Our study showed that Hsp–Cu(II) increased the abundances of Bacteroidota and Faecalibaculum in the T2DM mice, and the levels of DAO and D-LAC in the Hsp–Cu(II) groups were lower than those in the Diseased group, indicating that Hsp–Cu(II) significantly decreased intestinal permeability and improved the intestinal mucosal barrier function to alleviate T2DM. The gene discussed is DAO; the disease is type 2 diabetes mellitus.