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The role of palmitate in CaMKII-dependent metabolic memory formation

Grant number: 12/18818-7
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): December 01, 2012
Effective date (End): November 30, 2013
Field of knowledge:Biological Sciences - Physiology
Principal Investigator:Luiz Fernando de Rezende
Grantee:Ariane Cristina de Almeida Dias
Home Institution: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil
Associated research grant:11/09012-6 - Molecular mechanisms involved in the dysfunction and death of pancreatic beta cells in Diabetes Mellitus: strategies for the prevention of islet dysfunction and for islet mass recuperation in different cellular and animal models, AP.TEM

Abstract

Calcium ion (Ca2+) acts as a cell signaling mediator in eukaryotic cells, controlling many functions such as proliferation, gene expression, apoptosis and exocytosis.Calcium-calmodulin-dependent Kinase II (CaMKII), is a multifunctional protein which is intrinsically inhibited in low calcium environments thanks to its auto-inhibitory properties.After a peak in intracellular calcium levels, there is an increase in formation of calcium-calmodulin complex, which then binds to CaMKII exposing its catalytic site. This mechanism allows CaMKII to maintain its auto-phosphorylation and activity independently of the calcium-CaM complex, thus extending its actions and the effects initially generated by calcium.In this context, palmitate is a long-chain saturated fatty acid highly prevalent in mammals, and in particular, in pancreatic islets ²-cells, such as MIN6 cell lines. In MIN6 cells, palmitate hinders glucose-induced CaMKII phosphorylation while increasing glucose-stimulated insulin secretion (GSIS).Given that, the aim of the present project is to investigate the possibility that palmitate is involved in the formation of a long-term action of calcium effects over GSIS through CaMKII.