Nutrition (Burbank, Los Angeles County, Calif.) · 2005
Dietary phosphatidylcholine alleviates fatty liver induced by orotic acid.
СтатьяНазвание и аннотация: Перевод в очереди
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Buang Yohanes, Wang Yu-Ming, Cha Jae-Young, Nagao Koji, Yanagita Teruyoshi
Аннотация
OBJECTIVE: We compared the effect of dietary phosphatidylcholine (PC) with that of triacylglycerol (TG), both with the same fatty acid profiles, on fatty infiltration in orotic acid (OA)-induced fatty liver of Sprague-Dawley rats.
METHODS: Rats were fed an OA-supplemented diets containing TG (TG+OA group) or PC (20% of dietary lipid, PC+OA group) for 10 d. Rats fed the TG diet without OA supplementation served as the basal group.
RESULTS: Administering OA significantly increased the weights and TG accumulation in livers of the TG+OA group compared with the basal group. These changes were attributed to significant increases in the activities of fatty acid synthase, malic enzyme, and glucose-6-phosphate dehydrogenase, which are fatty acid synthetic enzymes, and phosphatidate phosphohydrolase, a rate-limiting enzyme of TG synthesis. However, the PC+OA group did not show TG accumulation and OA-induced increases of these enzyme activities. Further, a significant increase in the activity of carnitine palmitoyl transferase, a rate-limiting enzyme of fatty acid beta-oxidation, was found in the PC+OA group.
CONCLUSIONS: Dietary PC appears to alleviate the OA-induced hepatic steatosis and hepatomegaly, mainly through the attenuation of hepatic TG synthesis and enhancement of fatty acid beta-oxidation in Sprague-Dawley rats.
METHODS: Rats were fed an OA-supplemented diets containing TG (TG+OA group) or PC (20% of dietary lipid, PC+OA group) for 10 d. Rats fed the TG diet without OA supplementation served as the basal group.
RESULTS: Administering OA significantly increased the weights and TG accumulation in livers of the TG+OA group compared with the basal group. These changes were attributed to significant increases in the activities of fatty acid synthase, malic enzyme, and glucose-6-phosphate dehydrogenase, which are fatty acid synthetic enzymes, and phosphatidate phosphohydrolase, a rate-limiting enzyme of TG synthesis. However, the PC+OA group did not show TG accumulation and OA-induced increases of these enzyme activities. Further, a significant increase in the activity of carnitine palmitoyl transferase, a rate-limiting enzyme of fatty acid beta-oxidation, was found in the PC+OA group.
CONCLUSIONS: Dietary PC appears to alleviate the OA-induced hepatic steatosis and hepatomegaly, mainly through the attenuation of hepatic TG synthesis and enhancement of fatty acid beta-oxidation in Sprague-Dawley rats.