LECT2 and obesity disorder: Likewise, treated cells displayed upregulated lipogenic SREBP1c and SCD1 genes, accompanied by lipid overaccumulation in pre-adipocytes, and simultaneous breakdown of insulin receptor substrate (IRS-1) and Akt phosphorylation, indicating that LECT2 hepatokine greatly contributes to adipose tissue obesity, insulin resistance and inflammation through CD209/P38-dependent signaling and activation of downstream molecules [20].