A study led by Manuel Vázquez Carrera, group leader at the Diabetes and Associated Metabolic Diseases Networking Biomedical Research Center (CIBERDEM) at the University of Barcelona, reveals advances in the understanding and treatment of liver fibrosis, a serious complication in the context of metabolic fatty liver disease, also known as MASLD (metabolic dysfunction–associated steatotic liver disease). This study concludes that activation of the PPARβ/δ-AMPK pathway is an effective strategy to slow the development of liver fibrosis . The paper, published in the journal Biomedicine & Pharmacotherapy , also involved the collaboration of the groups led by experts Ángela Maria Valverde, from CIBERDEM, and Walter Wahli, from the University of Lausanne.
The most common chronic liver disease Metabolic fatty liver disease (MASLD) integrates a set of liver conditions ranging from simple isolated fat deposition in the liver to severe inflammation of the organ known as metabolic steatohepatitis, which in some cases can progress to fibrosis. For now, liver fibrosis is the most relevant risk factor for predicting both liver disease-related mortality and overall mortality. MASLD is a global health issue, as it is the most common chronic liver disease, affecting 25% of the world's population.
Numerous studies have shown that this condition often coexists with type 2 diabetes (DM2). In fact, DM2 can accelerate the progression of MASLD by aggravating both hepatic and extrahepatic prob.