In summary, through the animal experiments, cell experiments, and further mechanism exploration based on epigenetics, we concluded that vitamin D deficiency during pregnancy may promote the proliferation and differentiation of pre-adipocytes, which may be associated with methylation alterations of genes, such as Vldlr and Hif1α, ultimately leading to offspring obesity. The gene discussed is HIF1A; the disease is obesity due to melanocortin 4 receptor deficiency.