GLP-1 promotes mitochondrial metabolism in vascular smooth muscle cells by enhancing endoplasmic reticulum-mitochondria coupling
Author
dc.contributor.author
Morales, Pablo E.
Author
dc.contributor.author
Torres, Gloria
Author
dc.contributor.author
Sotomayor Flores, Cristian Alejandro
Author
dc.contributor.author
Peña Oyarzún, Daniel
Author
dc.contributor.author
Rivera Mejías, Pablo
Author
dc.contributor.author
Paredes, Felipe
Author
dc.contributor.author
Chiong Lay, Mario
Admission date
dc.date.accessioned
2018-12-20T15:10:56Z
Available date
dc.date.available
2018-12-20T15:10:56Z
Publication date
dc.date.issued
2014
Cita de ítem
dc.identifier.citation
Biochemical and Biophysical Research Communications, Volumen 446, Issue 1, 2018, Pages 410-416
Identifier
dc.identifier.issn
10902104
Identifier
dc.identifier.issn
0006291X
Identifier
dc.identifier.other
10.1016/j.bbrc.2014.03.004
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/158314
Abstract
dc.description.abstract
Incretin GLP-1 has important metabolic effects on several tissues, mainly through the regulation of glucose uptake and usage. One mechanism for increasing cell metabolism is modulating endoplasmic reticulum (ER)-mitochondria communication, as it allows for a more efficient transfer of Ca2+ into the mitochondria, thereby increasing activity. Control of glucose metabolism is essential for proper vascular smooth muscle cell (VSMC) function. GLP-1 has been shown to produce varied metabolic actions, but whether it regulates glucose metabolism in VSMC remains unknown. In this report, we show that GLP-1 increases mitochondrial activity in the aortic cell line A7r5 by increasing ER-mitochondria coupling. GLP-1 increases intracellular glucose and diminishes glucose uptake without altering glycogen content. ATP, mitochondrial potential and oxygen consumption increase at 3 h of GLP-1 treatment, paralleled by increased Ca2+ transfer from the ER to the mitochondria. Furthermore, GLP-1 increases lev