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Molecular pathways in non-alcoholic fatty liver disease

  • Datos identificativos

    Identificador: imarina:6387860
    Handle: https://hdl.handle.net/20.500.11797/imarina6387860
    Autores:
    Berlanga AGuiu-Jurado EPorras JAuguet T
    Resumen:
    Non-alcoholic fatty liver disease (NAFLD) is a clinicopathological change characterized by the accumulation of triglycerides in hepatocytes and has frequently been associated with obesity, type 2 diabetes mellitus, hyperlipidemia, and insulin resistance. It is an increasingly recognized condition that has become the most common liver disorder in developed countries, affecting over one-third of the population and is associated with increased cardiovascular- and liver-related mortality. NAFLD is a spectrum of disorders, beginning as simple steatosis. In about 15% of all NAFLD cases, simple steatosis can evolve into non-alcoholic steatohepatitis, a medley of inflammation, hepatocellular injury, and fibrosis, often resulting in cirrhosis and even hepatocellular cancer. However, the molecular mechanism underlying NAFLD progression is not completely understood. Its pathogenesis has often been interpreted by the double-hit hypothesis. The primary insult or the first hit includes lipid accumulation in the liver, followed by a second hit in which proinflammatory mediators induce inflammation, hepatocellular injury, and fibrosis. Nowadays, a more complex model suggests that fatty acids (FAs) and their metabolites may be the true lipotoxic agents that contribute to NAFLD progression; a multiple parallel hits hypothesis has also been suggested. In NAFLD patients, insulin resistance leads to hepatic steatosis via multiple mechanisms. Despite the excess hepatic accumulation of FAs in NAFLD, it has been described that not only de novo FA synthesis is increased, but FAs are also taken up from the serum. Furthermore, a decrease in mitochondrial FA oxidation and secretion of very-low-density lipoproteins has been reported. This review discusses the molecular mechanisms that underlie the

  • Otros:

    Autor según el artículo: Berlanga A; Guiu-Jurado E; Porras J; Auguet T
    Departamento: Medicina i Cirurgia
    Autor/es de la URV: Auguet Quintillà, Maria Teresa / BERLANGA BUSTOS, ALBA / GUIU JURADO, ESTHER / Porras Ledantes, Jose Antonio
    Palabras clave: Non-alcoholic fatty liver disease Molecular pathways Insulin resistance Fatty acid metabolism molecular pathways insulin resistance fatty acid metabolism
    Resumen: Non-alcoholic fatty liver disease (NAFLD) is a clinicopathological change characterized by the accumulation of triglycerides in hepatocytes and has frequently been associated with obesity, type 2 diabetes mellitus, hyperlipidemia, and insulin resistance. It is an increasingly recognized condition that has become the most common liver disorder in developed countries, affecting over one-third of the population and is associated with increased cardiovascular- and liver-related mortality. NAFLD is a spectrum of disorders, beginning as simple steatosis. In about 15% of all NAFLD cases, simple steatosis can evolve into non-alcoholic steatohepatitis, a medley of inflammation, hepatocellular injury, and fibrosis, often resulting in cirrhosis and even hepatocellular cancer. However, the molecular mechanism underlying NAFLD progression is not completely understood. Its pathogenesis has often been interpreted by the double-hit hypothesis. The primary insult or the first hit includes lipid accumulation in the liver, followed by a second hit in which proinflammatory mediators induce inflammation, hepatocellular injury, and fibrosis. Nowadays, a more complex model suggests that fatty acids (FAs) and their metabolites may be the true lipotoxic agents that contribute to NAFLD progression; a multiple parallel hits hypothesis has also been suggested. In NAFLD patients, insulin resistance leads to hepatic steatosis via multiple mechanisms. Despite the excess hepatic accumulation of FAs in NAFLD, it has been described that not only de novo FA synthesis is increased, but FAs are also taken up from the serum. Furthermore, a decrease in mitochondrial FA oxidation and secretion of very-low-density lipoproteins has been reported. This review discusses the molecular mechanisms that underlie the pathophysiological changes of hepatic lipid metabolism that contribute to NAFLD. © 2014 Berlanga et al.
    Áreas temáticas: Medicina iii Medicina i Gastroenterology & hepatology Gastroenterology
    Acceso a la licencia de uso: https://creativecommons.org/licenses/by/3.0/es/
    ISSN: 11787023
    Direcció de correo del autor: joseantonio.porras@urv.cat mariateresa.auguet@urv.cat
    Identificador del autor: 0000-0001-6418-1822 0000-0003-0396-6428
    Fecha de alta del registro: 2023-02-26
    Versión del articulo depositado: info:eu-repo/semantics/publishedVersion
    Referencia al articulo segun fuente origial: Clinical And Experimental Gastroenterology. 7 (1): 221-239
    Referencia de l'ítem segons les normes APA: Berlanga A; Guiu-Jurado E; Porras J; Auguet T (2014). Molecular pathways in non-alcoholic fatty liver disease. Clinical And Experimental Gastroenterology, 7(1), 221-239. DOI: 10.2147/CEG.S62831
    URL Documento de licencia: https://repositori.urv.cat/ca/proteccio-de-dades/
    Entidad: Universitat Rovira i Virgili
    Año de publicación de la revista: 2014
    Tipo de publicación: Journal Publications

  • Palabras clave:

    Gastroenterology,Gastroenterology & Hepatology
    Non-alcoholic fatty liver disease
    Molecular pathways
    Insulin resistance
    Fatty acid metabolism
    molecular pathways
    insulin resistance
    fatty acid metabolism
    Medicina iii
    Medicina i
    Gastroenterology & hepatology
    Gastroenterology

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