Table 1.
Deoxynivalenol content in different dietary groups.
Table 2.
Composition and nutrient levels of basal diet (as-fed basis)1.
Figure 1.
Blood anti-oxidative capacity in each group.
A: CAT activity in each group. B: H2O2 concentration in each group. C: MDA concentration in each group. D: NO concentration in each group. Dietary treatments were NC, an uncontaminated basal diet, DON, the basal contaminated with 4 mg/kg deoxynivalenol, GLU, uncontaminated basal diet with 2% (g/g) glutamic acid supplementation, and DG, deoxynivalenol-contaminated (4 mg/kg) basal diet with 2% (g/g) glutamic acid supplementation. Data are presented as means ± SEM, n = 7, with a–c used to indicate a statistically significant difference (P<0.05, one way ANOVA method). CAT: catalase (U/ml); H2O2: hydrogen peroxide (mmol/L); MDA: methane dicarboxylic aldehyde (nmol/ml); NO: nitric oxide (µmol/L).
Figure 2.
Liver and kidney anti-oxidative capacity in each group.
A: MDA concentrations of liver and kidney in each group. B: H2O2 concentrations of liver and kidney in each group. C: T-AOC of liver and kidney in each group. Dietary treatments were NC, an uncontaminated basal diet, DON, the basal contaminated with 4 mg/kg deoxynivalenol, GLU, uncontaminated basal diet with 2% (g/g) glutamic acid supplementation, and DG, deoxynivalenol-contaminated (4 mg/kg) basal diet with 2% (g/g) glutamic acid supplementation. Data are presented as means ± SEM, n = 7, with a–b used to indicate a statistically significant difference (P<0.05, one way ANOVA method). MDA: methane dicarboxylic aldehyde (nmol/ml); H2O2: hydrogen peroxide (mmol/L); T-AOC: total antioxidant capacity (U/mg).
Figure 3.
Ileum and jejunum anti-oxidative capacity in each group.
A: T-AOC of ileum and jejunum in each group. B: MDA concentrations of ileum and jejunum in each group. Dietary treatments were NC, an uncontaminated basal diet, DON, the basal contaminated with 4 mg/kg deoxynivalenol, GLU, uncontaminated basal diet with 2% (g/g) glutamic acid supplementation, and DG, deoxynivalenol-contaminated (4 mg/kg) basal diet with 2% glutamic acid supplementation. Data are presented as means ± SEM, n = 7, with a–c used to indicate a statistically significant difference (P<0.05, one way ANOVA method). MDA: methane dicarboxylic aldehyde (nmol/ml); T-AOC: total antioxidant capacity (U/mg).
Figure 4.
Plasma DAO activity and D-lactate levels in each group.
A: Plasma D-lactate levels in each group on day 15 and day 30. B: Plasma DAO activity in each group on day 15 and day 30. C: DAO activity of kidney and liver in each group. D: DAO activity of ileum and jejunum in each group. Dietary treatments were NC, an uncontaminated basal diet, DON, the basal contaminated with 4 mg/kg deoxynivalenol, GLU, uncontaminated basal diet with 2% (g/g) glutamic acid supplementation, and DG, deoxynivalenol-contaminated (4 mg/kg) basal diet with 2% (g/g) glutamic acid supplementation. Data are presented as means ± SEM, n = 7, with a–d used to indicate a statistically significant difference (P<0.05, one way ANOVA method). DAO: dianine oxidase (U/mg).
Figure 5.
Image of ileal goblet cells and ileal lymphocytes.
A: Ileal goblet cells (×250). B: Ileam lymphocytes (×400). Dietary treatments were NC, an uncontaminated basal diet, DON, the basal contaminated with 4 mg/kg deoxynivalenol, GLU, uncontaminated basal diet with 2% (g/g) glutamic acid supplementation, and DG, deoxynivalenol-contaminated (4 mg/kg) basal diet with 2% (g/g) glutamic acid supplementation. n = 7 for treatments.
Figure 6.
Image of jejunum goblet cells and jejunum lymphocytes.
A: Jejunum goblet cells (×250). B: Jejunum lymphocytes (×400). Dietary treatments were NC, an uncontaminated basal diet, DON, the basal contaminated with 4 mg/kg deoxynivalenol, GLU, uncontaminated basal diet with 2% (g/g) glutamic acid supplementation, and DG, deoxynivalenol-contaminated (4 mg/kg) basal diet with 2% (g/g) glutamic acid supplementation. n = 7 for treatments.
Table 3.
Effect of glutamic acid supplementation on ileal and jejunum morphology in piglets fed a deoxynivalenol-contaminated diet.
Table 4.
Effect of dietary supplementation with glutmic acid on serum amino acids levels (µg/ml) in piglets fed a deoxynivalenol-contaminated diet on day 15.
Table 5.
Effect of dietary supplementation with glutmic acid on serum amino acids levels (µg/ml) in piglets fed a deoxynivalenol-contaminated diet on day 30.
Table 6.
Effect of dietary supplementation with glutmic acid on serum amino acids levels in piglets fed deoxynivalenol-contaminated feed on day 37.
Figure 7.
(Up) Representative western blots of total 4EBP1(T-4EBP1), phosphorylated 4EBP1 (Ser65) (P-4EBP1), total Akt (T-Akt), phosphorylated Akt (Ser473) (P-Akt), total mTOR (T- mTOR), phosphorylated mTOR (Ser2448) (P- mTOR) in ileal of piglets fed the various dietary treatments. β-actin was the loading control. (Down) Quantification by image analysis of 4EBP1, Akt and mTOR phosphorylation. Dietary treatments were NC, an uncontaminated basal diet, DON, the basal contaminated with 4 mg/kg deoxynivalenol, GLU, uncontaminated basal diet with 2% (g/g) glutamic acid supplementation, and DG, deoxynivalenol-contaminated (4 mg/kg) basal diet with 2% (g/g) glutamic acid supplementation. n = 7 for treatments.
Figure 8.
Activation of mTOR in jejunum.
(Up) Representative western blots of total 4EBP1(T-4EBP1), phosphorylated 4EBP1 (Ser65) (P-4EBP1), total Akt (T-Akt), phosphorylated Akt (Ser473) (P-Akt), total mTOR (T- mTOR), phosphorylated mTOR (Ser2448) (P- mTOR) in jejunum of piglets fed the various dietary treatments. β-actin was the loading control. (Down) Quantification by image analysis of 4EBP1, Akt and mTOR phosphorylation. Dietary treatments were NC, an uncontaminated basal diet, DON, the basal contaminated with 4 mg/kg deoxynivalenol, GLU, uncontaminated basal diet with 2% (g/g) glutamic acid supplementation, and DG, deoxynivalenol-contaminated (4 mg/kg) basal diet with 2% (g/g) glutamic acid supplementation. n = 7 for treatments.