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Genes or environment to determine alcoholic liver disease and non-alcoholic fatty liver disease

Lookup NU author(s): Professor Chris Day

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Abstract

While the vast majority of heavy drinkers and individuals with obesity, insulin resistance, and the metabolic syndrome will have steatosis, only a minority will ever develop steatohepatitis, fibrosis, and cirrhosis. Genetic and environmental risk factors for advanced alcoholic liver disease (ALD) and non-alcoholic fatty liver disease (NAFLD) seem likely to include factors that influence the severity of steatosis and oxidative stress, the cytokine milieu, the magnitude of the immune response, and/or the severity of fibrosis. For ALD, the dose and pattern of alcohol intake, along with obesity are the most important environmental factors determining disease risk. For NAFLD, dietary saturated fat and antioxidant intake and small bowel bacterial overgrowth may play a role. Family studies and interethnic variations in susceptibility suggest that genetic factors are important in determining disease risk. For ALD, functional polymorphisms in the alcohol dehydrogenases and aldehyde dehydrogenase alcohol metabolising genes play a role in determining susceptibility in Oriental populations. No genetic associations with advanced NAFLD have been replicated in large studies. Preliminary data suggest that polymorphisms in the genes encoding microsomal triglyceride transfer protein, superoxide dismutase 2, the CD14 endotoxin receptor, TNF-α, transforming growth factor-β, and angiotensinogen may be associated with steatohepatitis and/or fibrosis. © 2006 Blackwell Munksgaard.


Publication metadata

Author(s): Day CP

Publication type: Review

Publication status: Published

Journal: Liver International

Year: 2006

Volume: 26

Issue: 9

Pages: 1021-1028

ISSN (print): 1478-3223

ISSN (electronic): 1478-3231

URL: http://dx.doi.org/10.1111/j.1478-3231.2006.01323.x

DOI: 10.1111/j.1478-3231.2006.01323.x


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