For example, FGF19 has been shown in rodent models of metabolic diseases to suppress hepatic gluconeogenesis by regulating the peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC-1α)/cyclic AMP (cAMP) response element binding protein (CREB) pathway25, increase fatty acid oxidation and energy expenditure26 and improve glucose effectiveness through the hypothalamus-pituitary-adrenal axis27, 28. This evidence concerns the gene FGF19 and metabolic disease.