Impact of Vitamin D Deficit on the Rat Gut Microbiome
Metadatos
Afficher la notice complèteAuteur
Robles-Vera, Iñaki; Callejo, María; Ramos, Ricardo; Duarte Pérez, Juan Manuel; Pérez-Vizcaíno, FranciscoEditorial
MDPI
Materia
Microbiota 16S rRNA sequencing Vitamin D deficit
Date
2019-10-24Referencia bibliográfica
Robles-Vera, I., Callejo, M., Ramos, R., Duarte, J., & Perez-Vizcaino, F. (2019). Impact of Vitamin D Deficit on the Rat Gut Microbiome. Nutrients, 11(11), 2564.
Patrocinador
This study is supported by grants from Mineco (SAF2016-77222-R and SAF2017-8489-R), with funds from the European Union (Fondo Europeo de Desarrollo Regional FEDER) and Fundación Contra la Hipertensión Pulmonar (Empathy grant). I.R.V and M.C. are funded by Mineco (FPU grant) and Universidad Complutense de Madrid, respectively. FPV was funded by a Mobility grant from CIBERESRésumé
Inadequate immunologic, metabolic and cardiovascular homeostasis has been related to
either an alteration of the gut microbiota or to vitamin D deficiency. We analyzed whether vitamin
D deficiency alters rat gut microbiota. Male Wistar rats were fed a standard or a vitamin D-free
diet for seven weeks. The microbiome composition was determined in fecal samples by 16S rRNA
gene sequencing. The vitamin D-free diet produced mild changes on alpha- diversity but no effect on
-diversity in the global microbiome. Markers of gut dysbiosis like Firmicutes-to-Bacteroidetes ratio or
the short chain fatty acid producing bacterial genera were not significantly affected by vitamin D
deficiency. Notably, there was an increase in the relative abundance of the Enterobacteriaceae, with
significant rises in its associated genera Escherichia, Candidatus blochmannia and Enterobacter in vitamin
D deficient rats. Prevotella and Actinomyces were also increased and Odoribacteraceae and its genus
Butyricimonas were decreased in rats with vitamin D-free diet. In conclusion, vitamin D deficit does
not induce gut dysbiosis but produces some specific changes in bacterial taxa, which may play a
pathophysiological role in the immunologic dysregulation associated with this hypovitaminosis.