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- W4048526 abstract "Alcoholic liver disease (ALD), such as fatty liver, hepatitis, or fibrosis, is frequently observed in patients with a long history of excessive alcohol intake. These types of ALD are considered alcohol-associated lifestyle diseases and involve both genetic and environmental factors [1]. Interactions between alcohol and nutritional status, which are one of the secondary risk factors, may also be important. Indeed, the presence and extent of protein-calorie malnutrition have important roles in determining the outcome of patients with ALD. Micronutrient abnormalities, such as hepatic vitamin A depletion or depressed vitamin E levels, may also potentially aggravate liver disease [2]. Additionally, obesity and excess body weight have been associated with an increased risk of ALD [3, 4]. Alcoholic and nonalcoholic fatty liver each begin with the accumulation of lipids in the liver, which, although a reversible condition, is understood to play an important role in the development of advanced liver disease. With continued alcohol intake, the development of steatosis may progress to hepatitis and fibrosis and might lead to liver cirrhosis. Excessive alcohol intake adversely influences the liver through the production of toxic products such as acetaldehyde and potentially highly reactive oxygen molecules, which are generated by alcohol dehydrogenase and the microsomal ethanol oxidizing system. These products can directly and indirectly interfere with the normal metabolism of other nutrients, particularly lipids, contributing to liver cell damage [5]." @default.
- W4048526 created "2016-06-24" @default.
- W4048526 creator A5011798844 @default.
- W4048526 creator A5031577921 @default.
- W4048526 creator A5046180354 @default.
- W4048526 date "2012-07-24" @default.
- W4048526 modified "2023-10-16" @default.
- W4048526 title "Dietary Fatty Acids and Alcoholic Liver Disease" @default.
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- W4048526 doi "https://doi.org/10.1007/978-1-62703-047-2_41" @default.
- W4048526 hasPublicationYear "2012" @default.
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