Honarbakhsh, Maryam. The effects of different forms of vitamin A on intestinal health: insights from a genetic mouse model of vitamin A deficiency. Retrieved from https://doi.org/doi:10.7282/t3-8ajh-a231
DescriptionVitamin A deficiency (VAD) is one of the most widespread micronutrient deficiencies affecting hundreds of millions of children and pregnant women in over half of the countries worldwide, despite the implementation of numerous intervention programs. Emerging evidence suggests that VAD can impact intestinal microbiota diversity and fitness suggesting a combined effect of dietary vitamin A and status. Not only vitamin A can be obtained from food of animal origin as preformed vitamin A, but also from vegetables and fruits containing provitamin A carotenoids, mainly as βC. In fact, βC is the most abundant dietary source of vitamin A worldwide, and often the sole source of the vitamin in certain regions of the world. Yet, its impact on intestinal functions and microbiome is unknown, especially during VAD.
The goal of this study was to understand the impact of different forms of dietary vitamin A (preformed retinoids or provitamin A carotenoids) vs. vitamin A status on intestinal health during VAD. To address this question, we used a genetic mouse model of VAD, the Lrat-/-Rbp-/- mice. Unable to store and deliver retinoids (vitamin A and its derivatives) to peripheral tissues, these mice display a tenuous vitamin A status. Fecal 16S rRNA gene analysis showed that VAD in our genetic model was concomitant with fecal microbial dysbiosis and dietary vitamin A did not impact the fecal microbial taxonomic profile. Also, VAD resulted in impaired structure and functions of the intestinal barrier as manifested by reduced mucins and antimicrobial defense, leaky gut, increased inflammation and oxidative stress, and impaired mucosal immunocytokine profiles. We also showed that that -carotene, as the sole source of the vitamin, not only improved the vitamin A status of the vitamin A deficient mutant mice but also improved intestinal dysfunctions and modified the taxonomic profile of the fecal microbiome of VAD.