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Low extracellular magnesium does not impair glucose-stimulated insulin secretion

There is an increasing amount of clinical evidence that hypomagnesemia (serum Mg(2+) levels < 0.7 mmol/l) contributes to type 2 diabetes mellitus pathogenesis. Amongst other hypotheses, it has been suggested that Mg(2+) deficiency affects insulin secretion. The aim of this study was, therefore, t...

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Detalles Bibliográficos
Autores principales: Gommers, Lisanne M. M., Hill, Thomas G., Ashcroft, Frances M., de Baaij, Jeroen H. F.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6548430/
https://www.ncbi.nlm.nih.gov/pubmed/31163064
http://dx.doi.org/10.1371/journal.pone.0217925
Descripción
Sumario:There is an increasing amount of clinical evidence that hypomagnesemia (serum Mg(2+) levels < 0.7 mmol/l) contributes to type 2 diabetes mellitus pathogenesis. Amongst other hypotheses, it has been suggested that Mg(2+) deficiency affects insulin secretion. The aim of this study was, therefore, to investigate the acute effects of extracellular Mg(2+) on glucose-stimulated insulin secretion in primary mouse islets of Langerhans and the rat insulinoma INS-1 cell line. Here we show that acute lowering of extracellular Mg(2+) concentrations from 1.0 mM to 0.5 mM did not affect glucose-stimulated insulin secretion in islets or in insulin-secreting INS-1 cells. The expression of key genes in the insulin secretory pathway (e.g. Gck, Abcc8) was also unchanged in both experimental models. Knockdown of the most abundant Mg(2+) channel Trpm7 by siRNAs in INS-1 cells resulted in a 3-fold increase in insulin secretion at stimulatory glucose conditions compared to mock-transfected cells. Our data suggest that insulin secretion is not affected by acute lowering of extracellular Mg(2+) concentrations.