ライフサイエンスコーパス: HOMA-IR

1 HOMA-IR (p < 0.0001), WHR (p < 0.0001), and the presence

2 HOMA-IR did not mediate the association between ox-LDL a

3 HOMA-IR was analyzed both as linear and categorical (med

4 HOMA-IR was computed as fasting insulin (mIU/L) x fastin

5 HOMA-IR was not associated with HCV markers in unadjuste

6 had greater decreases in insulin (P=0.009), HOMA-IR (P=0.015), and weight loss (P=0.018) than those

7 pared with 8.0 (7.2, 8.9) muU/mL; P = 0.02], HOMA-IR by 15% [2.0 (1.8, 2.3) compared with 1.7 (1.6, 2

8 ed with +1.2 muU/mL for placebo; P = 0.026), HOMA-IR (-1.363 compared with +0.27 for placebo; P = 0.0

9 A HOMA-IR value greater than 2.5 was arbitrarily considere

10 associations between early growth and adult HOMA-IR in linear regression models and used a nonparame

11 tnatal weight velocity (0-4 months) on adult HOMA-IR, although indirect effects through BMI and waist

12 sex was observed such that, in women alone, HOMA-IR was significantly lower after the red meat diet

13 /e'-PICP, IL-18 (both beta=0.18, P<0.01) and HOMA IR (beta=0.16, P<0.04).

14 f fasting insulin (median = 12.98 mU/mL) and HOMA IR values (significant difference among the four ph

15 +/- 0.6 mg/dL), Hb A1c (-0.02 +/- 0.0%), and HOMA-IR (-0.04 +/- 0.0) after adjustment for all covaria

16 insulin (P = 0.04), HbA1c (P = 0.0001), and HOMA-IR (P = 0.02), and a lesser increase in HOMA-B (P =

17 95% CI: -21.41, -5.53 pmol/L; P < 0.001) and HOMA-IR (WMD: -0.57 units; 95% CI: -0.76, -0.37 units; P

18 nsulin (19.35 vs. 8.80 mIU/L, p < 0.001) and HOMA-IR index (6.48 to 2.52, p < 0.001) were reduced aft

19 beta +/- SE: -8.76 +/- 4.13%; P = 0.03), and HOMA-IR (beta +/- SE: -10.52 +/- 4.39%; P = 0.01) in par

20 ncentrations (P for interaction = 0.032) and HOMA-IR (P for interaction = 0.011) and reversed associa

21 duction in HbA1c (r(2) = 0.42; p = 0.04) and HOMA-IR (r(2) = 0.54; p = 0.02).

22 etween CAP and insulin levels (r = 0.54) and HOMA-IR (r = 0.54) was also found.

23 ociated with insulin (P = 1.83 x 10(-7)) and HOMA-IR (P = 1.60 x 10(-9)).

24 lin (beta = -2.01; 95% CI: -3.24, -0.78) and HOMA-IR (beta = -0.39; -0.64, -0.14) values at the end o

25 tion in the association between the ADII and HOMA-IR suggests that inflammation might be one of the p

26 assessed the associations between HOMA-B and HOMA-IR and DM by haplogroup.

27 out HIV), PLWH had higher initial HOMA-B and HOMA-IR than people living without HIV.

28 HOMA-B and HOMA-IR were calculated using FG and FI data.

29 etween cumulative soft drink consumption and HOMA-IR change, we performed robust linear regression mo

30 oted between adipose tissue EPA plus DHA and HOMA-IR.

31 en cumulative consumption of soft drinks and HOMA-IR change after 7 y of follow-up in participants (n

32 sure, BMI, WHR, body weight, FAT%, FINS, and HOMA-IR in T2DM patients decreased significantly, wherea

33 ad the lowest QUICKI and the highest FSI and HOMA-IR values for all age-sex groups.

34 L- and total cholesterol, insulin, HbA1c and HOMA-IR (p < 0.005, 0.01, < 0.001, < 0.005, 0.03 and 0.0

35 telets, total cholesterol, hypertension, and HOMA-IR, but not ethnicity, were significantly associate

36 s and smaller decreases in serum insulin and HOMA-IR (all P </= 0.02 in an additive pattern), whereas

37 gnificantly greater increases in insulin and HOMA-IR (P = .008 and P = .004, respectively).

