Open AccessMechanism of Ethanol-Induced Insulin Secretion from INS-1 and INS-1E Tumor Cell Lines
Author(s) -
Roman Hafko,
Martina Orečná,
Zuzana Bačová,
Gabriela Kolláriková,
Igor Lacı́k,
Vladimír Štrbák
Publication year - 2009
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000257482
Subject(s) - secretion , mechanism (biology) , insulin , cell culture , ethanol , cancer research , chemistry , microbiology and biotechnology , endocrinology , medicine , biology , biochemistry , genetics , philosophy , epistemology
Alcohol causes reactive hypoglycemia by attenuating the release of counter regulatory hormones, redistribution of pancreatic blood flow and direct stimulation of insulin secretion. Objective of this study was characterization of ethanol-induced insulin secretion. Signaling of ethanol- and glucose-induced insulin release from INS-1 and INS-1E cells was compared. Both cell lines responded similarly to all experimental interventions. In contrast to glucose, ethanol-induced insulin secretion was not hindered in calcium depleted medium or by addition of 10 microM BAPTA/AM (intracellular chelator). Inhibitor of protein kinase C Bisindolylmaleimide (3 microM) abolished glucose- but not ethanol-induced insulin secretion. Tetanus toxin (20 nM), inhibitor of SNARE proteins complex formation, blocked ethanol-induced insulin secretion. Both 5 mM N-ethylamaleimide and 10 microM ZnCl(2) (inhibitor of protein tyrosine phosphatases), which block disassembly of SNARE complexes and their further participation in exocytosis, increased basal insulin secretion. In contrast to glucose, already high insulin secretion was further increased after ethanol stimulation in either treatment.