Researchers in a previous work found that higher leptin levels significantly suppressed LDLR in HepG2 cells and increased PCSK9 expression [35], suggesting that leptin plays a role in regulating PCSK9 expression and hepatic LDLR, which could explain the mechanism responsible for dyslipidemia in obesity [35]. This evidence concerns the gene LDLR and obesity due to melanocortin 4 receptor deficiency.