Class
Article
College
College of Agriculture and Applied Sciences
Faculty Mentor
Abby Benninghoff
Presentation Type
Oral Presentation
Abstract
The composition of the human gut microbiome can be affected by environmental factors, such as a poor diet. A Western dietary pattern is associated with dysbiosis and adverse health outcomes, including obesity and metabolic disorders. The 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, which promotes 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 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. 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 presentation dosing regimen. 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. As expected, consumption of the DIO diet resulted in a significant increase in body weight, fat mass and glucose intolerance. In conclusion, fecal transfer of bacteria from obese human donors did not alter the phenotype of recipient mice, in terms of weight gain or metabolic syndrome symptoms despite recipient mice having distinct microbiomes.
Location
Room 421
Start Date
4-12-2018 1:30 PM
End Date
4-12-2018 2:45 PM
Impact of basal diet on obesity phenotype of host mice following fecal transfer from obese or lean human donors
Room 421
The composition of the human gut microbiome can be affected by environmental factors, such as a poor diet. A Western dietary pattern is associated with dysbiosis and adverse health outcomes, including obesity and metabolic disorders. The 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, which promotes 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 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. 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 presentation dosing regimen. 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. As expected, consumption of the DIO diet resulted in a significant increase in body weight, fat mass and glucose intolerance. In conclusion, fecal transfer of bacteria from obese human donors did not alter the phenotype of recipient mice, in terms of weight gain or metabolic syndrome symptoms despite recipient mice having distinct microbiomes.