INS and metabolic dysfunction-associated steatotic liver disease: The two variants prevent insulin binding and thus increase the levels of APOC3 messenger RNA and protein.17 APOC3 is transported on circulating lipoproteins and limits clearance of TG-rich particles.18 Petersen et al.13 proposed that the sequence variants lead to increased uptake of chylomicron remnants by the liver, and this results in NAFLD and hepatic insulin resistance.