Is the DNA synthesis of pancreatic islets influenced by the MHC and/or the genetic background?

Neonatal pancreatic rat islets were used to investigate the effect of MHC haplotype RT1u on islet replication measured by incorporation of 3H-thymidine and autoradiography. The special interest in RT1u resulted from the fact that BB rats, which develop an insulin-dependent diabetes, belong to the RT1u haplotype. Thus, the RT1u, when influencing the replication, may be involved in the development of the B-cell deficiency observed in diabetic rats. The incorporation of labeled thymidine into islets obtained from rat strains carrying the RT1u or RTIa haplotype revealed no differences. No matter whether the islets were isolated from Lewis, Wistar, or BB rats, no alteration of islet replication by RT1u islets was found. However, islets obtained from Wistar rats had a higher replicatory activity than islets from Lewis rats. This finding was confirmed by a decrease in DNA synthesis of BB rat islets, in which the Wistar background was substituted by the Lewis background. We conclude from our results that MHC has no influence on islet replication, whereas genetic background seems to be involved in the regulation of islet DNA synthesis.