The loss of beta cell mass, which results in decreased insulin production, is one of the factors underlying the development of type 2 diabetes.
Once lost, β cell mass cannot be restored. In contrast, infants with focal hyperinsulinism of infancy exhibit rapid expansion of the β cell mass due to a silencing of a region of chromosome 11 that includes the gene encoding the cell cycle inhibitor p57Kip2
. In this issue of the Journal of Clinical Investigation
, Klaus Kaestner and colleagues at the University of Pennsylvania demonstrate that silencing the gene encoding p57Kip2
in isolated adult human islets promotes β cell replication and that these new cells exhibit many properties associated with β cells. This study provides an explanation for excessive β cell expansion in children with focal hyperinsulinism and suggests that targeting the p57Kip2
pathway in adults with type 2 diabetes may improve β cell function.