G protein-coupled receptor kinase 2 regulates: The development of non-alcoholic fatty liver disease

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Campo DC	Valor	Lengua/Idioma
dc.contributor.author	Cruces-Sande, Marta	es_ES
dc.contributor.author	Vila-Bedmar, Rocío	es_ES
dc.contributor.author	Lucas, Elisa	es_ES
dc.contributor.author	González-Rodríguez, Águeda	es_ES
dc.contributor.author	Valverde, Ángela M.	es_ES
dc.contributor.author	Mayor Menéndez, Federico	es_ES
dc.contributor.author	Murga, Cristina	es_ES
dc.date.accessioned	2015-11-23T14:48:20Z	-
dc.date.available	2015-11-23T14:48:20Z	-
dc.date.issued	2014	-
dc.identifier.citation	XXXVII Congreso SEBBM (2014)	es_ES
dc.identifier.uri	http://hdl.handle.net/10261/125552	-
dc.description	Resumen del póster presentado al XXXVII Congreso de la Sociedad Española de Bioquímica y Biología Molecular, celebrado en Granada del 9 al 12 de septiembre de 2014.-- et al.	es_ES
dc.description.abstract	[Background]: Insulin resistance (IR) and obesity are major health problems and important risk factors for the development of non-alcoholic fatty liver disease (NAFLD), a disease spectrum that includes hepatic steatosis, non-alcoholic steatohepatitis (NASH), fibrosis, and cirrhosis. G proteincoupled receptor kinase 2 (GRK2), fi rst identifi ed as a G protein-coupled receptor regulator, has been recently described to play a relevant role in IR and obesity in vivo. GRK2 hemizygous (GRK2+/-) mice are protected against high fat diet (HFD)-induced systemic and hepatic insulin resistance and obesity. However, the effect of GRK2 in the development of HFD-induced NAFLD has not been studied. [Materials and methods]: Given the lack of a potent and specific GRK2 inhibitor, we used a global tamoxifen (Tx)-inducible murine model in which GRK2 levels are decreased once HFD-induced IR has been established. Also, a long term chronic state of IR and obesity was triggered by feeding wild type (WT) and GRK2+/- mice a 32 week-long HFD. To discriminate the effects of the differential body weight gain, we fed mice with a methionine-choline defi cient diet (MCD), which induces NAFLD independently of fat mass accretion. [Results]: Systemic insulin sensitivity was preserved after decreasing GRK2 levels in the middle of a high fat feeding using tamoxifen, and accordingly enhanced insulin signaling was observed in the liver of HFD-fed Tx-induced GRK2-/- mice. Moreover, hepatic steatosis, a hallmark of NAFLD, was decreased in these mice. Also, different signs of infl ammation present in WT mice were absent in Tx-induced GRK2-/- animals. Nevertheless, after a long term HFD we found no differences in steatosis between WT and GRK2+/- mice, despite the decrease in body weight gain and liver weight. Finally, we found an increase in GRK2 protein levels in the liver of mice fed a MCD, a well established model of NASH, similar to what is detected during HFD feeding in WT animals, and we are further characterizing this model. [Conclusion]: Taken together, these results suggest a role for GRK2 in the establishment and development of NAFLD.	es_ES
dc.language.iso	eng	es_ES
dc.publisher	Sociedad Española de Bioquímica y Biología Molecular	es_ES
dc.rights	closedAccess	es_ES
dc.title	G protein-coupled receptor kinase 2 regulates: The development of non-alcoholic fatty liver disease	es_ES
dc.type	póster de congreso	es_ES
dc.description.peerreviewed	Peer reviewed	es_ES
dc.relation.csic	Sí	es_ES
dc.type.coar	http://purl.org/coar/resource_type/c_6670	es_ES
item.openairetype	póster de congreso	-
item.languageiso639-1	en	-
item.fulltext	No Fulltext	-
item.grantfulltext	none	-
item.cerifentitytype	Publications	-
item.openairecristype	http://purl.org/coar/resource_type/c_18cf	-
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