ライフサイエンスコーパス: HOMA-IR

1 HOMA-IR > 4 had the lowest misclassification rate (75% s

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

3 HOMA-IR accounted for only 15% of variability in SSPG in

4 HOMA-IR decreased significantly (-50%) from baseline by

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

6 HOMA-IR in subjects with IFG was similar to that in subj

7 HOMA-IR was independently associated with PAD (OR, 2.06;

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

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

10 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

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

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

13 with worsening glucose tolerance and across HOMA-IR quartiles in the normal and abnormal glucose tol

14 After age and sex adjustments, HOMA-IR scores were significantly and positively correla

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

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

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

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

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

20 +/- 0.6 mg/dL), Hb A1c (-0.02 +/- 0.0%), and HOMA-IR (-0.04 +/- 0.0) after adjustment for all covaria

21 BMI (P < 0.0001) and HOMA-IR (P < 0.0001) but not A1C (P = 0.65) increased wi

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

23 ine intra-abdominal fat area (P = 0.002) and HOMA-IR (P < 0.001) were independently associated with i

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

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

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

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

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

29 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

30 [-5.4 to -2.1] vs +5.5 kg [3.2 to 7.8]); and HOMA-IR (-1.52 [-1.93 to -1.01] vs +0.90 [-0.07 to 2.05]

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

32 iators were significantly related to BMI and HOMA-IR.

33 cOC, glucose, and insulin concentrations and HOMA-IR (1.24 +/- 0.15 for the control group compared wi

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

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

36 d that the effect of the Q allele on FPG and HOMA-IR was stronger in those with a higher BMI (P = 0.0

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

38 minally related to lower fasting glucose and HOMA-IR in the MAGIC consortium (P<0.05).

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

40 ctors, blood pressure and lipids, HbA1c, and HOMA-IR, FH remained a significant determinant of EDV (p

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

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

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

44 D4B) and one influencing fasting insulin and HOMA-IR (near IGF1).

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

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

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

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

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

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

51 etic correlation between fasting insulin and HOMA-IR (rho(G) > 0.86, P < 0.05), as well as insulin 30

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

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

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

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

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

57 unreported promising effects on insulin and HOMA-IR.

58 two loci associated with fasting insulin and HOMA-IR.

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

60 Associations with 2-h glucose, insulin, and HOMA-IR remained significant after further adjustment fo

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

62 x, predicted CAC scores, but only leptin and HOMA-IR provided value beyond risk factors, metabolic sy

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

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

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

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

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

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

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

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

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

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

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

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

75 by an elevated homeostasis model assessment (HOMA-IR) index, had lower levels of B-type natriuretic p

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

77 ucose/insulin, homeostasis model assessment (HOMA-IR), quantitative insulin sensitivity check index (

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

79 resistance by homeostasis model assessment (HOMA-IR; all P = 0.01-0.006).

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

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

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

83 6 (36%), and 165 (29%) patients had baseline HOMA-IR <2, 2 to <4, and >/= 4, respectively.

84 2 patients were randomized; 578 had baseline HOMA-IR and other prognostic data and were included in t

85 osteocalcin at baseline had higher baseline HOMA-IR (P = 0.006 and P = 0.02, respectively).

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

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

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

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

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

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

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

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

94 The common HOMA-IR cutoff of < or =3 to define insulin resistance h

95 fasting insulin and glucose concentrations, HOMA-IR, or HbA(1c).

96 f approximately 200% in ucOC concentrations, HOMA-IR was similar in the 2 groups at 6 and 12 mo (at 6

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

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

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

100 reduced insulin action as assessed by either HOMA-IR in 2,549 nondiabetic full-heritage Pima Indians

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

102 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

103 djusting for BMI but not after adjusting for HOMA-IR (P = 0.013).

104 lic syndrome components, while adjusting for HOMA-IR did not (P = 0.0028).

105 capacity was attenuated after adjusting for HOMA-IR.

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

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

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

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

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

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

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

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

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

115 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

116 ions of leptin were associated with a higher HOMA-IR index, even after adjustment for age, race, sex,

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

118 14-3.48 P = 0.0145, respectively) and higher HOMA-IR (OR = 1.78, 95% CI:1.02-3.13, P = 0.041).

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

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

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

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

123 ale ALL survivors had a significantly higher HOMA-IR (CRT, mean 4.0, 95% CI, 2.8 to 5.6; no CRT, mean

124 ale ALL survivors had a significantly higher HOMA-IR (CRT, mean 4.6, 95% CI, 3.6 to 5.7; no CRT, mean

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

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

127 d osteocalcin was not associated with higher HOMA-IR at baseline or at 3-y follow-up.

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

129 -3%,+2%) p = 0.70, with identical results if HOMA-IR was used.

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

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

132 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

133 IFG and HOMA-IR (or insulin), 10-y change in HOMA-IR (or insulin), and the age 9-10 y insulin x total

134 as inversely associated with a 3-y change in HOMA-IR (P = 0.002).

135 of osteocalcin at baseline and 3-y change in HOMA-IR were examined in 162 adults (mean age: 69 y; 63%

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

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

138 36 animals showed an artifactual decrease in HOMA-IR (i.e., increased sensitivity).

