Combination of GLP-1 Receptor Activation and Glucagon Blockage Promotes Pancreatic β-Cell Regeneration In Situ in Type 1 Diabetic Mice

Pancreatic β-cell neogenesis in vivo holds great promise for cell replacement therapy diabetic patients, and discovering the relevant clinical therapeutic strategies would push it forward to application. Liraglutide, a widely used antidiabetic glucagon-like peptide-1 (GLP-1) analog, has displayed diverse β-cell-protective effects type 2 animals. Glucagon receptor (GCGR) monoclonal antibody (mAb), preclinical agent that blocks glucagon pathway, can promote recovery of functional mass 1 mice. Here, we conducted 4-week treatment two drugs alone or combination Although liraglutide neither lowered blood glucose level nor increased plasma insulin level, immunostaining showed expanded through self-replication, differentiation from precursor cells, transdifferentiation pancreatic α cells β-cells. The more significantly after GCGR mAb treatment, while group did not further increase area. However, compared with group, combined reduced proportion β-cells/α-cells. Our study evaluated liraglutide, monotherapy, strategy control islet regeneration provided useful clues future application diabetes.