In animal models of metabolic syndrome and T2DM, Cr supplementation inhibited hepatic gluconeogenesis by decreasing mRNA expression of fructose 1,6-bisphosphatase (FBPase), phosphoenolpyruvate carboxykinase (PEPCK), and glucose-6-phosphatase (G6Pase) and promoted hepatic glycogen synthesis by upregulating glucokinase (Gk) mRNA expression in the liver (32–34). This evidence concerns the gene FBP1 and metabolic syndrome.