| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Endocrinology, Vol 118, 1498-1503, Copyright © 1986 by Endocrine Society
ARTICLES |
RV Farese, PE DiMarco, DE Barnes, MA Sabir, RE Larson, JS Davis and AD Morrison
Glucose effects on islet phospholipids were examined during direct incubation or after 3 days of 32P prelabeling in primary culture. In both cases, glucose increased the 32P content of phosphatidic acid (PA), phosphatidylinositol (PI), and polyphosphoinositides (PPI). Glucose-induced increases in PA, PI, and PPI in the culture-prelabeling experiments were evident within 1 min, dose related, and reflective of increases in phospholipid mass, which was confirmed in direct incubations by measurement of PI phosphorus. Thus, in addition to increasing PI-PPI hydrolysis, glucose increases de novo phospholipid synthesis in pancreatic islets. The latter may result from enhanced glycolysis and substrate availability for PA-PI-PPI synthesis, since glyceraldehyde and pyruvic acid also increased PI levels. Our findings raise the possibility that increases in PA, PI, and PPI synthesis could serve as a mechanism to enhance the generation of intracellular mediators, which are purported to regulate insulin secretion.
This article has been cited by other articles:
![]() |
Y. Q. Liu, J. A. Moibi, and J. L. Leahy Chronic High Glucose Lowers Pyruvate Dehydrogenase Activity in Islets through Enhanced Production of Long Chain Acyl-CoA: PREVENTION OF IMPAIRED GLUCOSE OXIDATION BY ENHANCED PYRUVATE RECYCLING THROUGH THE MALATE-PYRUVATE SHUTTLE J. Biol. Chem., February 27, 2004; 279(9): 7470 - 7475. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Prentki, E. Joly, W. El-Assaad, and R. Roduit Malonyl-CoA Signaling, Lipid Partitioning, and Glucolipotoxicity: Role in {beta}-Cell Adaptation and Failure in the Etiology of Diabetes Diabetes, December 1, 2002; 51(90003): S405 - 413. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Gilon and J.-C. Henquin Mechanisms and Physiological Significance of the Cholinergic Control of Pancreatic {beta}-Cell Function Endocr. Rev., October 1, 2001; 22(5): 565 - 604. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. C. Yaney, H. M. Korchak, and B. E. Corkey Long-Chain Acyl CoA Regulation of Protein Kinase C and Fatty Acid Potentiation of Glucose-Stimulated Insulin Secretion in Clonal {beta}-Cells Endocrinology, June 1, 2000; 141(6): 1989 - 1998. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. E. Corkey, J. T. Deeney, G. C. Yaney, K. Tornheim, and M. Prentki The Role of Long-Chain Fatty Acyl-CoA Esters in {beta}-Cell Signal Transduction J. Nutr., February 1, 2000; 130(2): 299 - 299. [Abstract] [Full Text] |
||||
![]() |
H. Ishihara, Y. Shibasaki, N. Kizuki, H. Katagiri, Y. Yazaki, T. Asano, and Y. Oka Cloning of cDNAs Encoding Two Isoforms of 68-kDa Type I Phosphatidylinositol4-phosphate 5-Kinase J. Biol. Chem., September 27, 1996; 271(39): 23611 - 23614. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |