Literature DB >> 3004919

Rapid glucose-dependent increases in phosphatidic acid and phosphoinositides in rat pancreatic islets.

R V Farese, P E DiMarco, D E Barnes, M A Sabir, R E Larson, J S Davis, A D Morrison.   

Abstract

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.

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Year:  1986        PMID: 3004919     DOI: 10.1210/endo-118-4-1498

Source DB:  PubMed          Journal:  Endocrinology        ISSN: 0013-7227            Impact factor:   4.736


  12 in total

1.  Stimulation of insulin release by phospholipase D. A potential role for endogenous phosphatidic acid in pancreatic islet function.

Authors:  S A Metz; M Dunlop
Journal:  Biochem J       Date:  1990-09-01       Impact factor: 3.857

2.  Diacylglycerol synthesis de novo from glucose by pancreatic islets isolated from rats and humans.

Authors:  B A Wolf; R A Easom; M L McDaniel; J Turk
Journal:  J Clin Invest       Date:  1990-02       Impact factor: 14.808

3.  Palmitate dependence of insulin secretion, "de novo" phospholipid synthesis and 45Ca2+-turnover in glucose stimulated rat islets.

Authors:  E Vara; O Fernández-Martín; C García; J Tamarit-Rodríguez
Journal:  Diabetologia       Date:  1988-09       Impact factor: 10.122

4.  Protein kinase C is activated in glomeruli from streptozotocin diabetic rats. Possible mediation by glucose.

Authors:  P A Craven; F R DeRubertis
Journal:  J Clin Invest       Date:  1989-05       Impact factor: 14.808

5.  Glucose and carbachol generate 1,2-diacylglycerols by different mechanisms in pancreatic islets.

Authors:  B Peter-Riesch; M Fathi; W Schlegel; C B Wollheim
Journal:  J Clin Invest       Date:  1988-04       Impact factor: 14.808

6.  Activation of protein kinase C by elevation of glucose concentration: proposal for a mechanism in the development of diabetic vascular complications.

Authors:  T S Lee; K A Saltsman; H Ohashi; G L King
Journal:  Proc Natl Acad Sci U S A       Date:  1989-07       Impact factor: 11.205

7.  Lipid composition of glucose-stimulated pancreatic islets and insulin-secreting tumor cells.

Authors:  I Rustenbeck; A Matthies; S Lenzen
Journal:  Lipids       Date:  1994-10       Impact factor: 1.880

8.  Activators of protein kinase C depolarize insulin-secreting cells by closing K+ channels.

Authors:  C B Wollheim; M J Dunne; B Peter-Riesch; R Bruzzone; T Pozzan; O H Petersen
Journal:  EMBO J       Date:  1988-08       Impact factor: 11.598

9.  Fiber-dependent and -independent toxicity of islet amyloid polypeptide.

Authors:  Diana E Schlamadinger; Andrew D Miranker
Journal:  Biophys J       Date:  2014-12-02       Impact factor: 3.699

Review 10.  Roles of Sphingolipid Metabolism in Pancreatic β Cell Dysfunction Induced by Lipotoxicity.

Authors:  Julien Véret; Lara Bellini; Paola Giussani; Carl Ng; Christophe Magnan; Hervé Le Stunff
Journal:  J Clin Med       Date:  2014-06-20       Impact factor: 4.241

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