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Regulation of Glycosylphosphatidylinositol-Specific Phospholipase D Secretion from ßTC3 cells¹

Division of Endocrinology and Metabolism, Department of Medicine, Indiana University School of Medicine, and the Richard L. Roudebush Veterans Affairs Medical Center, Indianapolis, Indiana 46202; and the Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington, and the Seattle Veterans Affairs Medical Center (C.B.V.), Seattle, Washington 98108

Address all correspondence and requests for reprints to: Mark Deeg, M.D., Ph.D., Division of Endocrinology and Metabolism (111E), Roudebush Veterans Affairs Medical Center, 1481 West 10th Street, Indianapolis, Indiana 46202-2884. E-mail: deeg.mark{at}indianapolis.va.gov

Glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD) is abundant in mammalian serum, but the source of the circulating enzyme is unknown. Pancreatic islets have been reported to contain and secrete GPI-PLD. In this report we examined the regulation of GPI-PLD secretion from ßTC3 cells, a mouse insulinoma cell line. In the absence of glucose, phorbol myristic acid (0.1 µM) stimulated insulin secretion by 2.5-fold and GPI-PLD secretion by 2-fold. Carbachol (5 µM), glucagon-like peptide I-(7–36) amide (0.1 µM), and isobutylmethylxanthine (0.1 mM) had no significant effect on insulin or GPI-PLD secretion in the absence of glucose. Glucose (16.7 mM) stimulated both GPI-PLD and insulin secretion from ßTC3 cells by 55% and 235%, respectively. In addition, glucose potentiated the secretagogue effect of isobutylmethylxanthine, phorbol myristic acid, and glucagon-like peptide I on both insulin and GPI-PLD secretion. By immunohistochemistry and confocal microscopy, ßTC3 cells contain both insulin and GPI-PLD, which generally colocalized intracellularly. However, GPI-PLD secretion differed from insulin secretion by a higher rate of basal release (2.8% vs. 0.23%/h), a lower magnitude of response to secretagogues, and a more prolonged period of increased secretion. These results demonstrate that ßTC3 cells secrete GPI-PLD in response to insulin secretagogues and suggest that GPI-PLD may be secreted via the regulated pathway in these cells.

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