As VLDLR is known to reduce the blood cholesterol level (Turunen et al., 2016), this upregulation of VLDLR is likely a protective feedback response due to hyperlipidemia induced by prenatal inflammatory stimulation, which might explain the relatively mild obesity and insulin resistance phenotype in offspring-pLPS and TLR2-deficient offspring-pLPS. This evidence concerns the gene TLR2 and obesity due to melanocortin 4 receptor deficiency.