Abstract

It is recently known that individuals with long-standing type 1 diabetes (T1D) still have surviving functional β cells. Thus, strategies to promote β-cell protection/replication should be used in the adjuvant therapy of T1D. Our lab has extensively characterized Lyn kinase as a critical regulator of β-cell mass. We herein hypothesized that pharmacological activation of Lyn could stimulate β-cell regeneration and improve glucose control in animal models of T1D. A short treatment of 7 days with MLR1023, a specific activator of Lyn, was sufficient to improve glucose tolerance, and to induce a 2-fold increase in β-cell mass in diabetic NOD mice.

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