alexa Non-Alcoholic Fatty Steatohepatitis an Inflammatory Disorder Beyond the Liver
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Review Article

Non-Alcoholic Fatty Steatohepatitis an Inflammatory Disorder Beyond the Liver

Sergio Cerpa-Cruz¹, Verónica González-Díaz¹, Gloria Martínez-Bonilla¹, Sergio Gutiérrez-Ureña¹, Elsa Rodríguez-Cortés¹, Lizbeth A. Garcia- Espinosa¹, Miguel A Martínez-Valles¹, J Antonio Velarde-Ruiz-Velazco²
1Rheumatology and Immunology Department, Hospital Civil de Guadalajara “Fray Antonio Alcalde”, Guadalajara, Jalisco, México
2Gastroenterology and Hepatology Department, Hospital Civil de Guadalajara “Fray Antonio Alcalde”, Guadalajara, Jalisco, México
Corresponding Author : Sergio Cerpa-Cruz
Rheumatology and Immunology Department
Hospital Civil de Guadalajara “Fray Antonio Alcalde”
Guadalajara, Jalisco, México
E-mail: [email protected]
Received: June 24, 2013; Accepted: August 14, 2013; Published: August 21, 2013
Citation: Cerpa-Cruz S, González-Díaz V, Martínez-Bonilla G, Gutiérrez-Ureña S, Rodríguez-Cortés E, et al. (2013) Non-alcoholic Fatty Steatohepatitisan Inflammatory Disorder Beyond the Liver. J Clin Cell Immunol 4:159. doi:10.4172/2155-9899.1000159
Copyright: © 2013 Cerpa-Cruz S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Non-alcoholic fatty liver disease (NAFLD) has emerged as the most prevalent chronic liver disease in the United States. Non-alcoholic steatohepatitis (NASH), the most severe form of NAFLD, has an increased risk for progression to cirrhosis and associated comorbidities such as cardiovascular disease. Metabolic syndrome (MS) including insulin resistance and obesity is central to the development of NASH. It is now estimated to affect 30% of adults and about 10% of children in the U.S. Hispanics are disproportionably affected with not only higher rates of NAFLD but also more severe disease. Emerging data indicate that NASH progression results from parallel events originating from the liver as well as from the adipose tissue, the gut and the gastrointestinal tract. Thus, dysfunction of the adipose tissue through enhanced flow of free fatty acids and release of adipocytokines, and alterations in the gut microbiome generate pro-inflammatory signals that increase NASH progression. Additional ‘extrahepatic hits’ include dietary factors and gastrointestinal hormones. Within the liver, hepatocyte apoptosis, ER stress and oxidative stress are key contributors to hepatocellular injury. In addition, lipotoxic mediators and danger signals activate Kupffer cells which initiate and perpetuate the inflammatory response by releasing inflammatory mediators that contribute to inflammatory cell recruitment and development of fibrosis. Inflammatory and fibrogenic mediators include chemokines, the inflammasome and activation of pattern-recognition receptors.

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