Searchable abstracts of presentations at key conferences in endocrinology

ea0073aep267 | Diabetes, Obesity, Metabolism and Nutrition | ECE2021

p63 induces the fibrosis in NASH

Fondevila Marcos F , Novoa Eva , Uxía Fernández , María J González-Rellán , Lima Natalia , Begoña Porteiro , Juan Cuñarro , Tovar Sulay , Fidalgo Miguel , Martinez-Chantar Maria Luz , Sabio Guadalupe , Marcos Miguel , Lopez Miguel , Dieguez Carlos , Rubén Nogueiras

p53 family controls several metabolic and cellular functions. The p63 member regulates lipid metabolism in hepatocytes and contributes to the development of liver steatosis. Here we show that p63 plays an important role in liver fibrosis. P63 is upregulated in patients with NASH, correlating positively with fibrosis score and collagen 1a1 expression. P63 expression is also increased in different animal models of diet-induced NASH and chemically induced liver fibrosis. Mice wit...

ea0073oc7.4 | Oral Communications 7: Diabetes, Obesity, Metabolism and Nutrition | ECE2021

Liver GPR55 regulates NAFLD progression from steatosis to fibrosis

Fernández Uxía , Fernández Fondevila Marcos , González Rellán María Jesús , Da Silva Lima Natalia , Buque Xabier , González Rodríguez Marta , Delgado Teresa , Varela Rey Marta V , Eva Novoa , Tojo Marta , Marta Miguel , Diéguez Carlos , Diéguez Miguel , DiéguezMaría Luísa , Arrese Marco , García-Monzón Carmelo , Mato Jose , Aspichueta Jose , Nogueiras Rubén

Background and aimsG protein-coupled receptor 55 (GPR55) is a putative cannabinoid receptor, and l-α-lysophosphatidylinositol (LPI) is its only known endogenous ligand. Although GPR55 has been linked to energy homeostasis in different organs, its specific role in lipid metabolism in the liver and its contribution to the pathophysiology of non-alcoholic fatty liver disease (NAFLD) remains unknown.MethodWe...