38 e top two signals replicated for insulin and HOMA-IR (P = 5.75 x 10(-3) and P = 3.35 x 10(-2), respec

39 led to a greater improvement of insulin and HOMA-IR (P for genotype-time interaction </=0.009) in pa

40 te genotype effect on changes in insulin and HOMA-IR (P</=0.05) was observed in participants assigned

41 were more evident on changes in insulin and HOMA-IR (P-interaction < 0.008).

42 nts in triglycerides (p = 0.01), insulin and HOMA-IR (p-values < 0.05).

43 OMA-IR improved IR, with reduced insulin and HOMA-IR concentrations after consumption of the HMUFA an

44 he genotype effect on changes in insulin and HOMA-IR remained significant in the highest-carbohydrate

45 became null for changes in serum insulin and HOMA-IR resulting from weight regain.

46 te genotype effect on changes in insulin and HOMA-IR was observed in the low-fat diet group (P=0.02 a

47 ing plasma levels of glucose and insulin and HOMA-IR, and poorer cognitive scores, together with wide

48 fasting plasma glucose, fasting insulin and HOMA-IR.

49 nge the interactions for fasting insulin and HOMA-IR.

50 unreported promising effects on insulin and HOMA-IR.

51 ctin), fasting glucose, fasting insulin, and HOMA-IR values were measured at baseline and at 2 follow

52 sterol, triglycerides, glucose, insulin, and HOMA-IR, independent of simple anthropometrics.

53 h-OGTT), HbA1c, triglyceride (TG) levels and HOMA-IR and positively with free fatty acid (FFA) and HD

54 rease in serum TNF-alpha and IL-6 levels and HOMA-IR scores in individuals with obesity and with a de

55 fasting and post-prandial glucose levels and HOMA-IR.

56 iated with fasting plasma insulin levels and HOMA-IR.

57 glycemia, post-prandial glucose levels, and HOMA-IR in models that adjusted for age, sex, race, and

58 Associations between metabolites and HOMA-IR were assessed using elastic net regression analy

59 Relations between FA patterns and HOMA-IR were analyzed in a sample of 922 participants wi

60 s inverse association between child PFAS and HOMA-IR was more pronounced in females [e.g., PFOA: -15.

61 tration estimated by land use regression and HOMA-IR, glucose, insulin, HbA1c, leptin, and high-sensi

62 orted improved TC, HDL cholesterol, SBP, and HOMA-IR.

63 on of therapy, hepatitis C virus status, and HOMA-IR index); the adjusted effect was -0.04 (95% confi

64 ulin Sensitivity Oral Glucose Tolerance, and HOMA-IR were high, and did not improve after RDN.

65 relationship between these two variants and HOMA-IR in the Atherosclerosis Risk in Communities (ARIC

66 hort, Hispanic ethnicity, male sex, VAT, and HOMA-IR were independently associated with greater LFF.

67 stimated using homeostasis model assessment (HOMA-IR), by HCV status.

68 ed by a higher homeostasis model assessment (HOMA-IR).

69 differed significantly according to average HOMA-IR values when lagged 6-18 h for PM2.5, 15-19 h for

70 t-hip-ratio (WHR), glucose, insulin, HOMA-B, HOMA-IR, and HbA1c.

71 We compared HOMA-B, HOMA-IR, and incident DM by haplogroups and assessed the

72 Baseline HOMA-IR also predicted resolution with those in the top

73 Baseline HOMA-IR was associated with SVR in univariate analysis,

74 e evaluated the association between baseline HOMA-IR and pretreatment factors on sustained virologic

75 ts with prior PR treatment failure, baseline HOMA-IR correlated with SVR in univariate but not multiv

76 6 (36%), and 165 (29%) patients had baseline HOMA-IR <2, 2 to <4, and >/= 4, respectively.

77 2 patients were randomized; 578 had baseline HOMA-IR and other prognostic data and were included in t

78 s stage were associated with higher baseline HOMA-IR.

