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Articles in PresS, published online ahead of print July 30, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00474.2001
Submitted on October 22, 2001
Accepted on June 19, 2002
and nPKC isoforms
1 Obesity Research Center, Department of Medicine, Boston University School of Medicine, Boston, MA, USA
2 Immunology Division, Children's Hospital of Philadelphia, University of Pennsylvania, Philadelphia, PA, USA
* To whom correspondence should be addressed. E-mail: gyaney{at}bu.edu.
Culturing clonal ß-cells (HIT-T15) overnight in the presence of phorbol ester (PMA) enhanced insulin secretion while causing downregulation of some protein kinase C (PKC) isoforms and most PKC activity. We show here that this enhanced secretion required the retention of PMA in the cell. Hence, it could not be due to long-lived phosphorylation of cellular substrates by the isoforms that were downregulated, namely PKC-, ßII and 
, but could be due to the continued activation of the two remaining diacylglycerol sensitive isoforms, 
and µ. The enhanced secretion did not involve changes in glucose metabolism, cell membrane potential or intracellular Ca2+ handling, suggesting a distal effect. PMA washout caused the loss of the enhanced response, but secretion was then stimulated by acute re-addition of PMA or bombesin. The magnitude of this re-stimulation appeared dependent on the mass of PKC- which was rapidly resynthesized during PMA washout. Therefore, stimulation of insulin secretion by PMA, and presumably by endogenous diacylglycerol, involves the activation of PKC isoforms and/or µ, and also PKC-.
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