New factors involved in the non-alcoholic fatty liver disease
A new study identified new factors involved in the development of the non-alcoholic fatty liver disease, the most common liver alteration among people. The study was published in the journal Molecular Metabolism, and is led by the team of the lecturer Manuel Vázquez Carrera, from the Pharmacology and Pharmacognosy Unit of the Faculty of Pharmacy and Food Sciences and the Institute of Biomedicine (IBUB) of the UB, and the Diabetes and Associated Metabolic Diseases Networking Biomedical Research Centre (CIBERDEM).
A new study identified new factors involved in the development of the non-alcoholic fatty liver disease, the most common liver alteration among people. The study was published in the journal Molecular Metabolism, and is led by the team of the lecturer Manuel Vázquez Carrera, from the Pharmacology and Pharmacognosy Unit of the Faculty of Pharmacy and Food Sciences and the Institute of Biomedicine (IBUB) of the UB, and the Diabetes and Associated Metabolic Diseases Networking Biomedical Research Centre (CIBERDEM).
Non-alcoholic fatty liver disease is distinguished for the presence of the deposit of fat in the liver, in patients who do not drink alcohol. It includes injuries ranging from an excessive accumulation of triglycerides in the liver (hepatic steatosis) to the non-alcoholic steatohepatitis, which sometimes can evolve up to an hepatic cirrhosis.
In the study, researchers proved the receptor of low-density lipoproteins (VLDLR) ─a distinguished modulator in the development of hepatic steatosis ─ is regulated by the PPARβ/δ receptor and the FGF21 hormone (fibroblast growth factor 21).
Using cell and animal models, the study reveals that a PPARβ/δ and FGF21 deficency favour the increase of VLDLR levels, and therefore, the development of hepatic steatosis. Furthermore, hepatic biopsies in patients with hepatic steatosis showed an increase of VLDLR and a reduction of PPARβ/δ activity and levels. Therefore, everything points out that the PPARβ/δ and FGF21 modulation could open new therapeutic strategies to treat hepatic steatosis through the regulation of VLDLR levels.
The following experts have also participated in the study: Francesc Villarroya and Tània Quesada-López, from the Faculty of Biology and IBUB, and the Physiopathology of Obesity and Nutrition Networking Biomedical Research Centre (CIBERobn), Ángela M. Valverde, Joan Carles Escolà-Gil and Francisco Blanco-Vaca (CIBERDEM), Walter Wahli (University of Lausanne, Switzerland) and Reza Zali (Shahid Beheshti University, Iran), among others.