Implications of Vitamin D Research in Chickens can Advance Human Nutrition and Perspectives for the Future

Abstract

The risk of vitamin D insufficiency in humans is a global problem that requires improving ways to increase vitamin D intake. Supplements are a primary means for increasing vitamin D intake, but without a clear consensus on what constitutes vitamin D sufficiency, there is toxicity risk with taking supplements. Chickens have been used in many vitamin-D-related research studies, especially studies involving vitamin D supplementation. Our state-of-the-art review evaluates vitamin D metabolism and how the different hydroxylated forms are synthesized. We provide an overview of how vitamin D is absorbed, transported, excreted, and what tissues in the body store vitamin D metabolites. We also discuss a number of studies involving vitamin D supplementation with broilers and laying hens. Vitamin D deficiency and toxicity are also described and how they can be caused. The vitamin D receptor (VDR) is important for vitamin D metabolism; however, there is much more to understand about VDR in chickens. Potential research aims involving vitamin D and chickens should explore VDR mechanisms that could lead to newer insights into VDR. Utilizing chickens in future research to help elucidate vitamin D mechanisms has great potential to advance human nutrition. Finding ways to increase vitamin D intake will be necessary because the coronavirus disease 2019 (COVID-19) pandemic is leading to increased risk of vitamin D deficiency in many populations. Chickens can provide a dual purpose with addressing pandemic-caused vitamin D deficiency: 1) vitamin D supplementation gives chickens added-value with the possibility of leading to vitamin-D-enriched meat and egg products; and 2) using chickens in research provides data for translational research. We believe expanding vitamin-D-related research in chickens to include more nutritional aims in vitamin D status has great implications for developing better strategies to improve human health.

Keywords: VDR; broiler; chicken; egg; human nutrition; laying hen; tibial dyschondroplasia; vitamin D; vitamin D supplementation; vitamin D toxicity.

FIGURE 1

Comparison of vitamin D precursors and their nutritionally relevant forms vitamin D₃ and D₂. In animals, when ultraviolet B rays (UVB) or sunlight hits 7-dehydrocholesterol (7-DHC) on the skin, then 7-DHC will undergo multiple reactions and be converted to cholecalciferol (vitamin D₃). In fungi and microalgae, ergosterol undergoes the same pathway as 7-DHC to become ergocalciferol (vitamin D₂).

FIGURE 2

Biochemical reactions of 7-dehydrocholesterol (7-DHC) that leads to synthesis of vitamin D₃ and potential noncalcemic metabolites. When ultraviolet B rays (UVB) or sunlight hits 7-dehydrocholesterol (7-DHC) on the skin, 7-DHC is converted to previtamin D₃ which is then converted to vitamin D₃, lumisterol-3, or tachysterol-3 by thermal isomerization. Vitamin D₃ enters the blood circulation to be hydroxylated to its more active forms. Vitamin D₃ in the skin can be converted to 5,6-trans-vitamin D₃ by UVB if it does not go into the circulation. Adapted with permission from (27) and (32).

FIGURE 3

Metabolic pathway of vitamin D₃ to its subsequent metabolite forms. Vitamin D₃ in circulation goes to the liver to be converted to 25-hydroxycholecalciferol (25-OH-D₃). 25-OH-D₃ can be further hydroxylated to either 24,25-dihydroxycholecalciferol [24,25-(OH)₂-D₃] or 1,25-dihydroxycholecalciferol [1,25-(OH)₂-D₃]. When 1,25-(OH)₂-D₃ binds to the vitamin D receptor, then biological effects are exerted through gene transcription. 1,25-(OH)₂-D₃ can also be further hydroxylated by 24-hydroxylase to 1,24,25-trihydroxycholecalciferol and undergoes a series of reactions to ultimately become calcitroic acid, a water-soluble metabolite that is safely excreted in urine. Adapted with permission from (27) and (32).