title: Proteomic and genomic studies of non-alcoholic fatty liver disease--clues in the pathogenesis.
abstract: Non-alcoholic fatty liver disease (NAFLD) is a widely prevalent hepatic disorder that covers wide spectrum of liver pathology. NAFLD is strongly associated with liver inflammation, metabolic hyperlipidaemia and insulin resistance. Frequently, NAFLD has been considered as the hepatic manifestation of metabolic syndrome. The pathophysiology of NAFLD has not been fully elucidated. Some patients can remain in the stage of simple steatosis, which generally is a benign condition; whereas others can develop liver inflammation and progress into non-alcoholic steatohepatitis, fibrosis, cirrhosis and hepatocellular carcinoma. The mechanism behind the progression is still not fully understood. Much ongoing proteomic researches have focused on discovering the unbiased circulating biochemical markers to allow early detection and treatment of NAFLD. Comprehensive genomic studies have also begun to provide new insights into the gene polymorphism to understand patient-disease variations. Therefore, NAFLD is considered a complex and mutifactorial disease phenotype resulting from environmental exposures acting on a susceptible polygenic background. This paper reviewed the current status of proteomic and genomic studies that have contributed to the understanding of NAFLD pathogenesis. For proteomics section, this review highlighted functional proteins that involved in: (1) transportation; (2) metabolic pathway; (3) acute phase reaction; (4) anti-inflammatory; (5) extracellular matrix; and (6) immune system. In the genomic studies, this review will discuss genes which involved in: (1) lipolysis; (2) adipokines; and (3) cytokines production.
authors.affiliation: Jun Wei Lim, John Dillon, Michael Miller, Department of Gastroenterology, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, United Kingdom.
authors.forename: Jun Wei
authors.initials: JW
authors.lastname: Lim
authors.affiliation: Jun Wei Lim, John Dillon, Michael Miller, Department of Gastroenterology, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, United Kingdom.
authors.forename: John
authors.initials: J
authors.lastname: Dillon
authors.affiliation: Jun Wei Lim, John Dillon, Michael Miller, Department of Gastroenterology, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, United Kingdom.
authors.forename: Michael
authors.initials: M
authors.lastname: Miller
mesh_terms: D000818:Animals; D018450:Disease Progression; D005786:Gene Expression Regulation; D005819:Genetic Markers; D023281:Genomics / Q000379:methods*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D008099:Liver / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D008103:Liver Cirrhosis / Q000235:genetics / Q000378:metabolism; D065626:Non-alcoholic Fatty Liver Disease / Q000175:diagnosis / Q000235:genetics* / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D011237:Predictive Value of Tests; D011379:Prognosis; D011506:Proteins / Q000235:genetics* / Q000378:metabolism*; D040901:Proteomics / Q000379:methods*; D015398:Signal Transduction
chemical_list: D005819:Genetic Markers; D018836:Inflammation Mediators; D011506:Proteins
keywords: Genomics; Metabolic syndrome; Non-alcoholic fatty liver disease; Pathophysiology; Proteomics