Abstract :
More than 95% of heavy drinkers develop fatty liver, but only up to 35% of this population develops more
severe forms of alcoholic liver disease (ALD), including fibrosis, alcoholic hepatitis, cirrhosis, and HCC. Many
risk factors have been proposed for the severe forms of ALD. Alcohol consumption and comorbid factors act in
synergy to accelerate the progression of ALD. Alcohol consumption can directly (via acetaldehyde) or indirectly
(via regulation of multiple factors) up-regulate the expression of SREBP-1c and down-regulate the expression of
PPAR α , leading to the induction of fatty acid synthesis and inhibition of fatty liver β -oxidation, which results in the
development of alcoholic fatty liver. Alcohol consumption can also modify many factors, including HIF-1, C3,
C1qa, PKC , and iNOS, that subsequently contribute to the development of liver injury. The mechanisms underly-
ing the effects of these factors remain unclear necessary for further investigation. |
file/Thai-Journal-of-gastroenterology-vol-14-no-1-376342.pdf