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Pubmed ID: 19135240
Publication Date: 2009/01/08

Regulation of PKD by the MAPK p38delta in insulin secretion and glucose homeostasis.


Dysfunction and loss of insulin-producing pancreatic beta cells represent hallmarks of diabetes mellitus. Here, we show that mice lacking the mitogen-activated protein kinase (MAPK) p38delta display improved glucose tolerance due to enhanced insulin secretion from pancreatic beta cells. Deletion of p38delta results in pronounced activation of protein kinase D (PKD), the latter of which we have identified as a pivotal regulator of stimulated insulin exocytosis. p38delta catalyzes an inhibitory phosphorylation of PKD1, thereby attenuating stimulated insulin secretion. In addition, p38delta null mice are protected against high-fat-feeding-induced insulin resistance and oxidative stress-mediated beta cell failure. Inhibition of PKD1 reverses enhanced insulin secretion from p38delta-deficient islets and glucose tolerance in p38delta null mice as well as their susceptibility to oxidative stress. In conclusion, the p38delta-PKD pathway integrates regulation of the insulin secretory capacity and survival of pancreatic beta cells, pointing to a pivotal role for this pathway in the development of overt diabetes mellitus.
Authors: Sumara Grzegorz , Formentini Ivan , Collins Stephan , Sumara Izabela , Windak Renata , Bodenmiller Bernd , Ramracheya Reshma , Caille Dorothée , Jiang Huiping , Platt Kenneth A , Meda Paolo , Aebersold Rudolf , Rorsman Patrik , Ricci Romeo ,

Reference:

  1. ncbi.nlm.nih.gov. [Last access 2009/01/08].

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