The rise in TAG-rich lipoprotein particles seen in metabolic disorders (e.g., insulin resistance, type II diabetes) results predominantly from the overproduction of apoB100-containing VLDL by the liver, competition of VLDL and CM for binding to lipoprotein lipase in peripheral tissues, and inefficient uptake of TAG-rich lipoprotein remnants by hepatic LDLR [51,52]. This evidence concerns the gene LPL and metabolic disease.