This study determined the associations of apolipoprotein A1 (ApoA1), high-density lipoprotein cholesterol (HDL-C), and HDL-C/ApoA1 ratio with fasting blood glucose (FBG) and evaluated the mediating effects of high-sensitivity C-reactive protein (hsCRP) and body mass index (BMI). A cross-sectional study with 4805 coronary artery disease (CAD) patients was performed. In multivariable analyses, higher ApoA1, HDL-C, and HDL-C/ApoA1 ratio were associated with significantly lower FBG level (Q [quartile] 4 vs Q1: 5.67 vs 5.87 mmol/L for ApoA1; 5.64 vs 5.98 mmol/L for HDL-C; 5.63 vs 6.01 mmol/L for HDL-C/ApoA1 ratio). Moreover, inverse associations of ApoA1, HDL-C, and HDL-C/ApoA1 ratio with abnormal FBG (AFBG) were found with odd ratios (95% confidence interval) of .83 (.70-.98), .60 (.50-.71), and .53 (.45-.64) in Q4 compared with Q1. Path analyses indicated that \"ApoA1 (or HDL-C)-FBG\" associations were mediated by hsCRP and \"HDL-C-FBG\" association was mediated by BMI. Our data suggested that higher ApoA1, HDL-C, and HDL-C/ApoA1 ratio were favorably associated with a lower FBG level in CAD patients and these associations might be mediated by hsCRP or BMI. Collectively, higher concentrations of ApoA1, HDL-C, and HDL-C/ApoA1 ratio might decrease the risk of AFBG.

Scarce data explored the associations of apolipoproteins with hemoglobin glycation index (HGI) and triglyceride-glucose (TyG) index. This study determined associations of serum apolipoproteinA1 (ApoA1) and high density lipoprotein cholesterol (HDL-C) with HGI and TyG index in coronary artery disease (CAD) patients.
A total of 10,803 CAD patients were included in this cross-sectional pilot study. Serum concentrations of ApoA1 and HDL-C were measured. Analyses of covariance were used to compare the mean differences in glucose metabolism indices (e.g., HGI, TyG index, hemoglobin glycation [HbA1c], fasting blood glucose [FBG]) among the quartiles of ApoA1, HDL-C and HDL-C/ApoA1 ratio.
In multivariate analysis, higher ApoA1, HDL-C and HDL-C/ApoA1 ratio were associated with significantly lower HGI (Quartile [Q]4 vs. Q1: -0.032 % vs. 0.017 % for ApoA1; -0.072 % vs. 0.079 % for HDL-C; -0.083 % vs. 0.085 % for HDL-C/ApoA1 ratio). Intermediate ApoA1 level was inversely associated with TyG index (Q2 vs. Q1: 296.278 vs. 306.794). The mean TyG index were significantly decreased with increased HDL-C and HDL-C/ApoA1 ratio (Q4 vs. Q1: 298.584 vs. 309.221 for HDL-C; 300.405 vs. 315.218 for HDL-C/ApoA1 ratio). Moreover, the inverse associations of ApoA1, HDL-C and HDL-C/ApoA1 ratio with HbA1c and FBG also were observed. In path analysis, the associations of HDL-C and HDL-C/ApoA1 ratio with TyG index were mediated by obesity.
This study provided further support for the hypoglycemic effects of ApoA1 and HDL-C in patients with CAD. Replication of these findings is warranted in further longitudinal studies in different populations.