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Papers In Press, published online ahead of print May 27, 2006
Medicine, Washington University School of Medicine, Saint Louis, MO 63110
Corresponding Author: jturk{at}wustl.edu
Studies involving pharmacologic or molecular biologic manipulation of Group VIA Phospholipase A2 (iPLA2ß) activity in pancreatic islets and insulinoma cells suggest that iPLA2ß participates in insulin secretion. It has also been suggested that iPLA2ß is a housekeeping enzyme that regulates cell 2-lysophosphatidylcholine (LPC) levels and arachidonate incorporation into phosphatidylcholine (PC). We have generated iPLA2ß-null mice by homologous recombination and have reported that they exhibit reduced male fertility and defective motility of spermatozoa. Here we report that pancreatic islets from iPLA2ß-null mice have impaired insulin secretory responses to D-glucose and forskolin. Electrospray ionization mass spectrometric analyses indicate that the abundance of arachidonate-containing PC species of islets, brain, and other tissues from iPLA2ß-null mice is virtually identical to that of wild-type mice, and no iPLA2ß mRNA was observed in any tissue from iPLA2ß-null mice at any age. Despite the insulin secretory abnormalities of isolated islets, fasting and fed blood glucose concentrations of iPLA2ß-null and wild-type mice are essentially identical under normal circumstances, but iPLA2ß-null mice develop more severe hyperglycemia than wild-type mice after administration of multiple low doses of the ß-cell toxin streptozotocin, suggesting an impaired islet secretory reserve. A high-fat diet also induces more severe glucose intolerance in iPLA2ß-null mice than in wild-type mice, but PLA2ß-null mice have greater responsiveness to exogenous insulin than do wild-type mice fed a high fat diet. These and previous findings thus indicate that iPLA2ß-null mice exhibit phenotypic abnormalities in pancreatic islets in addition to testes and macrophages.
J. Biol. Chem, 10.1074/jbc.M600075200
Submitted on January 4, 2006
Accepted on May 19, 2006
Insulin secretory responses and phospholipid composition of pancreatic islets from mice that do not express group via phospholipase A2 and effects of metabolic stress on glucose homeostasis
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