Abstract

As the understanding of the pathways involved in such effect are quite limited, we investigated the gene pathways that modulate lipid metabolism in layers and the fatty acid profiles of the yolk of layers that were challenged with dietary vanadium (V) and supplemented with epigallo-catechin-3-gallate (EGCG). For this purpose, a total of 120 hens were divided into four groups which were fed the following experimental diets for a period of 8weeks: control (basal diet), V10 (control + 10mg/kg V), EGCG130 (V10 + 130mg/kg EGCG), and EGCG217 (V10 + 217mg/kg EGCG). Blood total cholesterol, triglyceride, glucose, and very low-density lipoprotein-cholesterol concentration were lower in V10, EGCG130, and EGCG217 groups compared to the control group, while total cholesterol and triglyceride content in blood were lower in the EGCG217 group than in V10 group (P < 0.05). Hens consumed V10 diet had the highest triglyceride content in liver among treatments, whereas EGCG130 and EGCG217 groups had lower values when compared to those observed in the control group (P < 0.01). Dietary inclusion of V increased yolk polyunsaturated fatty acid (PUFA) and total unsaturated fatty acid (UFA) content compared to the control group (P < 0.05), whereas the addition of either 130 or 217mg/kg EGCG in V containing diet resulted in similar yolk PUFA and UFA contents with those observed in the control group. Treatment with V alone upregulated the expression of hepatic fatty acid synthase (FAS) and sterol-regulator element-binding protein 1 (SREBP1), while EGCG downregulated FAS and SREBP1 expressions in contrast to V10 treatments (P < 0.01). Liver gene expression peroxisome proliferator-activated receptor gamma (PPARγ) was lower in the V10 than in the control group while EGCG inclusion groups upregulated their expression (P < 0.05). In conclusion, the data gathered in this study indicate that dietary V and EGCG alter the layers' lipid metabolism and fat deposition pattern in egg yolk, which might be associated with their modulatory effect on lipogenesis-related gene (FAS, SREBP1, and PPARγ) expression.

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