Mitochondrial protein UCP2, which is involved in congenital hyperinsulinism, also plays a role in endocrine pancreas development during the fetal period

Mitochondrial protein UCP2 is a C4 metabolite transporter. Mutations in the Ucp2 gene lead to congenital hyperinsulinism. In mice, the knock-out of Ucp2 leads to an increased number of endocrine cells in the adult pancreas. Our recent data indicate that the absence of Ucp2 is also responsible for an amplification of the pool of endocrine cells during the foetal and perinatal periods.