Our taste system plays the role of gatekeeper for whatever we ingest, warning us of aversive tasting foods, indicating the dangers of rotten or rancid food, and potentially poisonous bitter compounds. It also stimulates reward circuits in the brain when we ingest compounds triggering the appetitive tastes of sweet, salty, fat, and umami, indicating calories, minerals, lipids and protein. In the modern environment, where hyper palatable foods are bountiful, an altered sense of taste can lead to overconsumption of these energy dense appetitive compounds. Indeed, in the obese, researchers have noted altered taste responses, which may contribute altered eating behaviors, and drive the worldwide epidemic of overnutrition. Work in our own lab has implicated certain proinflammatory cytokines as associated with a damaged taste phenotype in mice, with obese mice having fewer taste buds than lean littermates. Where the initial inflammatory insult comes from remains a mystery, but recent work on the microbiome has associated obese phenotypes with altered microbial communities. We conceived this work to test whether an altered microbiome may be the ultimate culprit in damage to the taste system observed with obesity. We found that prebiotic supplementation to a high fat diet, which altered the composition of the microbiome, did protect mice from taste damage associated with obesity. However, we were unable to recapitulate the microbial dysbiosis present in obese mice through gavages to lean mice. This was partially due to the presence of a consortia of colonization resistant microbes that blunted the effectiveness of fecal transplants. As most fecal transplants are carried out in germ-free mice, the discovery of this consortia will be of use to other researchers without access to germ-free models and may be of interest to the burgeoning microbiome field as a whole.