Abstract

Abdominal fat or fatty liver cause huge economic losses in the poultry industry, and nonalcoholic fatty liver disease (NAFLD) is also a global health issue in humans. More than 90% of de novo lipogenesis in humans and chickens is undertaken by the liver, which is proved to be full of lipids in new-born chickens. Folic acid was thought to have correlation with lipid metabolism. Primary hepatocytes from new-born chickens were employed as a natural model of early stage fatty liver in vitro and further to explore whether folic acid could prevent fatty liver in the current study. We found that folic acid addition reduced triglyceride deposition by suppressing de novo fatty acid synthesis and coordinately promoting triglyceride hydrolysis and exportation in primary chicken hepatocytes from new-born chickens. In addition, lipogenesis suppression was through the PI3K/AKT/SREBP pathway mediated by weakening insulin/IGF signal. Our data suggested that folic acid may be considered as a precautionary strategy for abdominal fat deposition in broilers or fatty liver in laying hens and humans. In addition, mechanism regulation also implied that an IGF2 inhibitor and PI3K inhibitor may be used for the NAFLD precautionary measure to reduce TG deposition.

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