A Spanish study led by Federico Mayor and Cristina Murga, researchers of the Center for Biomedical Research in Network for Cardiovascular Diseases (CIBERCV) at the Autonomous University of Madrid, has shown that the levels of GRK2 protein are increased in the liver of patients with non-alcoholic fatty liver.
Researchers have used genetically modified mice in the gene of GRK2, which show partially reduced levels of this protein. The results showed that genetic reduction of GRK2 protects these animals against the development of steatohepatitis after feeding them with a high-fat diet that causes this pathology.
“We have observed that the reduction in the levels of GRK2 in mice decreases the accumulation of fat in the liver, reduces inflammation in this tissue and improves the cellular response to this diet“, explains Marta Cruces-Sande, first author of the work and researcher of the CIBERCV in the UAM.
The results, published in the journal BBA Molecular Basis of Disease, are the result of collaboration between groups of several Biomedical Research Centers in the Network (CIBEREHD, CIBERDEM and CIBERER) and the Sanitary Research Institute La Princesa, among other institutions.
“These advances identify GRK2 protein as a possible therapeutic target in the treatment of fatty liver disease, steatohepatitis and other pathologies related to the metabolic syndrome,” the researchers conclude.
The accumulation of fat in the liver is the most common cause of chronic liver disease in the world, above that caused by alcohol or hepatitis C virus, and is commonly consequence of sedentary lifestyle and Western diet.
“Fatty liver disease can be aggravated by the development of liver inflammation in non-alcoholic steatohepatitis, which causes significant pathological changes, increases the risk of suffering from cirrhosis or liver cancer, and is associated with cardiovascular diseases,” says Cristina Murga.