Apoa 1

Samples were collected in the fasting state. Triglycerides and LDL‐C were measured on fresh serum samples using traditional enzymatic methods. Non‐HDL‐C was calculated as total cholesterol minus HDL‐C. All other measurements of apolipoproteins and lipoprotein particle subclasses (triglyceride‐rich lipoprotein particles [TRLP], LDLP and high‐density lipoprotein particles [HDLP]) were performed on available frozen plasma EDTA or serum samples from the modified intent‐to‐treat population (mITT) population. Lipoprotein particle concentration and average lipoprotein particle size were measured by nuclear magnetic resonance (NMR) spectroscopy at baseline and 26 weeks (LabCorp, Burlington, NC, USA). The lipoprotein insulin resistance (LPIR) score, a weighted combination of six lipoprotein subclass measures (large TRLP, large HDLP, small LDLP and mean sizes of TRLP, LDLP and HDLP), was also calculated.²⁷ Preheparin serum LPL mass was measured by enzyme‐linked immunosorbent assay (ALPCO, Salem, NH, USA). ApoA‐I, apoB (Roche, Indianapolis, IN, USA) and apoC‐III (Kamiya, Seattle, WA, USA) were measured by immunoturbidimetry at baseline and at 4, 12 and 26 weeks.

The following biochemical indicators were detected in this study: total Cholesterol (TC), triglyceride (TG), HDLC, low-density lipoprotein cholesterol (LDLC), APOA1, apolipoprotein B (APOB), lipoprotein a (LPA), hypersensitive C-reactive protein (CRP), TRSF, homocysteine (HCY), and AAT. The commercially available enzymatic colorimetric assays (TC, TG, HDLC, LDLC, APOA1, APOB, LPA, CRP, and TRSF were purchased from Roche Diagnostics, Switzerland; HCY were purchased from Jiuqiang, Beijing; AAT were purchased from DIALAB diagnostic, Austria) and an automated analyzer system (Cobas 8000 modular device Roche Diagnostics, Switzerland) were used.