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Table 3 The cross-lagged path coefficients by HOMA-IR status in the total sample, with adjustment for covariates

From: Changes in triglycerides and high-density lipoprotein cholesterol may precede peripheral insulin resistance, with 2-h insulin partially mediating this unidirectional relationship: a prospective cohort study

 

Normal (n = 2, 516)

IR (n = 809)c

IR status difference

β1

β2

β1

β2

P for β1

P for β2

Model 1 a

TG ↔ Gutt index

−0.094**

−0.029

−0.173**

0.040

0.047

NS

HDL-C ↔ Gutt index

0.091**

0.016

0.177**

0.016

0.030

NS

TG ↔ HOMA-%β

−0.103*

−0.117*

−0.051

−0.047

NS

NS

HDL ↔ HOMA-%β

0.093**

0.136**

0.114**

0.062

NS

NS

TG ↔ 2-h insulin

0.113**

0.044*

0.128*

0.029

NS

NS

HDL-C ↔ 2-h insulin

−0.094**

−0.020

−0.147**

−0.010

NS

NS

Model 2 b

NS

NS

2-h insulin ↔ Gutt index

−0.095**

−0.023

−0.153**

−0.025

NS

NS

  1. Data are cross-lagged path coefficients
  2. NS, non-significant; TG, triglycerides; HDL-C, high-density lipoprotein cholesterol; BMI, body mass index
  3. Gutt index = [75,000 + (fasting glucose − 2-h glucose) × 0.19 × body weight]/(120 × log [(fasting insulin + 2-h insulin)/2] × [(fasting glucose + 2-h glucose)/2])
  4. Covariates included age, gender, BMI, alcohol consumption, smoking, regular exercise and caloric intake
  5. aModel 1: β1 describes the path from the baseline TG/HDL-C to the follow-up Gutt index, HOMA-models or 2-h insulin, and β2 describes the path from the baseline Gutt index, or 2-h insulin to the follow-up TG/HDL-C
  6. bModel 2: β1 describes the path from the baseline 2-h insulin to the follow-up Gutt index, and β2 describes the path from the baseline Gutt index to the follow-up 2-h insulin
  7. cInsulin resistance (IR) was defined as the upper quartile of HOMA-IR
  8. * P < 0.05 for β1 and β2 being different from 0, ** P < 0.01 for β1 and β2 being different from 0