Study of the effects of vitamin A metabolism on the gut commensal based on its dietary sources
Vitamin A (VA) enables some of the most crucial functions in the mammalian body - immune cell maturation, tissue regeneration, and vision. Its human deficiency is linked to infectious disease, blindness, and delayed growth. While preformed VA is naturally found in animal-based foods, the body can convert only specific plant-derived pro-VA carotenoids, notably beta-carotene, into VA. The metabolic pathways involved in the metabolism of pre- and pro-formed vitamin A into its active metabolite, retinoic acid (RA) are well studied and reveal their key role in regulating multiple aspects of mammalian physiology. Our recent work has shown that in mice besides the dedicated host intrinsic vitamin A metabolism, commensal bacteria residing in the gastrointestinal tract are also capable of metabolizing preformed dietary retinoids into active forms thus significantly expanding the vitamin A metabolic capabilities of the host. However, whether the human microbiome also has the vitamin A metabolic capacity and if this bacteria's intrinsic vitamin A metabolic capacity also extends to the pro-form of vitamin A such as beta-carotene forms a significant source of vitamin A in the human diet. This study assessed the human microbiome's metabolic capacity to process preformed acetate and pro-VA in the form of beta-carotene. Our research demonstrates that RA production by gut bacteria on pre-VA coincides with microbial dysbiosis, characterized by the bloom of Proteobacteria in the gut lumen.