Low apoA-I is associated with insulin resistance in patients with impaired glucose tolerance: a cross-sectional study

Xiaomeng Feng; Xia Gao; Zhi Yao; Yuan Xu

Low apoA-I is associated with insulin resistance in patients with impaired glucose tolerance: a cross-sectional study

2017

Xiaomeng Feng | Xia Gao | Zhi Yao | Yuan Xu

Abstract Background Low apolipoprotein A-I (apoA-I) is an independent risk factor for atherosclerotic cardiovascular diseases. Insulin resistance predicts the progression of abnormal glucose metabolism, which is the main cause of atherosclerotic cardiovascular disease. In this study, we assessed the potential association between apoA-I levels and insulin resistance in patients with impaired glucose tolerance (IGT) and the possible link between apoA-I and IGT. Methods This study evaluated a cross-sectional study of 108 participants with impaired glucose tolerance (IGT group) and 84 controls (control group). ApoA-I and clinical characteristics were measured, and a homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. Results The IGT group exhibited significantly lower apoA-I and higher HOMA-IR levels than the control group (apoA-I: 1.37 ± 0.36 vs 1.57 ± 0.39 g/L; HOMA-IR: 4.21 ± 1.56 vs 2.15 ± 0.99; P < 0.001 for both). ApoA-I was negatively correlated with HOMA-IR in both the IGT and control groups (IGT group: r = −0.269, P = 0.005; control group: r = −0.262, P = 0.016). Multiple stepwise regression analysis showed that low apoA-I levels (β = −1.470, P = 0.002) were independently correlated with high HOMA-IR levels in the IGT group. Moreover, logistic regression analysis identified that low apoA-I was an independent influencing factor for IGT (β = −1.170, OR = 0.310, P = 0.007). Conclusions ApoA-I is inversely associated with insulin resistance in patients with impaired glucose tolerance, and low apoA-I is an independent risk factor for impaired glucose tolerance. These results indicate that apoA-I plays an important role in regulating insulin sensitivity and glucose metabolism in patients with IGT.

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