels but have lower fasting insulin levels.

241 /- 0.33; DM: -0.46 +/- 0.24; P = 0.001), and fasting insulin (LM: -2.01 +/- 1.10 mIU/mL; DM: -1.16 +/

242 No effects were seen on fasting insulin<100 pmol/L; above this, study numbers we

243 Metabolic health (e.g., HOMA-IR or fasting insulin) may be more biologically relevant and m

244 patients with type 2 diabetes, a decrease in fasting insulin (MD -7 microU/ml, 95% CI -11.5, -2.5) wa

245 : -7.6 +/- 2.1 kg; P = 0.015, time x group), fasting insulin (mean +/- SD: water: -2.84 +/- 0.77 mU/L

246 relative risk of incident HF associated with fasting insulin measured at study entry.

247 of 609 whites and 339 blacks who had BMI and fasting insulin measured twice in childhood (mean age =

248 Type I had the highest values of fasting insulin (median = 12.98 mU/mL) and HOMA IR value

249 both sexes, 5alphaR activity correlated with fasting insulin (men R = 0.53, P = 0.003; women R = 0.33

250 In striking contrast, HOMA-IR ([fasting insulin (muU/mL) x fasting glucose (mmol)]/22.5)

251 d hepatic insulin resistance as reflected by fasting insulin occur in the early stages of insulin res

252 y meaningful differences in fasting glucose, fasting insulin, or measures of insulin resistance despi

253 g glucose, 2-h glucose, glycated hemoglobin, fasting insulin, or thigh intramuscular fat.

254 ndependently related to S(I) (P < 0.001) and fasting insulin (P < 0.01), with individuals having grea

255 sulin sensitivity (P = 0.0005 to P = 0.023), fasting insulin (P = 0.022 to P = 0.033), triglycerides

256 RS was associated with a greater decrease in fasting insulin (P = 0.04), HbA1c (P = 0.0001), and HOMA

257 els of fasting glucose (P = 7.70 x 10-7) and fasting insulin (P = 4.79 x 10-6), but these association

258 ed with 2-h glucose (P for trend = 0.04) and fasting insulin (P for trend = 0.004), inversely associa

259 reater waist circumference (both P<0.05) and fasting insulin (P<0.01) and lower insulin sensitivity (

260 ortion of associations with CRP, Hb A1c, and fasting insulin (P-contribution </= 0.02 for all) but no

261 ositively associated with VF (P=3.0x10(-7)), fasting insulin (P=5.4x10(-32)), and triacylglycerols (P

262 rted not usually having breakfast had higher fasting insulin (percent difference 26.4%, 95% CI 16.6%-

263 One of these associations, fasting insulin/phosphofructokinase (PFKM), overlaps wit

264 0.01 to -0.12; P=0.01) lower log-transformed fasting insulin (pmol/L) and 21% lower odds (95% confide

265 ysiological significance of the reduction in fasting insulin produced by dietary methionine restricti

266 Adjustment for weight, fasting insulin, proinsulin, and other metabolic factors

267 AST and ALT were positively correlated with fasting insulin (r = 0.22 and r = 0.35, respectively), w

268 intile, fasting triglyceride correlated with fasting insulin (r = 0.59, P < 0.001) and with the fasti

269 Individuals carrying >/=17 fasting insulin-raising alleles (5.5% population) were s

270 gy compared with >12.5% of energy) had lower fasting insulin (ratio of geometric means: 0.82; 95% CI:

271 g insulin (r = 0.59, P < 0.001) and with the fasting insulin resistance index (r = 0.49, P < 0.009),

272 nsitivity was determined on the basis of the fasting insulin resistance index and with an oral-glucos

273 Waist-to-hip ratio and the fasting insulin resistance index were significantly grea

274 tradiol to sex hormone-binding globulin, the fasting insulin resistance index, and C-peptide and lept

275 gion close to the leptin locus was linked to fasting insulin response to exercise training in nondiab

276 trol of brain activity during deep sleep and fasting insulin secretion rate.

277 und significant heritability for measures of fasting insulin sensitivity and beta-cell function, for

278 independent of baseline age, sex, fat mass, fasting insulin, smoking status, and follow-up time.

279 s model assessment of insulin resistance and fasting insulin) through a systematic review and meta-an

280 Similarly, using fasting insulin to define metabolic health, metabolicall

281 d pressure (SBP), body mass index (BMI), and fasting insulin to LV mass and geometry.

282 here was significant evidence for linkage of fasting insulin to the short arm of chromosome 17 (logar

283 justment for age, sex, BMI, fasting glucose, fasting insulin, total triglycerides, and HDL cholestero

284 onatal 25(OH)D(3) was associated with higher fasting insulin, triglyceride, and cholesterol (in women

285 However, further adjustment for fasting insulin, triglyceride, and cholesterol levels at

286 d renal function, adjustments controlled for fasting insulin, triglyceride, and cholesterol levels.

287 nsortia data were used for metabolic traits (fasting insulin, triglyceride, total cholesterol, low-de

288 Body weight, food intake, adiposity index, fasting insulin, triglycerides and cholesterol levels we

289 sed to determine clustering of risk factors (fasting insulin, triglycerides, HDL-C, and systolic bloo

290 both) and inversely with insulin resistance (fasting insulin unadjusted, P < 0.001 for both; adjusted

291 Each 50-pmol/L increment in fasting insulin was associated with a 25% increase in ri

292 correlation between S(I) and either HOMA or fasting insulin was only approximately 50% accounted for

293 Fasting insulin was positively associated with adverse e

294 Fasting insulin was significantly higher after the dairy

295 (fasting nonesterified fatty acids [NEFAs] x fasting insulin) was calculated at baseline and after 16

296 To explore sex-specific genetic effects on fasting insulin, we tested for genotype-by-sex interacti

297 SBP, triglycerides, and fasting insulin were significantly higher and HDL-C sign

298 protein cholesterol, triglycerides, glucose, fasting insulin) were measured with the use of standard

299 higher GRS might have a greater reduction in fasting insulin when consuming a high-protein diet (P =

300 dipose DI was calculated as ATIS: (1/GlyRa x fasting insulin) x first-phase insulin secretion.