Figure 2.

Lipocalin-2 (LCN2) as a component in non-alcoholic steatohepatitis (NASH) pathology and diagnostics. NASH patients show elevated levels of LCN2 in urine, serum, and liver tissue, which makes it a potential biomarker for NASH. It is able to discriminate between simple steatosis (SS) and NASH, while the level of LCN2 correlates with inflammation (e.g., increase of CRP), insulin resistance, and fibrosis. It is induced by proinflammatory cytokines, high fat diet, glucose, and fructose overconsumption. Overexpression experiments have implicated LCN2 in the enhancement of lipolysis, fatty acid oxidation, mitochondrial activity, and immune cells crosstalk. In addition, LCN2 upregulation is associated with reduced de novo lipogenesis. All evidence points out that its role is hepatoprotective. However, the exact mechanisms are ought to be found.