Home Health A Spanish study finds a key to non-alcoholic fatty liver disease

A Spanish study finds a key to non-alcoholic fatty liver disease


Researchers from the CiMUS Molecular Metabolism group, from the University of Santiago de Compostela (USC), and the CIBER of Obesity and Nutrition (CIBEROBN) have discovered a new target involved in the development of non-alcoholic fatty liver disease for which , for now, there is no treatment.

This is the ATG3 protein, which is present at high levels in the liver of patients with this pathology, and that, by inhibiting it, improves fat metabolism by increasing mitochondrial function while decreasing the accumulation of fat and damage to this organ.

Various studies have shown that this disease is suffered by one in four people in the world today, which means almost two billion people affected. In the initial phases, this disease begins with the accumulation of fat in the liver (with 5% fat is enough to classify the liver as fatty), and can progress to more serious diseases, including steatohepatitis nonalcoholic, cirrhosis and cancer. The increased prevalence of NAFLD in both developed and underdeveloped countries has made it the most common cause of liver transplants.

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To carry out this study, published in the scientific journal ‘Journal of Hepatology‘, a cohort of 117 human patients was used, 85 with different stages of fatty liver disease and 32 patients with healthy liver.

“The use of human samples from up to 117 patients is a strong point of the work because helps verify that our discovery in preclinical models has validity and can potentially be applied to human beings, and, in addition, it involves a tremendous coordination effort by specialists from three national hospitals: Santa Cristina University Hospital (Madrid), Marqués de Valdecilla University Hospital (Santander) and Virgen del Rocío University Hospital (Sevilla)”, explain the CiMUS researchers involved in this work.

The results showed that patients with NAFLD have elevated levels of ATG3 in the liver, a protein which until now was known for its role in autophagy, a process by which the cell destroys useless cellular material. The same was observed in the liver of mice fed a high-fat diet, as well as in human liver cells.

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“It has been possible to demonstrate a mechanism for reversing the accumulation of fat in the liver, turning ATG3 into a possible therapeutic target against non-alcoholic fatty liver”, point out the main authors of the research, Natália Lima, Marcos Fernandez Fondevila and Eva Nóvoa. This happens because ATG3 inhibition causes an increase in Sirtuin 1 (SIRT1) and Carnitine Palmitoyltransferase 1a (CPT1a), two proteins involved in mitochondrial function.

This research is the result of the work of researchers Natalia da Silva Lima, Marcos Fernandez Fondevila and Eva Nóvoa Deaño of the CiMUS Molecular Metabolism group, coordinated by Dr. Rubén Nogueiras Pozo and in which CiMUS research teams (Dr. Miguel López and Dr. Carlos Diéguez) have participated, as well as groups from the University of the Basque Country, CIC bioGUNE ( Bilbao), the European Genomic Institute for Diabetes (France), the CNIC (Madrid), the University of Coimbra (Portugal), the University of Lübeck (Germany), the Santa Cristina University Hospital (Madrid), the August Pi iSunyer Biomedical Research Institute ( Barcelona), as well as CIBEREHD and CIBERDEM.

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