Two experiments were conducted to determine the stability of microencapsulated and non-microencapsulated forms of vitamins in diets during extrusion and pelleting. We investigated the recovery of vitamins in swine diets after extrusion at 100 °C, 140 °C, or 180 °C. Next, two diets were conditioned at 65 °C (low temperature; LT) or 85 °C (high temperature; HT), and pellets were formed using a 2.5 × 15.0 mm (low length-to-diameter ratio; LR) or 2.5 × 20.0 mm (high length-to-diameter ratio; HR) die. The extrusion temperature had a significant effect on the recovery of vitamins E, B₁, B₂, B₃, and B₅ in the diets. The diet extruded at 100 °C had higher B₁, B₂, B₃, and B₅ vitamin recoveries than diets extruded at 140 °C and 180 °C. Microencapsulated vitamins A and K₃ had greater stability than non-microencapsulated vitamins A and K₃ at 100 °C and 140 °C extrusion. In the diet extruded at 180 °C, microencapsulated vitamins A, D₃, and K₃ had higher recoveries than non-microencapsulated vitamins A, D₃, and K₃. The recovery of vitamin K₃ in diets after LTLR (low temperature + low length-to-diameter ratio) or HTLR (high temperature + low length-to-diameter ratio) pelleting was greater (p < 0.05) than after LTHR (low temperature + high length-to-diameter ratio) and HTHR (high temperature + high length-to-diameter ratio) pelleting. Our results clearly show that low extrusion temperature and low pellet temperature, and a low length-to-diameter ratio (L:D ratio) for pellet mill die are recommended for pig feed. Moreover, microencapsulated vitamins had greater stability compared to non-microencapsulated vitamins.

Vitamin K (VK), a fat-soluble vitamin, is essential for the clotting of blood because of its role in the production of clotting factors in the liver. Moreover, researchers continue to explore the role of VK as an emerging novel bioactive molecule with the potential function of improving bone health. This review focuses on the effects of VK on bone health and related mechanisms, covering VK research history, homologous analogs, dietary sources, bioavailability, recommended intake, and deficiency. The information summarized here could contribute to the basic and clinical research on VK as a natural dietary additive and drug candidate for bone health. Future research is needed to extend the dietary VK database and explore the pharmacological safety of VK and factors affecting VK bioavailability to provide more support for the bone health benefits of VK through more clinical trials.

Osteogenic activity of vitamin K₂ (VK₂), a small molecular nutrient, has been suggested. However, the underlying mechanisms have not been fully elucidated. Therefore, this study aimed to explore the mechanisms by which VK₂ promotes osteogenic differentiation. The effects of VK₂ on osteogenic differentiation indicators were determined in C3H10 T1/2 clone 8 cells. The RNA-seq analysis was used to explore the hypothesis that VK₂ promotes osteogenic differentiation. Small interfering RNA (siRNA) assay and plasmid transfection assay were used to determine the potential role of VK₂ in the modulation of Bcl-6/STAT axis and IL-6/JAK/STAT signaling pathway. VK₂ significantly increased alkaline phosphatase (ALP) activity, ALP, osteocalcin (OCN), and RUNX2 abundance, and RUNX2 protein expression. RNA-seq analysis showed that there were 314 differentially expressed genes (DEGs) upregulated and 1348 DEGs downregulated by VK₂. PPI analysis determined the top 10 hub genes upregulated or downregulated by VK₂. Overexpression of Bcl-6 increased osteogenic differentiation and decreased expression of STAT1. Administration with VK₂ restored the inhibition by siBcl-6 in osteogenic differentiation. Knockdown of IL-6 decreased the mRNA levels of genes associated with the JAK/STAT signaling pathway, and increased markers of osteoblast differentiation. Furthermore, treatment with VK₂ improved inhibition in osteogenic differentiation and decreased enhancement of JAK/STAT signaling pathway related genes by overexpression of IL-6. Our study suggests that VK₂ could improve osteogenic differentiation via the Bcl-6/STAT axis and IL-6/JAK/STAT signaling pathway.

