However, leptin overproduction, due to increased adipose tissue, acts as a pro-inflammatory and fibrogenic factor acting on metalloproteinases (TIMP metallopeptidase inhibitor 1 and matrix metalloproteinase-1), stimulating TGF-β, and upregulating CD14 on liver Kupffer cells, thus worsening liver steatosis [24,25,26,27]. This evidence concerns the gene LEP and Hepatic steatosis.