While reliable experimental data we initially applied to confirm that PQQ administration not only effectively mediated damaged lipid and cholesterol metabolism with an increased level of intracellular cholesterol, but also depressed the expression of PCSK9, up-regulating downstream target LDLR and the T-converting proteins in the LCs, therefore, which may be the potential mechanism where PQQ improves the obesity-incurred dysfunction of T synthesis. The gene discussed is PCSK9; the disease is obesity disorder.