79 Median baseline HOMA-IR was 2.6 (interquartile range [IQR] 1.7-4.3); 207

80 ored the prognostic significance of baseline HOMA-IR alone and adjusted for other pretreatment factor

81 y examined associations between the baseline HOMA-IR-related multimetabolite model and T2D incidence

82 L pattern was positively related to baseline HOMA-IR [adjusted geometric means (95% CIs) for quartile

83 There were strong correlation between HOMA-IR and visceral fat mass (r = 0.570, 95% confidence

84 e curve (AUC) for the discrimination between HOMA-IR extreme categories was 0.82 (95% CI: 0.74-0.90),

85 BMI, HOMA-IR, and SPISE were estimated; HOMA-IR values >= 2.6

86 to BMI and insulin resistance as defined by HOMA-IR values >/=2.5 and the presence of metabolic synd

87 lin sensitivity at the liver (as measured by HOMA-IR), which is contrary to what others have reported

88 n the left medial temporal lobe predicted by HOMA-IR was significantly related to worse performance o

89 In conclusion, HOMA-IR is of limited utility for detecting diet-induced

90 In striking contrast, HOMA-IR ([fasting insulin (muU/mL) x fasting glucose (mm

91 p showed no improvement in glycemic control (HOMA-IR mean change: -0.26; 95% CI: -0.64, 0.13).

92 provements in TC, HDL cholesterol, SBP, DBP, HOMA-IR, and acute/chronic FMD remained significant.

93 peanuts or tree nuts significantly decreased HOMA-IR and fasting insulin; there was no effect of nut

94 BMI, HOMA-IR, and SPISE were estimated; HOMA-IR values >= 2.6 were considered insulin resistance

95 the risk of NASH was modified by ethnicity: HOMA-IR was not a significant risk factor for NASH among

96 atios for insulin, 1.06 (CI, 0.98-1.16); for HOMA-IR, 1.06 (CI, 0.98-1.15); for TG/HDL-C, 1.11 (CI, 0

97 notably improved the predictive ability for HOMA-IR beyond classical risk factors and significantly

98 capacity was attenuated after adjusting for HOMA-IR.

99 er site in the same gene was significant for HOMA-IR and of borderline significance for insulin (P =

100 Metabolic health (e.g., HOMA-IR or fasting insulin) may be more biologically rel

101 e, insulin, C-reactive protein, and ghrelin, HOMA-IR, and lipid metabolism did not differ between tre

102 diabetes, plasma adiponectin, blood glucose, HOMA-IR and body mass index (BMI) in African Americans.

103 ed in the study (1287 visits), 323 (46%) had HOMA-IR > 2.77 for at least 1 follow-up visit and 319 (4

104 ctive of frequency) were less likely to have HOMA-IR > 2.77 (odds ratio [95% confidence interval], 0.

105 with age, BMI, waist/hip ratio, FBG, HbA1C, HOMA-IR and TG in the non-diabetic subjects.

106 High HOMA-IR was associated with a greater hazard of diabetes

107 timetabolite score (model 3) predicting high HOMA-IR (median value or higher) or HOMA-IR (continuous)

108 Higher HOMA-IR predicted hypermetabolism in MCI-progressors and

109 Higher HOMA-IR was associated with lower global glucose metabol

110 risk ratio 40.5/4.8, 8.4, p < 0/0001),higher HOMA-IR (3.7 vs. 1.9, p < 0.0001) and high triglycerides

111 This resulted in a higher HOMA-IR after the HDD (P = 0.027).

112 For AD, higher HOMA-IR predicted lower FDG in all ROIs.

113 14-3.48 P = 0.0145, respectively) and higher HOMA-IR (OR = 1.78, 95% CI:1.02-3.13, P = 0.041).

114 ssociated with excess body weight and higher HOMA-IR, especially in the presence of lower concentrati

115 erence was offset after adjusting for higher HOMA-IR at baseline among the former.

116 Higher likelihood of prediabetes, higher HOMA-IR, and lower Matsuda index were associated with lo

117 For MCI-progressors, higher HOMA-IR predicted higher FDG in the MTL and hippocampus.

118 CC carriers had a significantly higher HOMA-IR only when SFA:carbohydrate intake was high (P =

119 matter of <10 mum was associated with higher HOMA-IR (15.6% [95% CI 4.0; 28.6]) and insulin (14.5% [3

120 pendently and jointly associated with higher HOMA-IR in both white and black women, whereas a similar

121 lin-resistant MetS subjects with the highest HOMA-IR improved IR, with reduced insulin and HOMA-IR co

122 -3%,+2%) p = 0.70, with identical results if HOMA-IR was used.

123 Vitamin D3 at 3750 IU/d did not improve HOMA-IR compared with the Institute of Medicine Recommen

124 The surgery group had improved HOMA-IR (-4.6 vs +1.6; P = 0.0004) and higher diabetes r

125 bling in insulin of 1.21 (CI, 1.12-1.31), in HOMA-IR of 1.19 (CI, 1.11-1.28), in TG/HDL-C of 1.35 (CI

126 l analysis over 48 weeks showed no change in HOMA-IR, lipid or adipokine levels.

