Abstract
Type 2 diabetes develops due to functional β cell loss after insulin resistance. Sustained increased insulin demand compels β cells into apoptosis and dedifferentiation resulting in decreased β cell mass. In adult humans, β cell regeneration (proliferation, neogenesis or transdifferentiation) rarely occurs in a physiologic condition. Because of this stagnant nature of β cells, β cell mass are not sufficiently recovered once their numbers are severely decreased. Constant efforts have been made to replenish the decreased β cell mass in diabetic patients by islet or pancreas transplantation1,2 .
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