Pancreatic islet expression profiling in diabetes-prone C57BLKS/J mice reveals transcriptional differences contributed by DBA loci, including Plagl1 and Nnt.

ABSTRACT:

Background

C57BLKS/J (BLKS) mice are susceptible to islet exhaustion in insulin-resistant states as compared with C57BL6/J (B6) mice, as observed by the presence of the leptin receptor (Lepr) allele, Leprdb/db. Furthermore, DBA2/J (DBA) mice are also susceptible to beta-cell failure and share 25% of their genome with BLKS; thus the DBA genome may contribute to beta-cell dysfunction in BLKS mice.

Results

Here we show that BLKS mice exhibit elevated insulin secretion, as evidenced by improved glucose tolerance and increased islet insulin secretion compared with B6 mice, and describe interstrain transcriptional differences in glucose response. Transcriptional differences between BLKS and B6 mice were identified by expression profiling of isolated islets from both strains. Genom

SUBMITTER: Anderson AA 

PROVIDER: S-EPMC2642818 | biostudies-literature | 2009 Jan

REPOSITORIES: biostudies-literature