To address this, we treated HepG2 cell cultures (at 70–80 % confluence) with the typical proinflammatory cytokines and chemokine that are known to be upregulated in metabolic disease such as obesity and T2D and measured the expression of fetuin-A in supernatants for comparison with untreated controls. Here, AHSG is linked to obesity due to melanocortin 4 receptor deficiency.