Abstract
Abstract By 2030, half the human population will be obese contributing to diabetes, cancer and cardiovascular disease. The gut peptide, vasoactive intestinal peptide (VIP) that acts as a regulator of innate and adaptive immunity, is elevated in obese humans. VIP mediates immunity changes through binding two receptors, called VPAC1 and VPAC2. Unfortunately, the pathways linking VIP signaling to obesity are not known. We hypothesized that defective VIP signaling would have an anti-obesity effect by lowering the gut firmicutes/bacteroidetes (f:b) ratio. To this end, knockout mice deficient for VIP, VPAC1 or VPAC2, were used to collect 16S rRNA reads from fecal samples. Operational taxonomic units for each strain were compared against each other to determine changes in bacterial taxa. Moreover, differences in gene functions were analyzed using PICRUSt. These data revealed a significant decrease in the f:b ratio for mice deficient in VIP and VPAC2 compared to wild type controls. Heterozygous and homozygous littermates for the VIP mutation showed the greatest reduction in fecal bacterial richness and clustered differently when compared phylogenetically to wild type or VIP receptor knockout strains. Metabolome predictions indicated that genes regulating the circulatory system and cardiovascular disease were consistently altered in mice deficient for VIP or its two receptors. In summary, deficiency in the VIP signaling axis significantly alters the gut microbiota and microbiome.
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