Role of glucose metabolism and phosphoinositide hydrolysis in glucose-induced sensitization/desensitization of insulin secretion from mouse pancreatic islets
Author:
Publisher
Wiley
Subject
Physiology
Link
http://onlinelibrary.wiley.com/wol1/doi/10.1111/j.1748-1716.1995.tb09887.x/fullpdf
Reference39 articles.
1. The pentose cycle and insulin release in mouse pancreatic islets;Ashcroft;Biochem J,1972
2. Lack of glucose-induced priming of insulin release in the perfused mouse pancreas;Berglund;J Endocrinol,1987
3. Significance of the calcium content of mouse β cells in the preservation of glucose-induced insulin release during culture;Bergsten;J Endocrinol,1987
4. Characteristics of desensitization of insulin secretion in fully in vitro systems;Bolaffi;Endocrinology,1988
5. The importance of Ca2+ for glucose-induced priming in pancreatic islets;Chalmers;Biochim Biophys Acta,1989
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1. Glibenclamide inhibits islet carnitine palmitoyltransferase 1 activity, leading to PKC-dependent insulin exocytosis;American Journal of Physiology-Endocrinology and Metabolism;2003-08
2. Pancreatic islet insulin secretion and metabolism in adult rats malnourished during neonatal life;British Journal of Nutrition;2002-02
3. L-arginine stimulation of glucose-induced insulin secretion through membrane depolarization and independent of nitric oxide;European Journal of Endocrinology;1999-01-01
4. Inhibition of glucose-induced insulin secretion by the diacylglycerol lipase inhibitor RHC 80267 and the phospholipase A2 inhibitor ACA through stimulation of K+ permeability without diminution by exogenous arachidonic acid;Biochemical Pharmacology;1997-04
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