Insulin resistance lowers adipose LPL expression and raises endogenous LPL inhibitors— angiopoietin-like protein 3/angiopoietin-like protein 4 (ANGPTL3/ANGPTL4) and apolipoprotein C3 (APOC3)—slowing TRL hydrolysis and extending the lipemic phase from approximately 4–6 h to 8–12 h or longer, thereby sustaining exposure to atherogenic remnant particles (57–59). This evidence concerns the gene APOC3 and Insulin resistance.