Recent molecular studies have revealed a complex microbiota in the dog intestine, consisting of thousand bacterial, fungal, and viral phylotypes. Convincing evidence has been reported linking changes in microbial communities to acute and chronic gastrointestinal inflammation, especially in canine inflammatory bowel disease (IBD). Most common microbial changes observed in intestinal inflammation are decreases in the bacterial phyla Firmicutes (i.e., Lachnospiraceae, Ruminococcaceae, Fecalibacterium) and Bacteroidetes, with concurrent increases in Proteobacteria (i.e., E. coli). Due to the important role of microbial-derived metabolites for host health, it is important to elucidate the metabolic consequences of gastrointestinal dysbiosis and a better understanding of the physiological pathways is helpful to potentially pinpoint specific diseases. Novel approaches such as shotgun sequencing of DNA allow characterizing functional changes in the bacterial metagenome in gastrointestinal disease. Furthermore, wide scale and untargeted measurements of metabolic products derived by the host and the microbiota in intestinal samples allow a better understanding of the functional alterations that occur in gastrointestinal disease. For example, changes in bile acid metabolism, short-chain fatty acid concentrations, and tryptophan pathways have recently been reported in humans and dogs. Also, metabolites associated with the pentose phosphate pathway were significantly altered in chronic gastrointestinal inflammation and indicate the presence of oxidative stress in dogs with IBD. Better understanding of the interactions of microbial-derived metabolites and the host will yield insights into the pathophysiology of gastrointestinal diseases. Furthermore, some of these metabolic pathways can be targeted to develop better treatment approaches.