Two in vitro experiments were conducted to investigate the effects of choline chloride, copper sulfate (CuSO₄) and zinc oxide (ZnO) on the stability of vitamin A (VA), vitamin D₃ (VD₃), vitamin E (VE), vitamin K₃ (VK₃), vitamin B₁ (VB₁), vitamin B₂ (VB₂), vitamin B₆ (VB₆), niacin, and pantothenic acid in vitamin and vitamin/trace mineral (VTM) premixes for weanling piglets after 0, 1, 2, 3, 6 and 12 months of premix storage. We developed predicted equations to estimate vitamin retention during storage. Two vitamin premixes (with or without choline) were formulated and stored at 25 °C and 60% humidity to establish the storage stability of vitamin premixes. Additionally, four VTM premixes were used to evaluate the effect of choline chloride (0 vs. 40,000 mg/kg) and trace minerals (Low CuSO₄ + ZnO vs. High CuSO₄ + ZnO) on vitamin stability in VTM premixes stored at room temperature (22 °C). In general, as storage time increased, residual vitamin activity decreased (p < 0.05). The results confirmed that VD₃, VE, VB₂, VB₆, niacin and pantothenic acid were highly stable during storage, while the retention of VA, VK₃ and VB₁ was significantly affected by storage time and the presence of choline and high concentrations of Cu and Zn in the premix. After one year of storage, the retention of VE, VB₂, VB₆ niacin, and pantothenic acid was more than 90% in vitamin and VTM premixes. The retention of VD₃ was more than 90% in vitamin premixes and more than 80% in VTM premixes after one year of storage. We conclude that current microencapsulation techniques for vitamin premixes appear to be inadequate to guarantee VA, VK₃, and VB₁ concentrations in VTM premixes.

The objective of this study was to quantify the relative bioavailability of microencapsulated vitamins A and E in nursery pigs and compare the effects of vitamin forms and vitamin levels on the plasma vitamin content and growth performance of weaned piglets. In experiment (Exp.) 1, 12 nursery pigs (fitted with jugular catheters) were supplied at 0 h with non-microencapsulated or microencapsulated vitamin A and E. Blood samples were collected at 1, 3, 6, 9, 12, 16, 18, 21, 24, 27, 30, 36, 48, and 72 h after feeding to compare the bioavailability of oral vitamins A and E. In Exp. 2, a total of 216 crossbred weaned piglets were assigned to six treatments. This experiment was a 2 × 3 factorial arrangement, with two factors for vitamin forms (non-microencapsulated and microencapsulated) and three factors for vitamin levels (the National Research Council level of vitamins, 75% commercial recommendations of vitamins (CRV) level, and a 100% CVR level). In Exp. 1, the relative bioavailability of microencapsulated vitamin E was significantly greater than that of non-microencapsulated vitamin E. In Exp. 2, the pigs fed diets containing 75% or 100% CRV levels of vitamins increased their growth performance and plasma vitamin concentrations compared to the control group. In conclusion, microencapsulation can improve the bioavailability of vitamins, and supplementation with high levels of vitamins was able to improve the growth performance of the piglets.

This study was conducted to investigate the stability of five commercial vitamin A products in vitamin premixes and vitamin-trace mineral premixes. The five commercial products used were: Xinhecheng, Zhejiang medicine, Kingdomway, DSM, and BASF. The vitamin A products were stored in three vitamin premixes (for suckling, weanling, and finishing pigs) or in vitamin-trace mineral (VTM) premixes (for suckling, weanling, and finishing pigs). Vitamin premixes were stored in an environmentally controlled chamber set at 25 °C and 60% humidity. The VTM premixes were stored at room temperature (approximately 22 °C). Sampling was performed on d 0, 90, 180, 270, and 360. Stability was reported as the residual vitamin A activity (% of initial) at each sampling point. For the stability of vitamin premixes, all interactive and main effects of storage time and vitamin A product were not significant. For the stability of VTM premixes, there was no significant interaction effects between storage time, vitamin A product and main effect of vitamin A product, but the main effect of storage time was significant (p < 0.01). In conclusion, a longer storage time reduced vitamin A activity in VTM premixes but there was no difference in the stability of commercially available vitamin A.