Key Laboratory of Animal Disease-Resistance Nutrition, Ministry of Education, Key Laboratory of Animal Disease-Resistance Nutrition and Feed, Ministry of Agriculture, Animal Nutrition Institute, Sichuan Agricultural University, No. 211, Huimin Road, Wenjiang District, Chengdu, 611130, China.
Faculty of Veterinary and Agricultural Sciences, The University of Melbourne, Parkville, Australia.
Biol Trace Elem Res. 2019 Aug;190(2):501-508. doi: 10.1007/s12011-018-1562-0. Epub 2018 Nov 7.
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 8 weeks: control (basal diet), V10 (control + 10 mg/kg V), EGCG130 (V10 + 130 mg/kg EGCG), and EGCG217 (V10 + 217 mg/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 217 mg/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.
由于对参与这种作用的途径的了解相当有限，我们研究了调节蛋鸡脂质代谢的基因途径和蛋鸡蛋黄的脂肪酸谱，这些蛋鸡受到膳食钒（V）的挑战，并补充了表没食子儿茶素-3-没食子酸酯（EGCG）。为此，将 120 只母鸡分为四组，在 8 周的时间内分别用以下实验饲料喂养：对照组（基础日粮）、V10 组（对照+10mg/kg V）、EGCG130 组（V10+130mg/kg EGCG）和 EGCG217 组（V10+217mg/kg EGCG）。与对照组相比，V10、EGCG130 和 EGCG217 组的血液总胆固醇、甘油三酯、葡萄糖和极低密度脂蛋白胆固醇浓度较低，而 EGCG217 组的血液总胆固醇和甘油三酯含量低于 V10 组（P<0.05）。V10 组母鸡的肝脏甘油三酯含量最高，而 EGCG130 和 EGCG217 组的肝脏甘油三酯含量低于对照组（P<0.01）。与对照组相比，膳食中添加 V 增加了蛋黄多不饱和脂肪酸（PUFA）和总不饱和脂肪酸（UFA）的含量（P<0.05），而在含 V 的饮食中添加 130 或 217mg/kg 的 EGCG 则导致蛋黄 PUFA 和 UFA 的含量与对照组相似。单独用 V 处理可上调肝脂肪酸合酶（FAS）和固醇调节元件结合蛋白 1（SREBP1）的表达，而 EGCG 下调 V10 处理中 FAS 和 SREBP1 的表达（P<0.01）。V10 组的肝脏基因表达过氧化物酶体增殖物激活受体γ（PPARγ）低于对照组，而 EGCG 组则上调了其表达（P<0.05）。总之，本研究的数据表明，膳食 V 和 EGCG 改变了蛋鸡的脂质代谢和蛋黄中的脂肪沉积模式，这可能与它们对脂肪生成相关基因（FAS、SREBP1 和 PPARγ）表达的调节作用有关。
