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Abstract
Diabetes is the result of having inadequate supply of functional insulin-producing
β cells. Two possible approaches for replenishing the β cells are: (1) replacement
by transplanting cadaveric islets or β cells derived from human embryonic stem cells/induced
pluripotent stem cells and (2) induction of endogenous regeneration. This review focuses
on endogenous regeneration, which can follow two pathways: enhanced replication of
existing β cells and formation of new β cells from cells not expressing insulin, either
by conversion from a differentiated cell type (transdifferentiation) or differentiation
from progenitors (neogenesis). Exciting progress on both pathways suggest that regeneration
may have therapeutic promise.