Research Note: Effects of feeding corn naturally contaminated with aflatoxin B1, deoxynivalenol, and zearalenone on reproductive performance of broiler breeders and growth performance of their progeny chicks.

To evaluate the toxic effects of mycotoxin-contaminated corn (MC) on the breeders and their progeny chicks, a total of 480 fifty-wk-old Cobb broiler breeder hens were fed the following dies: 1) a corn-soybean meal diet (Control; containing 70.35% corn), 2) MC substituting for 50% of corn in Control (LM), 3) LM diet plus 2 g/kg 1 mycotoxin sequestrant, Toxy-Nil Plus (TNP) (LMT2.0), 4) MC substituting for 100% of corn in Control (HM), 5) HM diet plus 2 g/kg TN (HMT2.0), and 6) HM diet plus 2.5 g/kg TNP (HMT2.5). The MC contained 69.25 µg aflatoxin B1 (AFB1)/kg, 4,875 µg deoxynivalenol (DON)/kg, and 2,262 µg zearalenone (ZEN)/kg. At wk 4 after MC inclusion, all eggs laid were used for hatch, and all progeny chicks were fed the same mycotoxin-untreated diet for 14 d. Dietary MC inclusion decreased the hatchability of set eggs and increased embryo mortality during d 18 to 21.5. The TNP addition increased these aforementioned indices in MC-included diets. Maternal HM treatment decreased the BW of progeny chicks at age of 14 d and BWG of progeny chicks during d 1 to 14, whereas maternal LM treatment did not affect these indices. In parallel, maternal HM treatment decreased the concentrations of serum IgA, IgG, and lysozyme in the progeny chicks on d 14, but maternal LM treatment did not affect these indices. Overall, maternal dietary TNP treatments increased the growth of progeny chicks and had a trend to increase the concentrations of serum IgA and IgG on d 14 compared to maternal MC treatments. It was concluded that the feeding of relative high ratio of corn contaminated with low level of AFB1, DON, and ZEN negatively affected the reproductive performance of breeders and the growth performance of their progeny chicks, and TNP addition alleviated these toxic effects.

Molecular interactions governing the incorporation of cholecalciferol and retinyl-palmitate in mixed taurocholate-lipid micelles.

Cholecalciferol (D3) and retinyl palmitate (RP) are the two main fat-soluble vitamins found in foods from animal origin. It is assumed that they are solubilized in mixed micelles prior to their uptake by intestinal cells, but only scarce data are available on the relative efficiency of this process and the molecular interactions that govern it. The extent of solubilization of D3 and RP in micelles composed of lipids and sodium taurocholate (NaTC) was determined. Then, the molecular interactions between components were analyzed by surface tension and surface pressure measurements. The mixture of lipids and NaTC allowed formation of micelles with higher molecular order, and at lower concentrations than pure NaTC molecules. D3 solubilization in the aqueous phase rich in mixed micelles was several times higher than that of RP. This was explained by interactions between NaTC or lipids and D3 thermodynamically more favorable than with RP, and by D3 self-association.

25-Hydroxyvitamin D as a Biomarker of Vitamin D Status and Its Modeling to Inform Strategies for Prevention of Vitamin D Deficiency within the Population.

There is substantial evidence that the prevalence of vitamin D deficiency is unacceptably high in the population, and this requires action from a public health perspective. Circulating 25-hydroxyvitamin D [25(OH)D] is a robust and reliable marker of vitamin D status and has been used by numerous agencies in the establishment of vitamin D dietary requirements and for population surveillance of vitamin D deficiency or inadequacy. In a wider context, modeling of serum 25(OH)D data and its contributory sources, namely dietary vitamin D supply and UVB availability, can inform our understanding of population vitamin D status. The aim of this review is to provide the current status of knowledge in relation to modeling of such vitamin D-relevant data. We begin by highlighting the importance of the measurement of 25(OH)D and its standardization, both of which have led to new key data on the prevalence of vitamin D deficiency and inadequacy in North America and Europe. We then overview how state-of-the-art modeling can be used to inform our understanding of the potential effect of ergocalciferol and 25(OH)D on vitamin D intake estimates and how meteorological data on UVB availability, when coupled with other key data, can help predict population serum 25(OH)D concentration, even accounting for seasonal fluctuations, and lastly, how these in silico approaches can help inform policymakers on strategic options on addressing low vitamin D status through food-based approaches and supplementation. The potential of exemplar food-based solutions will be highlighted, as will the possibility of synergies between vitamin D and other dairy food-based micronutrients, in relation to vitamin D status and bone health. Lastly, we will briefly consider the interactions between season and vitamin D supplements on vitamin D status and health.

Comparison of the Micellar Incorporation and the Intestinal Cell Uptake of Cholecalciferol, 25-Hydroxycholecalciferol and 1-α-Hydroxycholecalciferol.

In the context of the global prevalence of vitamin D insufficiency, we compared two key determinants of the bioavailability of 3 vitamin D forms with significant biopotencies: cholecalciferol, 25-hydroxycholecalciferol and 1-α-hydroxycholecalciferol. To this aim, we studied their incorporation into synthetic mixed micelles and their uptake by intestinal cells in culture. Our results show that 1-α-hydroxycholecalciferol was significantly more solubilized into mixed micelles compared to the other forms (1.6-fold and 2.9-fold improvement compared to cholecalciferol and 25-hydroxycholecalciferol, respectively). In Caco-2 TC7 cells, the hydroxylated forms were taken up more efficiently than cholecalciferol (p < 0.05), and conversely to cholecalciferol, their uptake was neither SR-BI(Scavenger-Receptor class B type I)- nor NPC1L1 (NPC1 like intracellular cholesterol transporter 1)-dependent. Besides, the apical membrane sodium-bile acid transporter ASBT (Apical Sodium-dependent Bile acid Transporter) was not involved, at least in vitro, in the uptake of any of the three vitamin D forms. Further investigations are needed to identify the uptake pathways of both 1-α-hydroxycholecalciferol and 25-hydroxycholecalciferol. However, considering its high bioavailability, our results suggest the potential interest of using 1-α-hydroxycholecalciferol in the treatment of severe vitamin D deficiency.

The distribution and relative hydrolysis of tocopheryl acetate in the different matrices coexisting in the lumen of the small intestine during digestion could explain its low bioavailability.

SCOPE: Vitamin E is present in feed and food mainly as d-α-tocopherol (d-α-TOL) but also as all-rac-α-tocopheryl acetate (rac-α-TAC) through supplementation. Its absorption efficiency is low compared to that of triacylglycerols. The aim of this work was thus to study the fate of TAC during digestion. METHODS AND RESULTS: Using an in vitro digestion model, we showed that TAC was distributed between mixed micelles (36%), liposomes (9%), and nonsolubilized food debris (52%). A significant fraction of TAC was also found in emulsions when fat hydrolysis was not complete. Among the candidate esterases tested, i.e. cholesteryl ester hydrolase, pancreatic lipase, and pancreatic lipase-related protein 2, only cholesteryl ester hydrolase was able to hydrolyze TAC to all-rac-α-TOL, about five times more efficiently when it was incorporated into mixed micelles or liposomes than into emulsions or in the food matrix. Caco-2 cells were able to hydrolyze TAC and to uptake TOL when TAC was incorporated into mixed micelles but not into emulsions. CONCLUSION: During digestion, most TAC is recovered in matrices where its hydrolysis and its uptake by intestinal cells are markedly less efficient than in mixed micelles.