127 nges in soft drink consumption and change in HOMA-IR.

128 and 2.77% (95% CI, -4.36, -1.77) decline in HOMA-IR and insulin respectively, and a 2.55% (95% CI, 0

129 changes in ucOC were linked to a decrease in HOMA-IR (beta coefficient: -0.31; 95% CI: -0.60, 0.03; P

130 36 animals showed an artifactual decrease in HOMA-IR (i.e., increased sensitivity).

131 06, 80-mg arm), there were no differences in HOMA-IR (estimated effect, 0.007; SE, 0.106) at 24 weeks

132 onsumption is associated with an increase in HOMA-IR, despite known risk factors.

133 The variance in HOMA-IR explained by the combination of metabolites and

134 ther secondary metabolic outcomes, including HOMA-IR (mean difference 0.2, 95% CI -0.9 to 0.9, p = 0.

135 odel assessment of insulin resistance index (HOMA IR; beta=-0.20, P<0.002); and for E/e'-PICP, IL-18

136 s model assessment insulin resistance index (HOMA-IR), and concentrations of glucose, triglycerides,

137 Although insulin, HOMA-IR, and TG/HDL-C remained associated with increased

138 r parameters, such as glucose, BMI, insulin, HOMA-IR and lipid profile, were also investigated.

139 cin and changes in fasting glucose, insulin, HOMA-IR, and HOMA-BCF.

140 higher glycated hemoglobin (HbA1c), insulin, HOMA-IR, triglycerides, liver fat, and adiposity and wit

141 s taking metformin had lower HbA1c, insulin, HOMA-IR, and tissue plasminogen activator compared with

142 ostic value of adding fasting serum insulin, HOMA-IR (homeostasis model assessment-insulin resistance

143 f either miRNA-93 or miRNA-223 with insulin, HOMA-IR, HOMA-beta or testosterone levels.

144 Median homeostasis model assessment of IR (HOMA-IR) was 3.3 (IQR, 1.7-5.3).

145 The homeostasis model assessment of IR (HOMA-IR) was used to measure IR.

146 ollowing were measured in the offspring: IR (HOMA-IR index); TNF-alpha and NF-kappaBp65 content in th

147 association with variant rs7627128 and lower HOMA-IR among men with minor allele A in the fully adjus

148 en with higher PFAS concentrations had lower HOMA-IR [e.g., -10.1% (95% CI: -17.3, -2.3) per interqua

149 rcaloric feeding despite significantly lower HOMA-IR indexes.

150 0.99; P = 0.04) and a tendency toward lower HOMA-IR (ratio of geometric means: 0.82; 95% CI: 0.66, 1

151 WDSW + saroglitazar had lower weight, lower HOMA-IR, triglycerides, total cholesterol, and ALT.

152 25.2 +/- 2.7 vs. 26 +/- 2.7), and with lower HOMA-IR (1.4 vs. 1.7) (P .70.001).

153 In contrast, subjects with lower HOMA-IR showed reduced body mass index and waist circumf

154 Median HOMA-IR increased from 1.5 at baseline to 2.0 at follow-

155 Median HOMA-IR indexes did not change compared with baseline co

156 quartile of BMI, subjects with above-median HOMA-IR, above-median WHR, or IFG had a higher LV mass-t

157 MetS subjects with a low to medium HOMA-IR exhibited reduced blood pressure, triglyceride,

158 - 17.9 mg/dL; insulin, -0.7 +/- 5.1 muIU/mL; HOMA-IR, -0.2 +/- 1.9; and QUICKI, 0.004 +/- 0.019 (all

159 tance was assessed by the homeostasis model (HOMA-IR) and circulating metabolites quantified by high-

160 the IR as measured by the homeostasis model (HOMA-IR).

161 subset of people with obesity have a normal HOMA-IR and no metabolic syndrome components.

162 The ability of HOMA-IR to detect diet-induced resistance was particular

163 We tested the ability of HOMA-IR to detect high-fat diet-induced insulin resistan

164 on analysis tested the statistical effect of HOMA-IR on global glucose metabolism.

165 The effect of HOMA-IR on the risk of NASH was modified by ethnicity: H

166 tabolites discriminating between extremes of HOMA-IR and able to predict HOMA-IR with high accuracy.

