Transcriptomics

Dataset Information

299

Transcription profiling of mouse pancreatic islets on day 14.5 of pregnancy


ABSTRACT: The inability of the beta-cell to meet the demand for insulin brought about by insulin resistance leads to type 2 diabetes. In adults, beta-cell replication is one of the mechanisms thought to cause the expansion of beta-cell mass. Efforts to treat diabetes require knowledge of the pathways that drive facultative beta-cell proliferation in vivo. A robust physiological stimulus of beta-cell expansion is pregnancy, and identifying the mechanisms underlying this stimulus may provide therapeutic leads for the treatment of type 2 diabetes. The peak in beta-cell proliferation during pregnancy occurs on day 14.5 of gestation in mice. Using advanced genomic approaches, we globally characterize the gene expression signature of pancreatic islets on day 14.5 of gestation during pregnancy. We identify a total of 1,907 genes as differentially expressed in the islet during pregnancy. We demonstrate that the islet's ability to compensate for relative insulin deficiency during metabolic stress is associated with the induction of both proliferative and survival pathways. A comparison of the genes induced in three different models of islet expansion suggests that diverse mechanisms can be recruited to expand islet mass. The identification of many novel genes involved in islet expansion during pregnancy provides an important resource for diabetes researchers to further investigate how these factors contribute to the maintenance of not only islet mass, but ultimately beta-cell mass.

ORGANISM(S): Mus musculus  

SUBMITTER: Peter White   Jonathan Schug   Klaus Kaestner   Sebastian Rieck  

PROVIDER: E-MTAB-120 | ArrayExpress | 2009-08-05

REPOSITORIES: ArrayExpress

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Publications

The transcriptional response of the islet to pregnancy in mice.

Rieck Sebastian S   White Peter P   Schug Jonathan J   Fox Alan J AJ   Smirnova Olga O   Gao Nan N   Gupta Rana K RK   Wang Zhao V ZV   Scherer Philipp E PE   Keller Mark P MP   Attie Alan D AD   Kaestner Klaus H KH  

Molecular endocrinology (Baltimore, Md.) 20090702 10


The inability of the ss-cell to meet the demand for insulin brought about by insulin resistance leads to type 2 diabetes. In adults, ss-cell replication is one of the mechanisms thought to cause the expansion of ss-cell mass. Efforts to treat diabetes require knowledge of the pathways that drive facultative ss-cell proliferation in vivo. A robust physiological stimulus of ss-cell expansion is pregnancy and identifying the mechanisms underlying this stimulus may provide therapeutic leads for the  ...[more]

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