GLP-1 receptor agonists can reverse immunosuppression-induced beta-cell dysfunction

It is well known that some of the agents commonly used during immunosuppressive (IS) therapy after solid organ transplantation can contribute to beta cell dysfunction and result in diabetes mellitus in the transplant recipient. Some of the risks associated with post-transplant diabetes mellitus (PTDM) include cardiovascular disease (CVD), graft failure and mortality. Since this significance was recognized, many studies are ongoing to refine the IS therapy regimen to reduce or discontinue corticosteroids and calcineurin inhibitors (CNI). A promising addition to the immunosuppression treatment regimen to treat PTDM is glucagon-like peptide-1 receptor (GLP-1R) agonists or incretin mimetics normally used in the treatment of type 2 diabetes (T2D). Studies show that adding GLP-1R agonists to the immunosuppression regimen after solid organ transplant is beneficial not only for the health of the islet beta cells but also positively affects immune function in metabolic disorders by suppressing the activation of CD4+ T lymphocyte cytokine expression. Additional benefits include decreased cardiac graft vasculopathy, improvement of hepatic steatosis, preservation of kidney function, enhanced graft survival and improved all-cause mortality rates for solid organ transplant recipients.