Data from: Diet- and genetically-induced obesity differentially affect the fecal microbiome and metabolome in Apc1638N mice

Obesity is a risk factor for colorectal cancer (CRC), and alterations in
the colonic microbiome and metabolome may be mechanistically involved in
this relationship. The relative contribution of diet and obesity per se
are unclear. We compared the effect of diet- and genetically-induced
obesity on the intestinal microbiome and metabolome in a mouse model of
CRC. Apc1638N mice were made obese by either high fat (HF) feeding or the
presence of the Leprdb/db (DbDb) mutation. Intestinal tumors were
quantified and stool microbiome and metabolome were profiled. Genetic
obesity, and to a lesser extent HF feeding, promoted intestinal
tumorigenesis. Each induced distinct microbial patterns: taxa enriched in
HF were mostly Firmicutes (6 of 8) while those enriched in DbDb were split
between Firmicutes (7 of 12) and Proteobacteria (5 of 12). Parabecteroides
distasonis was lower in tumor-bearing mice and its abundance was inversely
associated with colonic Il1b production (p<0.05). HF and genetic
obesity altered the abundance of 49 and 40 fecal metabolites respectively,
with 5 in common. Of these 5, adenosine was also lower in obese and in
tumor-bearing mice (p<0.05) and its concentration was inversely
associated with colonic Il1b and Tnf production (p<0.05). HF and
genetic obesity differentially alter the intestinal microbiome and
metabolome. A depletion of adenosine and P.distasonis in tumor-bearing
mice could play a mechanistic role in tumor formation. Adenosine and P.
distasonis have previously been shown to be anti-inflammatory in the colon
and we postulate their reduction could promote tumorigenesis by
de-repressing inflammation.