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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.

This experiment examined the egg quality of hens fed vanadium (V) and vitamin C (VC) during storage, as well as the V and VC withdrawal on egg quality and V residual in egg. A total of 360 laying hens (31 weeks old) were randomly allotted into a 3 × 2 factorial arrangement treatments (6 replicates and 10 chicks per replicate) with three levels of dietary V (0, 5, and 10 mg/kg) and two levels of VC (0 and 100 mg/kg) for 19 weeks (feeding V and VC 12 weeks, recovery 7 weeks). The V residual in eggs at 4, 8, and 12th weeks were increased (linear effect, P ≤ 0.01) as V levels increased and was not detected in albumen at 7th week after V withdrawal. Followed by 12-week feeding period, albumen height and Haugh unit of eggs during 2-week storage were decreased (linear and quadratic effect, P < 0.01) by dietary V supplementation. Lightness value was increased (linear effect, P < 0.01), whereas redness and yellowness value of the eggshell were lowered (linear effect, P < 0.01) in V-containing diet. During 7-week withdrawal period, eggs from groups pre-feeding 5 and 10 mg/kg V had lower (linear effect, P < 0.01) overall albumen height and Haugh unit. The reducing effect on albumen height and HU continued to be observed until the seventh week, whereas the bleaching effect on eggshell color disappeared after 1-week withdrawal. The results indicated that feeding 5 or 10 mg/kg V increases egg V residual and reduces egg albumen quality and bleached the shell color, and the impaired albumen quality induced by 10 mg/kg of V lasted at least 6 weeks after changing to no V supplementation diet. The addition of VC did not show to affect egg quality during storage or recovery phase.

Vanadium (V) is a trace element which can induce dysfunction of gastro-intestine and egg quality deterioration of laying hens. This study was conducted to determine the effect of tea polyphenols (TP) on intestinal morphology, microflora, and short-chain fatty acid (SCFA) profile of laying hens fed vanadium containing diets. A total of 120 Lohman laying hens (67-week-old) were randomly divided into 4 groups with 6 replicates and 5 birds each for a 35-day feeding trial. The dietary treatments were as follows: (1) control (CON), fed a basal diet; (2) vanadium treatment (V10), CON +10 mg V/kg; (3) TP treatment 1 (TP1): V10 + 600 mg TP/kg; (4) TP treatment 2 (TP2): V10 + 1000 mg TP/kg. Fed 10 mg V/kg diets to laying hens did not affect the cecum flora diversity index (H), degree of homogeneity (EH), and richness (S), but hens fed TP2 diet decreased the H, EH, and S (P < 0.05). The cecum butyrate acid concentration was lower in V10 treatment and higher in TP2 treatment (P < 0.05). Addition of 10 mg/kg V resulted in an increased (P < 0.01) duodenal cell apoptosis rate, and 1000 mg/kg TP supplementation overcame (P < 0.01) this reduction effect induced by vanadium. The results indicated that supplementation of 10 mg/kg vanadium increased duodenal cell apoptosis and reduced cecum butyrate acid content. Addition of 1000 mg/kg TP increased the SCFA production to affect cecum flora ecology and protected the duodenal cell from excess apoptosis caused by vanadium.

The study was conducted to assess the effect of vanadium (V) in high-fat diet on the liver and kidney of rats in a 5-week trial. Seventy-two female Wistar rats (BW = 95 ± 5 g) were randomly allotted into eight groups. Groups I, II, III, and IV obtained low-fat diet containing 0, 3, 15, and 30 mg/kg V, and V, VI, VII, and VIII groups received the respective vanadium doses with high-fat diet, respectively. There were lesions in the liver and kidney of V, VI, VII, and VIII groups, granular degeneration and vacuolar degeneration were observed in the renal tubular and glomerulus epithelial cells, and hepatocytes showed granular degeneration and vacuolar degeneration. Supplemented high-fat diet with vanadium was shown to decrease (P < 0.05) activities of superoxide dismutase, total antioxidant capacity, glutathione-S transferase, and NAD(P)H/quinone oxidoreductase 1 (NQO1) and increase malondialdehyde content in the liver and kidney. The relative expression of hepatic nuclear factor erythroid 2-related factor 2 (Nrf-2) and NQO1 mRNA was downregulated by V addition and high-fat diet, and the effect of V was more pronounced in high-fat diet (interaction, P < 0.05), with VIII group having the lowest mRNA expression of Nrf-2 and NQO1 in the liver and kidney. In conclusion, it suggested that dietary vanadium ranging from 15 to 30 mg/kg could lead to oxidative damage and vanadium accumulation in the liver and kidney, which caused renal and hepatic toxicity. The high-fat diet enhanced vanadium-induced hepatic and renal damage, and the mechanism was related to the modulation of the hepatic and renal mRNA expression of Nrf-2 and NQO1.