TAT-PBX1 Reverses Hyperglycemia Through β-Cell Regeneration and Functional Restoration in an STZ-Induced Diabetic Model.

ABSTRACT: Objective: β-cell dysfunction and loss are major pathological determinants of impaired islet function and hyperglycemia in diabetes. Given the inability of current therapies to restore β-cell viability or glucose-responsive insulin secretion, this study aimed to investigate whether a cell-permeable PBX1 fusion protein (TAT-PBX1) could rescue streptozotocin (STZ)-induced β-cell injury and restore β-cell functional integrity. Methods: A TAT-PBX1 recombinant fusion protein was produced using a prokaryotic expression system. Its protective effects were assessed in STZ-treated MIN6 β cells and in a mouse model of STZ-induced diabetes, with the glucokinase (GK) activator dorzagliatin included as a positive control. We evaluated β-cell apoptosis, DNA damage, ATP and NAD⁺/

SUBMITTER: Meng X 

PROVIDER: S-EPMC12845013 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature