Currently available antidiabetic treatments fail to halt, and may even exacerbate, pancreatic -cell exhaustion, a key feature of type 2 diabetes pathogenesis; thus, strategies to prevent, or reverse, -cell failure should be actively sought. The serine threonine kinase Akt has a key role in the regulation of -cell homeostasis; among Akt modulators, a central role is played by pleckstrin homology domain leucine-rich repeat protein phosphatase (PHLPP) family. Here, taking advantage of an in vitro model of chronic exposure to high glucose, we demonstrated that PHLPPs, particularly the second family member called PHLPP2, are implicated in the ability of pancreatic cells to deal with glucose toxicity.
View Article and Find Full Text PDFObjective: Two subtypes of angiotensin II (ATII) receptor have been defined on the basis of their differential pharmacological and biochemical properties: ATII-type1 receptors (AT(1)-R) and ATII-type2 receptors (AT(2)-R). It has been hypothesized that part of the protective effects on the cardiovascular system of AT(1)-R blockers is mediated by an ATII-mediated overstimulation of AT(2)-R. We hypothesized that the inhibition of AT(1)-R has a stronger impact on insulin-induced nitric oxide (NO) production than ATII-mediated overstimulation of AT(2)-R.
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