Paraoxonase (PON1) is an antioxidant enzyme that prevents LDL oxidation as well as detoxifies homocysteine thiolactone (HCTL), both of which can cause atherosclerosis. Chronic alcohol (ETOH) and high ω-3 polyunsaturated fatty acids (ω-3 PUFA) consumption may affect PON1 status presumably via reactive oxygen species by depleting liver glutathione (GSH), whereas betaine may counter their effects.
Experimental rats belonging to various dietary groups were pair-fed with Lieber-DeCarli low (2.8% the dietary calories as ω3-fatty acids) and high (13.8% the dietary calories as ω3-fatty acids) menhaden fish alcohol-liquid diets with and without betaine (10 g/l diet) for 8 weeks after which liver PON1 mRNA, GSH, lipid score, and serum PON1, HCTLase, and ALT activities were measured.
Betaine restored liver PON1 mRNA expressions in low and high ω-3 PUFA ETOH groups with parallel restorations of PON1 activity and liver GSH. Concomitantly, betaine reduced hepatosteatosis accompanied by alleviation of liver injury caused by chronic alcohol and high ω-3 PUFA.
Dietary betaine was atheroprotective by restoring liver glutathione (GSH) that quenches free radicals, but also may alleviate liver injury by reducing hepatosteatosis.
Varatharajalu et al (2009). "Betaine Protects Chronic Alcohol and Omega-3 PUFA-Mediated Down-Regulations of PON1 Gene, Serum PON1 and Homocysteine Thiolactonase Activities With Restoration of Liver GSH." Alcoholism: Clinical and Experimental Research. Epub Dec 17.
Tuesday, December 29, 2009
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