Male C57BL/6J mice were administered a control high fat diet, or one enriched in methyl donors (betaine and SAM) with or without alcohol for 4 wks using the enteral alcohol feeding model. As expected, attenuation of alcohol-induced liver injury (ALI)and an increase in GSH:GSSG ratio were achieved with methyl donor supplementation. Interestingly, methyl donors led to a 35% increase in blood alcohol elimination rate and, while there was no effect on alcohol metabolism in the stomach, a profound effect on liver alcohol metabolism was observed. The catalase-dependent pathway of alcohol metabolism was induced, yet the increase of CYP2E1 activity by alcohol was blunted which may be mitigating production of oxidants. Additional factors contributing to the protective effects of methyl donors in ALI were increased activity of low- and high-K(m) aldehyde dehydrogenases leading to lower hepatic acetaldehyde, maintenance of the efficient mitochondrial energy metabolism, and promotion of peroxisomal beta-oxidation.
Profound changes in alcohol metabolism represent additional important mechanism of the protective effect of methyl donors in ALI.
Powell et al (2010). "Mechanism for Prevention of Alcohol-Induced Liver Injury by Dietary Methyl Donors." Toxicol Sci. 115(1): 131-139
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