167 of 30 metabolites discriminating extremes of HOMA-IR were consistently selected.

168 The impact of HOMA-IR on incident DM was less significant in those wit

169 The proportions via the mediation of HOMA-IR were 29.0% (95% CI: 10.3%-55.5%), 35.0% (95% CI:

170 I 1.72-1.95) per unit increase in Z score of HOMA-IR and 2.03 (1.86-2.21) per unit decrease in Z scor

171 The intervention had no effect on HOMA-IR (adjusted geometric mean ratio [95%CI] 0.96 [0.8

172 Intensive treatment had no effect on HOMA-IR (adjusted geometric mean ratio, 0.96 [95% confid

173 ee nuts or peanuts had a favorable effect on HOMA-IR (WMD: -0.23; 95% CI: -0.40, -0.06; I2 = 51.7%) a

174 Effects on HOMA-IR and FMD remained stable to sensitivity analyses.

175 The influence of pancreatic function on HOMA-IR accuracy was assessed using the acute insulin re

176 not associated with leptin, adiponectin, or HOMA-IR in offspring.

177 ciation was observed with BMI, FBG, HbA1C or HOMA-IR in T2D subjects.

178 ing high HOMA-IR (median value or higher) or HOMA-IR (continuous) at baseline were 2.00 (95% CI: 1.58

179 , body fat-BF and waist circumference-WC) or HOMA-IR as dependent variables and the degree of PBMC L1

180 tan was demonstrated on the primary outcome (HOMA-IR), but there were marginal improvements with some

181 In T2DM patients, HOMA-IR was inversely correlated with functional connect

182 ncluding glucose, HbA1c, insulin, C-peptide, HOMA-IR, triglycerides, and blood pressure.

183 ween extremes of HOMA-IR and able to predict HOMA-IR with high accuracy.

184 ity from 0 to 24 months positively predicted HOMA-IR among males only, while indirect effects were si

185 st circumference, which positively predicted HOMA-IR.

186 er concentrations of 25(OH)D and higher PTH, HOMA-IR, HOMA-B, hs-CRP, and eGFR than white women (all

187 equivalent energy amount of glucose reduced HOMA-IR (MD: -0.36; 95% CI: -0.71, -0.02; SUCRAglucose:

188 similar efficacy as comparators in reducing HOMA-IR (WMD: 0.05, 95% CI: -0.49 to 0.59) and increasin

189 atic model assessment of insulin resistance (HOMA-IR%) were higher in the old ( approximately 50-85%,

190 sis model assessment for insulin resistance (HOMA-IR) (-2.4%; -4.6, -0.3; n = 30).

191 asis model assessment of insulin resistance (HOMA-IR) (MD: 0.13; 95% CI: -0.07, 0.34; P = 0.21), or g

192 asis model assessment of insulin resistance (HOMA-IR) (P = 0.028, P = 0.017, and P = 0.026, respectiv

193 atic model assessment of insulin resistance (HOMA-IR) [betaPFOS=0.39; 95% confidence interval (CI): 0

194 ht, fasting glucose, and insulin resistance (HOMA-IR) across genotypes by the low-fat and high-fat di

195 asis model assessment of insulin resistance (HOMA-IR) after adjustment for the confounders (all P for

196 asis model assessment of insulin resistance (HOMA-IR) among 837 nondiabetic participants in the Genet

197 asis model assessment of insulin resistance (HOMA-IR) and beta-cell function (HOMA-B).

198 in homeostatic model of insulin resistance (HOMA-IR) and diabetes remission.

199 atic model assessment of insulin resistance (HOMA-IR) and HDL, and pulmonary function were quantified

200 l assessment estimate of insulin resistance (HOMA-IR) and liver fibrosis defined using the aspartate

201 tic model assessment for insulin resistance (HOMA-IR) and Matsuda ISI.

202 atic model assessment of insulin resistance (HOMA-IR) and secondary outcomes (including blood pressur

203 asis model assessment of insulin resistance (HOMA-IR) and weight loss by genotypes.

204 asis model assessment of insulin resistance (HOMA-IR) at 2 y in white Americans (P-interaction = 0.02

205 asis model assessment of insulin resistance (HOMA-IR) at 24 weeks.

206 asis model assessment of insulin resistance (HOMA-IR) at the beginning and end of each period.

207 asis model assessment of insulin resistance (HOMA-IR) improved significantly after bariatric surgery.

