Dietary supplementation of zinc oxide modulates intestinal functionality during the post-weaning period in clinically healthy piglets.

BACKGROUND: To improve our understanding of host and intestinal microbiome interaction, this research investigated the effects of a high-level zinc oxide in the diet as model intervention on the intestinal microbiome and small intestinal functionality in clinically healthy post-weaning piglets. In study 1, piglets received either a high concentration of zinc (Zn) as zinc oxide (ZnO, Zn, 2,690 mg/kg) or a low Zn concentration (100 mg/kg) in the diet during the post weaning period (d 14-23). The effects on the piglet's small intestinal microbiome and functionality of intestinal tissue were investigated. In study 2, the impact of timing of the dietary zinc intervention was investigated, i.e., between d 0-14 and/or d 14-23 post weaning, and the consecutive effects on the piglet's intestinal functionality, here referring to microbiota composition and diversity and gene expression profiles. RESULTS: Differences in the small intestinal functionality were observed during the post weaning period between piglets receiving a diet with a low or high concentration ZnO content. A shift in the microbiota composition in the small intestine was observed that could be characterized as a non-pathological change, where mainly the commensals inter-changed. In the immediate post weaning period, i.e., d 0-14, the highest number of differentially expressed genes (DEGs) in intestinal tissue were observed between animals receiving a diet with a low or high concentration ZnO content, i.e., 23 DEGs in jejunal tissue and 11 DEGs in ileal tissue. These genes are involved in biological processes related to immunity and inflammatory responses. For example, genes CD59 and REG3G were downregulated in the animals receiving a diet with a high concentration ZnO content compared to low ZnO content in both jejunum and ileum tissue. In the second study, a similar result was obtained regarding the expression of genes in intestinal tissue related to immune pathways when comparing piglets receiving a diet with a high concentration ZnO content compared to low ZnO content. CONCLUSIONS: Supplementing a diet with a pharmaceutical level of Zn as ZnO for clinically healthy post weaning piglets influences various aspects intestinal functionality, in particular in the first two weeks post-weaning. The model intervention increased both the alpha diversity of the intestinal microbiome and the expression of a limited number of genes linked to the local immune system in intestinal tissue. The effects do not seem related to a direct antimicrobial effect of ZnO.

Dietary saturated fat/cholesterol, but not unsaturated fat or starch, induces C-reactive protein associated early atherosclerosis and ectopic fat deposition in diabetic pigs.

BACKGROUND: Diabetes is thought to accelerate cardiovascular disease depending on the type of diet. This study in diabetic subjects was performed to investigate the metabolic, inflammatory and cardiovascular effects of nutritional components typically present in a Western, Mediterranean or high glycaemic diet. METHODS: Streptozotocin-diabetic pigs (~45 kg) were fed for 10 weeks supplemental (40% of dietary energy) saturated fat/cholesterol (SFC), unsaturated fat (UF) or starch (S) in an eucaloric dietary intervention study. RESULTS: Fasting plasma total, LDL and HDL cholesterol concentrations were 3-5 fold higher (p < 0.01) in SFC compared to UF and S pigs. Fasting plasma NEFA concentrations (mmol/L) were highest (p < 0.05) in SFC (1.09 ± 0.17), intermediate in UF (0.80 ± 0.14) and lowest in S pigs (0.58 ± 0.14) whereas plasma glucose (~13 mmol/L), triglyceride (~0.5 mmol/L) and insulin (~24 pmol/L) concentrations were comparable among SFC, UF and S pigs. The postprandial response area under the curves (AUC, 0-4 h) for glucose but not for insulin and triglyceride responses were intermediate in SFC (617 ± 144) and lowest (p < 0.05) in UF (378 ± 157) compared to S pigs (925 ± 139). Fasting hepatic glucose production, hepatic and peripheral insulin sensitivity and blood pressure were not different among pigs. C-reactive protein (CRP) concentrations (mg/L) were highest (p < 0.05) in SFC (25 ± 4), intermediate in S (21 ± 3) and lowest in UF pigs (14 ± 2). Liver weights, liver and muscle triglyceride concentrations, and the surface area of aorta fatty streaks were highest (p < 0.01) in SFC pigs. A positive correlation between postprandial plasma CRP and aorta fatty streaks was observed in SFC pigs (R(2) = 0.95). Retroperitoneal fat depot weight (g) was intermediate in SFC (260 ± 72), lowest in S (135 ± 51) and highest (p < 0.05) in UF (571 ± 95) pigs. CONCLUSION: Dietary saturated fat/cholesterol induces inflammation, atherosclerosis and ectopic fat deposition whereas an equally high dietary unsaturated fat load does not induce these abnormalities and shows beneficial effects on postprandial glycaemia in diabetic pigs.

Surplus dietary tryptophan inhibits stress hormone kinetics and induces insulin resistance in pigs.

Recently we have shown that surplus dietary tryptophan (TRP) reduced the plasma concentrations of cortisol and noradrenaline in pigs. Stress hormones are known to affect insulin sensitivity and metabolism. We now investigated the long-term effects of surplus dietary TRP on 1) plasma and urinary stress hormone kinetics, 2) insulin sensitivity for glucose and amino acid clearance, and 3) whole body nitrogen balance. Pigs were fed for 3weeks a high (13.2%) vs normal (3.4%) TRP to large neutral amino acids (LNAA) diet, leading to reduced fasting (14 h) plasma cortisol (17.1+/-3.0 vs 28.9+/-4.3 ng/mL, p<0.05) and noradrenaline (138+/-14 vs 225+/-21 pg/mL, p<0.005) concentrations, lower daily urinary noradrenaline (313+/-32 vs 674+/-102 ng/kg day, p<0.001) and adrenaline (124+/-13 vs 297+/-42 ng/kg day, p<0.001) but higher dopamine (5.8+/-0.5 vs 1.5+/-0.2 microg/kg day, p<0.001) excretions, respectively. Insulin sensitivities for both glucose and amino acid clearance, (as measured by the intraportal hyperinsulinaemic (1 mU/kg min) euglycaemic euaminoacidaemic clamp technique), were lower by 22% in pigs on the high vs normal TRP/LNAA diet (14.8+/-1.4 vs 18.9+/-0.9, p<0.05 and 69.7+/-4.3 vs 89.7+/-6.8 mL/kg min, p<0.05, respectively) without affecting urinary nitrogen excretion (35.5+/-1.0 vs 36.6+/-1.0% of dietary nitrogen intake, p=ns). In conclusion, long-term feeding of surplus dietary TRP inhibits both baseline adrenocortical and sympathetic nervous system activity, it induces insulin resistance for both glucose and amino acid clearance but it does not affect whole body protein catabolism. This indicates that the bioactive amino acid TRP contributes to homeostasis in neuroendocrinology and insulin action and that low baseline adrenocortical and sympatho-adrenal axis activity are associated with insulin resistance.