139 ted with increases in S(i), and decreases in HOMA-IR were related to increases in adiponectin (r = -0

140 emained a significant predictor of increased HOMA-IR at 10-11 years even after adjustment for total s

141 were independently associated with increased HOMA-IR at 10-11 years in a multiple linear regression m

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

143 d by the homeostasis model assessment index (HOMA-IR).

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

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

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

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

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

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

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

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

152 ling calculation of homeostasis model of IR (HOMA-IR).

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

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

155 rcaloric feeding despite significantly lower HOMA-IR indexes.

156 0.99; P = 0.04) and a tendency toward lower HOMA-IR (ratio of geometric means: 0.82; 95% CI: 0.66, 1

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

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

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

160 Stratifying subjects on the basis of median HOMA-IR, we found that CRP >3 mg/L was no longer signifi

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

162 - 17.9 mg/dL; insulin, -0.7 +/- 5.1 muIU/mL; HOMA-IR, -0.2 +/- 1.9; and QUICKI, 0.004 +/- 0.019 (all

163 and control groups, respectively; at 12 mo, HOMA-IR was 2.13 +/- 0.38 and 1.47 +/- 0.22 in the exper

164 lar in the 2 groups at 6 and 12 mo (at 6 mo, HOMA-IR was 2.24 +/- 0.54 and 1.52 +/- 0.23 in the exper

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

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

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

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

169 After addition of HOMA-IR, VAT remained positively related to VLDL particl

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

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

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

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

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

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

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

177 1), but not with body mass index, insulin or HOMA-IR.

178 P = 0.0002 and P = <0.0001, respectively) or HOMA-IR (P = 0.0008 and P = <0.0001, respectively), wher

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

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

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

182 st circumference, which positively predicted HOMA-IR.

183 Repeat HOMA-IR measurements had higher within-person variation

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

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

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

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

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

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

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

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

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

193 asis model assessment of insulin resistance (HOMA-IR) and fasting insulin.

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

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

196 atic model assessment of insulin resistance (HOMA-IR) and the age 9-10 y HOMA-IR x percentage of calo

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

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

199 asis model assessment of insulin resistance (HOMA-IR) at 6 and 12 months.

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

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

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

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

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

205 ll function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 nondiabetic participants.

206 tic model assessment for insulin resistance (HOMA-IR) index, and serum adipocytokine (leptin, adipone

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

208 asis model assessment of insulin resistance (HOMA-IR) index, predicted CAC scores, but only leptin an

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

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

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

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

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

214 s is model assessment of insulin resistance (HOMA-IR) to the model.

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

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

217 asis model assessment of insulin resistance (HOMA-IR) was calculated and correlated with ucOC concent

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

219 asis model assessment of insulin resistance (HOMA-IR) was calculated from fasting plasma glucose and

220 asis model assessment of insulin resistance (HOMA-IR) was calculated.

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

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

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

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

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

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

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

228 asis model assessment of insulin resistance (HOMA-IR), and the insulin sensitivity index (ISI(0,120))

229 sis model assessment for insulin resistance (HOMA-IR), fasting plasma insulin level, Matsuda index, a

230 Insulin resistance (HOMA-IR), insulin production, and glucagon-like peptide

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

232 asis model assessment of insulin resistance (HOMA-IR), was associated with impaired endothelium-depen

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

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

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

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

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

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

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

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

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

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

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

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

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

246 asis model assessment of insulin resistance (HOMA-IR)] and structural equation models to estimate gen

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

248 asis model assessment of insulin resistance [HOMA-IR] = 1.3) and seven insulin-resistant (HOMA-IR = 6

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

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

251 ostatic model assessment-insulin resistance [HOMA-IR]) and peripheral insulin resistance (S(i)) and b

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

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

254 asis model assessment of insulin resistance [HOMA-IR], and glycemia (HbA(1c) [A1C]) to the levels of

255 asis model assessment of insulin resistance [HOMA-IR]: beta = -0.0059, P = 0.005), and metabolic synd

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

257 HOMA-IR] = 1.3) and seven insulin-resistant (HOMA-IR = 6.3) men, during suppression of endogenous ins

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

259 odel assessment of insulin resistance score (HOMA-IR) (P < 0.0001), and medications used for NAFLD (P

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

261 relates positively with insulin sensitivity (HOMA-IR index).

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

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

264 mbined IFG/IGT and significantly higher than HOMA-IR in subjects with IGT or NGT.

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 Of several metabolic markers, leptin and the HOMA-IR index had the most robust, independent associati

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

273 Insulin resistance was assessed by the HOMA-IR.

274 ion results in sustained improvements in the HOMA-IR index, suggesting that HCV could have a direct r

275 formed to evaluate whether the effect of the HOMA-IR index on the coronary calcium score is moderated

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

277 okine on insulin resistance according to the HOMA-IR index and on coronary artery calcification deter

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

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

280 ns showed a significant interaction with the HOMA-IR index (P for multivariate interaction = 0.02).

281 in (P = 0.98) showed no association with the HOMA-IR index.

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

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

284 expression and plasma CRP levels but not to HOMA-IR.

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

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

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

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

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

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

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

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

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

294 able analysis, steatosis was associated with HOMA-IR, body mass index, waist circumference, serum tri

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

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

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 tal adiposity was significantly related with HOMA-IR at 10-11 years in models that contained intra-ab

300 ulin resistance (HOMA-IR) and the age 9-10 y HOMA-IR x percentage of calories from fat interaction we