Although the exact mechanism whereby hypothalamic FFAR2/3 exert their metabolic actions is yet to be fully clarified, it has been shown that high fat diet exposure results in increased expression of FFAR3 in the PVN, associated with decreased butyrate levels, as putative contributing factor for development of inflammation and hypertension, while virogenetic silencing of FFAR3 in the PVN attenuated these adverse responses, i.e., tissue inflammation and hypertension, in rats (75). This evidence concerns the gene FFAR2 and hypertensive disorder.