Poster Topical Area: Obesity
Location: Hall D
Poster Board Number: 718
Approximately 100 trillion bacteria inhabit the human gastrointestinal tract. The composition of human gut microbiota can be affected by a variety of genetic and environmental factors, such as a poor diet. A Western dietary pattern is associated with dysbiosis and adverse health outcomes, including obesity and metabolic disorders. Objectives: The primary objective of this study was to examine the contribution of gut microbiota from lean or obese human donors on development of metabolic syndrome and weight gain in recipient mice fed one of three basal diets: 1) the standard AIN93G diet, designed to promote rodent health; 2) the total Western diet (TWD), which promotes inflammation-associated colorectal carcinogenesis; and 3) a 45% high fat diet-induced obesity (DIO) diet, which promotes excessive weight gain and symptoms of metabolic syndrome. We hypothesized that mice receiving gut bacteria from obese humans would develop an obese phenotype with symptoms of metabolic syndrome, which would be maintained by consumption of either TWD or DIO diets.
Methods: A 2x3 factorial experiment design was used, where mice received fecal transfer from either lean or obese human donors and were fed one of the three diets listed above for 20 weeks. Prior to fecal transfer, the resident gut microbiome was depleted using an established antibiotic/antifugal oral dosing regimen. Endpoints assessed included body weight and composition, food and energy intake, glucose tolerance and microbiota profiling of the human donor samples and fecal samples from recipient mice.
Results: Fecal transfer from obese or lean donors did not significantly differentially affect final body weight or body composition in recipient mice fed either the AIN, TWD or DIO diets. However, beta diversity analysis showed that obese recipient mice had a significantly different microbiome compared to lean recipient mice (P=0.01). As expected, consumption of the high fat DIO diet did result in a significant increase in body weight, fat mass and glucose intolerance (P<0.0001).
Conclusion: In this study, fecal transfer of bacteria from obese human donors did not alter the phenotype of recipient mice, in terms of weight gain or symptoms of metabolic syndrome despite recipient mice having distinct microbiomes.
Utah State University