Metabolic Memory Of ß-cells Controls Insulin Secretion And Is Mediated By Camkii.


Autoria(s): Santos, Gustavo Jorge Dos; Ferreira, Sandra Mara; Ortis, Fernanda; Rezende, Luiz Fernando; Li, Chengyang; Naji, Ali; Carneiro, Everardo Magalhães; Kaestner, Klaus H; Boschero, Antonio Carlos
Contribuinte(s)

UNIVERSIDADE DE ESTADUAL DE CAMPINAS

Data(s)

01/07/2014

27/11/2015

27/11/2015

Resumo

Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) functions both in regulation of insulin secretion and neurotransmitter release through common downstream mediators. Therefore, we hypothesized that pancreatic ß-cells acquire and store the information contained in calcium pulses as a form of metabolic memory, just as neurons store cognitive information. To test this hypothesis, we developed a novel paradigm of pulsed exposure of ß-cells to intervals of high glucose, followed by a 24-h consolidation period to eliminate any acute metabolic effects. Strikingly, ß-cells exposed to this high-glucose pulse paradigm exhibited significantly stronger insulin secretion. This metabolic memory was entirely dependent on CaMKII. Metabolic memory was reflected on the protein level by increased expression of proteins involved in glucose sensing and Ca(2+)-dependent vesicle secretion, and by elevated levels of the key ß-cell transcription factor MAFA. In summary, like neurons, human and mouse ß-cells are able to acquire and retrieve information.

3

484-9

Identificador

Molecular Metabolism. v. 3, n. 4, p. 484-9, 2014-Jul.

2212-8778

10.1016/j.molmet.2014.03.011

http://www.ncbi.nlm.nih.gov/pubmed/24944908

http://repositorio.unicamp.br/jspui/handle/REPOSIP/201499

24944908

Idioma(s)

eng

Relação

Molecular Metabolism

Mol Metab

Direitos

aberto

Fonte

PubMed

Palavras-Chave #Camkii #Insulin Secretion #Metabolic Memory
Tipo

Artigo de periódico