LEP and periodontitis: Periodontitis-derived virulence factors can induce endoplasmic reticulum stress (ERS) to promote leptin secretion.76 High levels of leptin inhibit the activation of Janus kinase 2 (JAK2) by the cell surface leptin receptor (LepRb) in an autocrine manner and inhibit downstream IRS signaling.113 Leptin also promotes the proliferation of macrophages in a paracrine manner, induces the expression of inflammatory factors,114 and participates in visceral adipose tissue IR.