## 4 Discussion  
### Plasma Kinetic Behavior of Different Forms of Vitamin A  
The compartmental model used in the present study fits the plasma kinetic data well. Regarding the implication of the image, the curves had an upswing mostly representing absorption, and a downswing mostly representing equilibration of plasma vitamin A (retinol) with the tissue pools. The plasma kinetics of retinol after feeding with non-microencapsulated or microencapsulated vitamin A showed very similar characteristics to thus prolonged period. The plasma concentration of retinol reached its peak at approximately 10 h after feeding. After the peak, the plasma levels of retinol decreased gradually. Our result reveal the slow distribution of vitamin A, which is responsible for the long terminal half-life of vitamin A. Vitamin A is administered orally and enters the bloodstream rapidly, where it is distributed to the peripheral compartment slowly [16]. Based on current knowledge of the many parallels in gastrointestinal tract function between pigs and humans, it is unsurprising that the plasma retinol responses obtained in this study are similar to the kinetic parameters found in humans (9.8 h) [17]. When providing a single oral dosage of 3,000 IU/kg of vitamin A for dogs, the peak plasma vitamin A concentration was observed at 8 h after feeding; then, the blood vitamin A content decreased to the baseline by 72 h after oral administration [18]. The different responses of  
\begin{table}
\begin{tabular}{c c c c c c c c c c c} \hline \hline \multirow{2}{*}{**Form**} & \multicolumn{3}{c}{**Non-Microencapsulated**} & \multicolumn{4}{c}{**Microencapsulated**} & \multicolumn{4}{c}{\(p\)-Value**} \\ \cline{2-10}  & \multicolumn{3}{c}{**CRV**} & \multicolumn{2}{c}{**CRV**} & \multicolumn{2}{c}{**CRV**} & \multicolumn{2}{c}{**SEM**} & \multirow{2}{*}{**Form**} & \multirow{2}{*}{**Level**} & \multirow{2}{*}{**Form**} & \multirow{2}{*}{**Level**} & \multirow{2}{*}{**Form**} \(\times\) \\  & \multicolumn{3}{c}{**75\%**} & \multicolumn{1}{c}{**100\%**} & \multicolumn{1}{c}{**NRC**} & & & & & & & \\ \hline Reinol, ng/mL & 196.12 & 202.81 & 188.84 & 201.38 & 218.58 & 205.68 & 19.42 & 0.432 & 0.752 & 0.947 \\
25(OHJ)D\({}_{3}\), ng/mL & 29.84 & 33.23 & 33.17 & 34.38 & 34.56 & 30.89 & 3.95 & 0.716 & 0.868 & 0.696 \\ \(\alpha\)-tocopherol, ng/mL & 0.31 b\({}^{\text{  
plasma vitamin A may have resulted from species differences, and the vitamin's form and dose may have potential effects on vitamin absorption. In addition, [PERSON] et al. reported that the plasma retinol value after feeding is associated with the relative growth rate and physiological status [19; 20]. Another objective of this study was to investigate the relative bioavailability of microencapsulated vitamin A compared to non-microencapsulated vitamin A. Bioavailability is determined by comparing the AUC. We observed a similar AUC for retinol from both non-microencapsulated vitamin A and microencapsulated vitamin A. This observation implies that microencapsulated vitamin A is equally as effective as non-microencapsulated vitamin A, which is contrary to our hypothesis. [PERSON] et al. performed in vitro and in vivo studies [21] and revealed a prolonged ocular retention time and improved bioavailability of microencapsulated vitamin A compared with non-microencapsulated vitamin A. In our study, there was no significant improvement in the bioavailability of microencapsulated vitamin A, because the designed release mechanism for microencapsulation was not suitable for swine digestion in this case. Moreover, the release mechanisms vary with the type of encapsulating agent used to insert or encapsulate the active ingredient, the method of preparation, and the environment where the release occurs. The encapsulating agent is very important because it influences the microencapsulation efficiency and stability of the finial product. The main mechanisms involved in the core release are diffusion, degradation, and pH release [22].