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ABSTRACT:
Alcohol is absorbed mainly in the digestive tract . 90% of the absorbed alcohol is metabolized in
the liver while remaining 10% is discharged via expiration, urine and perspiration. Alcohol is
oxidized to acetaldehyde by various liver enzymes, such as alcohol dehydrogenase, catalase, etc.,
which is further enzymatically oxidized to harmless acetic acid. Meanwhile, alcohol is readily
metabolized to acetaldehyde by enteric microorganisms that modifies gut permeability and
microbiota equilibrium which in turn result in increased levels of pathogen-associated molecular
patterns such as lipopolysaccharide, bacterial translocation, etc., causing direct hepatocyte
damage. In patients who consume alcohol over a long period, an increment of Gram negative
bacteria cause endotoxemia and hyperactivation of the immune system.
Recently, probiotics, live lactic acid bacteria and other genus (i.e. Bacillus spp.) in the intestine
have been reported to convert ethanol into acetaldehyde and further to acetic acid, thereby
suppressing the absorption of alcohol and acetaldehyde, associated with hepato-protective
activity by reducing or preventing the progression of ALD. A potential mechanism is
transformation of intestinal microbiota by probiotics. However, not all enteric bacteria have such
a function.
While this appears to be a promising therapeutic strategy for the treatment of intestinal barrier
dysfunction, there is a scarcity of research that studies probiotics in the context of ALD.
Therefore, there is a need for developing the bacterial compositions that functions to prevent the
absorption of alcohol and acetaldehyde and protect the liver.
Keywords:
Probiotics; Alcohol; Alcoholic Liver Disease; Intestinal microbiota; Lactic acid bacteria.