In addition, glucose can stimulate pancreatic β-cells to release hepcidin.[77] Therefore, serum hepcidin in patients with NAFLD is higher than that in normal people, and the increase in serum hepcidin leads to a decrease in FPN expression and cell iron output,[78] which further stimulates iron deposition in hepatocytes. The gene discussed is HAMP; the disease is metabolic dysfunction-associated steatotic liver disease.