208 asis model assessment of insulin resistance (HOMA-IR) in a subset of adult participants (n= 716; mean

209 atic model assessment of insulin resistance (HOMA-IR) in mid-childhood.

210 atic model assessment of insulin resistance (HOMA-IR) in observational studies.

211 asis model of assessment-insulin resistance (HOMA-IR) index, cognitive performance on the MATRICS Con

212 asis model assessment of insulin resistance (HOMA-IR) index, or fasting insulin level, within the low

213 asis model assessment of insulin resistance (HOMA-IR) index.

214 atic model assessment of insulin resistance (HOMA-IR) index] and fasting and postprandial glucose, la

215 ostasis model assessment insulin resistance (HOMA-IR) levels.

216 asis model assessment of insulin resistance (HOMA-IR) mean change: -0.92; 95% CI: -1.17, -0.67)].

217 asis model assessment of insulin resistance (HOMA-IR) measures, and quantitative insulin sensitivity

218 model assessment of the insulin resistance (HOMA-IR) score was calculated before and 3 months after

219 the homeostasis model of insulin resistance (HOMA-IR) through the use of elastic net regression analy

220 asis model assessment of insulin resistance (HOMA-IR) using the DerSimonian and Laird random-effects

221 asis model assessment of insulin resistance (HOMA-IR) values were significantly lower and liver enzym

222 del assessment index for insulin resistance (HOMA-IR) was calculated (n = 1,543).

223 asis model assessment of insulin resistance (HOMA-IR) was calculated at baseline and at the 2-y follo

224 asis model assessment of insulin resistance (HOMA-IR) were assessed through multivariable linear regr

225 ostasis model assessment-insulin resistance (HOMA-IR) were primary and secondary outcomes, respective

226 asis model assessment of insulin resistance (HOMA-IR) were randomly assigned to 4 diets: an HSFA diet

227 asis model assessment of insulin resistance (HOMA-IR) were significantly associated with NASH.

228 associated with BMI and insulin resistance (HOMA-IR) while positively associated with the expression

229 del assessment-estimated insulin resistance (HOMA-IR), a marker for insulin resistance, has been asso

230 t, homoeostatic model of insulin resistance (HOMA-IR), akathisia, and sedation.

231 atic model assessment of insulin resistance (HOMA-IR), alkaline phosphatase, body mass index, waist c

232 ty, homeostasis model of insulin resistance (HOMA-IR), and duration of follow-up on effect estimates

233 atic model assessment of insulin resistance (HOMA-IR), and secondary outcomes (including blood pressu

234 atic model assessment of insulin resistance (HOMA-IR), and total energy and macronutrient intake at b

235 ll function (HOMA-B) and insulin resistance (HOMA-IR), as well as incident diabetes mellitus (DM), am

236 atic model assessment of insulin resistance (HOMA-IR), is widely applied despite known inaccuracies i

237 ated hemoglobin (HbA1c), insulin resistance (HOMA-IR), uric acid, C-reactive protein (CRP), alanine t

238 circumference, and HOMA-insulin resistance (HOMA-IR).

239 ostasis Model Assessment-Insulin Resistance (HOMA-IR).

240 asis model assessment of insulin resistance (HOMA-IR).

241 assessment of peripheral insulin resistance (HOMA-IR).

242 orrelated inversely with insulin resistance (HOMA-IR).

243 asis model assessment of insulin resistance (HOMA-IR).

244 and homeostatic model of insulin resistance (HOMA-IR).

245 asis model assessment of insulin resistance (HOMA-IR).

246 asis model assessment of insulin resistance (HOMA-IR).

247 asis model assessment of insulin resistance (HOMA-IR).

248 asis model assessment of insulin resistance (HOMA-IR).

249 atic model assessment of insulin resistance (HOMA-IR): beta-adjusted = 3.5% per SD (95% CI: 0.6%, 6.3

250 atic model assessment of insulin resistance (HOMA-IR); and a 2-hour oral glucose tolerance test was a

251 Insulin resistance (HOMA-IR: -0.67; 95% CI: -0.98, -0.36) was improved by ch

252 atic model assessment of insulin resistance [HOMA-IR] between 2.0 and 8.0) to weekly healthy lean don

253 atic model assessment of insulin resistance [HOMA-IR] of at least 2.0 mmol/L.mU/L), BMI greater than

254 ulin resistance (HOMA of insulin resistance [HOMA-IR]) and beta-cell dysfunction (HOMA of beta-cell f

255 atic model assessment of insulin resistance [HOMA-IR]) and cannabis use were assessed.

