The function of β-cells is regulated by nutrient uptake and metabolism. The cells" metabolic state can be expressed as concentration ratios of AMP, ADP and ATP. Relative changes in these ratios regulate insulin release. An increase in the intracellular ATP concentration causes closure of K(ATP) channels and cell membrane depolarization, which triggers stimulus-secretion coupling (SSC). In addition to K(ATP) channels, the AMP-dependent protein kinase (AMPK), a major cellular fuel sensor in a variety of cells and tissues, also affects insulin secretion and β-cell survival. In a previous study we found that the widely used AMPK inhibitor compound C retards proliferation and induces apoptosis in the rat β-cell line INS-1E. We therefore tested the effects of AMPK activators (AICAR and metformin), and compound C on AMPK phosphorylation, insulin secretion, K(ATP) channel currents, cell membrane potential, intracellular calcium concentration, apoptosis and cell cycle distribution of INS-1E cells under standard cell culture conditions (11 mM glucose).
Useful keywords (using NLM MeSH Indexing)
AMP-Activated Protein Kinases/chemistry*
AMP-Activated Protein Kinases/metabolism
Cell Line, Tumor
Cell Proliferation/drug effects
Membrane Potentials/drug effects
Find related publications in this database (Keywords)AMP kinase