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. Author manuscript; available in PMC: 2019 Jan 17.
Published in final edited form as: Adv Exp Med Biol. 2015;815:217–238. doi: 10.1007/978-3-319-09614-8_13

Fig. 7.

Fig. 7

Proposed biochemical mechanism explaining origin of genetic background-independent noninvasive biomarkers of alcohol-induced liver disease in Ppara-null mice. Together with impairment of NAD+ biosynthesis in these mice, oxidation of alcohol leads to a marked shift in redox balance occurs with an increased NADH/NAD+ ratio resulting in impairment of fatty acid oxidation and steatosis in alcohol-treated Ppara-null mice. Concurrent increase in aspartate aminotransferase activity (EC 2.6.1.1) due to liver injury might enhance the deamination of phenylalanine and tryptophan to produce α-keto acids: phenylpyruvic acid and indole-3-pyruvic acid. The elevated NADH/NAD+ ratio could drive the reduction α-keto acid intermediates to the corresponding α-hydroxy acids: phenyllactic acid and indole-3-lactic acid. Enzyme numbers mentioned in blue and light gray indicate enzymes annotated and unannotated in mammals, respectively