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Articles by P. E Scherer
Total Records ( 2 ) for P. E Scherer
  A Villasenor , Z. V Wang , L. B Rivera , O Ocal , I. W Asterholm , P. E Scherer , R. A Brekken , O Cleaver and T. M. Wilkie
  Alethia Villasenor, Zhao V. Wang, Lee B. Rivera, Ozhan Ocal, Ingrid Wernstedt Asterholm, Philipp E. Scherer, Rolf A. Brekken, Ondine Cleaver, and Thomas M. Wilkie

Diabetes is characterized by the loss, or gradual dysfunction, of insulin-producing pancreatic β-cells. Although β-cells can replicate in younger adults, the available diabetes therapies do not specifically target β-cell regeneration. Novel approaches are needed to discover new therapeutics and to understand the contributions of endocrine progenitors and β-cell regeneration during islet expansion. Here, we show that the regulators of G protein signaling Rgs16 and Rgs8 are expressed in pancreatic progenitor and endocrine cells during development, then extinguished in adults, but reactivated in models of both type 1 and type 2 diabetes. Exendin-4, a glucagon-like peptide 1 (Glp-1)/incretin mimetic that stimulates β-cell expansion, insulin secretion and normalization of blood glucose levels in diabetics, also promoted re-expression of Rgs16::GFP within a few days in pancreatic ductal-associated cells and islet β-cells. These findings show that Rgs16::GFP and Rgs8::GFP are novel and early reporters of G protein-coupled receptor (GPCR)-stimulated β-cell expansion after therapeutic treatment and in diabetes models. Rgs16 and Rgs8 are likely to control aspects of islet progenitor cell activation, differentiation and β-cell expansion in embryos and metabolically stressed adults.

  S Rieck , P White , J Schug , A. J Fox , O Smirnova , N Gao , R. K Gupta , Z. V Wang , P. E Scherer , M. P Keller , A. D Attie and K. H. Kaestner
 

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 treatment of type 2 diabetes. The peak in ß-cell proliferation during pregnancy occurs on d 14.5 of gestation in mice. Using advanced genomic approaches, we globally characterize the gene expression signature of pancreatic islets on d 14.5 of gestation during pregnancy. We identify a total of 1907 genes as differentially expressed in the islet during pregnancy. 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 ß-cell mass.

 
 
 
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