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Inadequate compensatory beta cell hyperplasia in insulin-resistant states triggers the development of overt diabetes. The mechanisms that underlie this crucial adaptive response are not fully defined. Here we show that the compensatory islet-growth response to insulin resistance in 2 models--insulin receptor (IR)/IR substrate-1 (IRS-1) double heterozygous mice and liver-specific IR KO (LIRKO) mice--is severely restricted by PDX-1 heterozygosity. Six-month-old IR/IRS-1 and LIRKO mice both showed up to a 10-fold increase in beta cell mass, which involved epithelial-to-mesenchymal transition. In both models, superimposition of PDX-1 haploinsufficiency upon the background of insulin resistance completely abrogated the adaptive islet hyperplastic response, and instead the beta cells showed apoptosis resulting in premature death of the mice. This study shows that, in postdevelopmental states of beta cell growth, PDX-1 is a critical regulator of beta cell replication and is required for the compensatory response to insulin resistance.
Pubmed ID: 15372107
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Core that offers support for data-driven projects related to basic, clinical and translational research, with a particular emphasis on diabetes. The core aims to ensure that researchers take advantage of the most modern and robust methods available in the field of Bioinformatics and Biostatistics.
View all literature mentionsTHIS RESOURCE IS NO LONGER IN SERVICE. Documented on October 27,2023. Core that provides cell sorting and flow cytometry services. Specific services include cell analysis, large object sorting,magnetic cell enrichment, and automatic cell counting.
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View all literature mentionsTHIS RESOURCE IS NO LONGER IN SERVICE. Documented on October 27,2023. Core that provides technically advanced physiological evaluation of metabolism in diabetes, obesity, and their associated complications in rodents for DRC investigators and outside users. It also provides training of investigators and trainees in several physiological procedures.
View all literature mentionsTHIS RESOURCE IS NO LONGER IN SERVICE. Documented on October 27,2023. Core that provides services for genetic and genomic analysis, including DNA extraction from blood, access to DNA collections from the Core?s repository, SNP genotyping, and support for gene expression studies based on both high-density oligonucleotide arrays and real-time quantitative PCR.
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View all literature mentionsSix component core which facilitates the exchange of research information and discussions among investigators, fellows and students within the Joslin Diabetes Center, as well as between Joslin Staff and outside researchers with similar interests.
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