256 atic model assessment of insulin resistance [HOMA-IR]) and WHR were used for cardiometabolic phenotyp

257 asis Model Assessment of Insulin Resistance [HOMA-IR]), and concentrations of lipids, high sensitivit

258 atic model assessment of insulin resistance [HOMA-IR]), trunk-to-leg fat ratio, resting energy expend

259 (HOMA-IR < 3, n = 9) and insulin-resistant (HOMA-IR > 7, n = 9) obese subjects were assayed by micro

260 to evaluate the association between IR risk (HOMA-IR > 2.77) and cannabis use (occasional, regular, d

261 al in 126 overweight, non-insulin sensitive (HOMA-IR >=1.30), Chinese, Malay, and Asian-Indian males

262 from duodenal samples of insulin-sensitive (HOMA-IR < 3, n = 9) and insulin-resistant (HOMA-IR > 7,

263 ht, QUICKI (whole-body insulin sensitivity), HOMA-IR (hepatic insulin resistance), and fasting lipids

264 ciated with type 2 diabetes mellitus (T2DM), HOMA-IR and FFA.

265 virologic response to TVR-based therapy than HOMA-IR.

266 Adjusted analyses showed that HOMA-IR was predicted by the baseline HOMA index and BMI

267 The HOMA-IR decline from entry to 24 weeks after EOT was sig

268 The HOMA-IR group difference at week 12 favoured aripiprazol

269 In addition, subjects above the HOMA-IR threshold (HOMA-IR >2.6) had 47% (9-99%) larger

270 0.28, 1.26; P < 0.01) without affecting the HOMA-IR (MD: 0.18; 95% CI: -0.02, 0.39; P = 0.08) or glu

271 leptin concentrations were assessed, and the HOMA-IR was calculated.

272 ssociations with waist circumference and the HOMA-IR.

273 more insulin resistant as determined by the HOMA-IR index.

274 Insulin resistance was assessed by the HOMA-IR.

275 mption of soft drinks and IR by means of the HOMA-IR in Mexican adults.

276 resistance as evaluated with the use of the HOMA-IR.

277 eta = -0.17 (95% CI: -0.31, -0.02)] with the HOMA-IR in subjects with a waist circumference </=88 cm

278 showed no significant interactions with the HOMA-IR index (each P > 0.05).

279 tissue ALA was inversely associated with the HOMA-IR.

280 ition, subjects above the HOMA-IR threshold (HOMA-IR >2.6) had 47% (9-99%) larger odds of cognitive d

281 verage change between baseline and follow-up HOMA-IR showed an increase of 1.11 units (95% CI: 0.74,

282 IR and sensitivity were calculated using HOMA-IR and Matsuda indices.

283 ally healthy overweight women, defined using HOMA-IR, were not at elevated risk of breast cancer comp

284 Caution should be exercised when using HOMA-IR to detect insulin resistance when pancreatic fun

285 ed a voxelwise analysis to determine whether HOMA-IR predicted regional glucose metabolism.

286 Of greater significance is whether HOMA-IR can detect changes in insulin sensitivity induce

287 Two sensitivity analyses with HOMA-IR values as a continuous variable and a cutoff val

288 ep duration, AHIREM was only associated with HOMA-IR (beta = 0.04; 95% CI, 0.1-0.07; P = 0.01), where

289 position and saturation were associated with HOMA-IR (P < 0.0005 for 20 metabolite measures).

290 k consumption was positively associated with HOMA-IR change.

291 Neither APOC3 variant was associated with HOMA-IR in the Dallas Heart Study; this lack of associat

292 in activation was positively associated with HOMA-IR in the nucleus accumbens, right and left insula,

293 Nitrogen dioxide was associated with HOMA-IR, glucose, insulin, and leptin.

294 f metabolite levels were not associated with HOMA-IR, with the exception of a variant in GCKR associa

295 set of baseline metabolites associated with HOMA-IR.

296 ites were also significantly associated with HOMA-IR.

297 was highly and independently correlated with HOMA-IR as a marker of insulin resistance in children.

298 cts with asthma and directly correlated with HOMA-IR.

299 with positive associations among those with HOMA-IR >= 1.6 while associations were closer to the nul

300 oser to the null or inverse among those with HOMA-IR < 1.6.