Targeting a cell cycle inhibitor promotes beta cell replication
One of the factors underlying the development of type 2 diabetes is loss of β cell mass, resulting in decreased insulin production. 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.
Decreased insulin production is a problem because without enough insulin, sugar can’t be pulled out of the blood for use by cells. High blood sugar results in damage to your organs by oxidation.