In another study, METRNL treatment in myoblasts was reported to stimulate glucose uptake via calcium-mediated AMPKα phosphorylation and the downstream p38 MAPK pathway, and intraperitoneal injection of GST-METRNL improved glucose intolerance in HFD mice, as well as in db/db mice [47], suggesting the therapeutic role of METRNL in metabolic disease. This evidence concerns the gene METRNL and Other metabolic disease.