Trimethylamine-N-oxide (TMAO) is an important biomarker of atherosclerosis. TMAO is the product of a hepatic conversion of trimethylamine (TMA). Releasing of TMA moieties is dependent on the adaptation of the gut microbiota to dietary TMA containing substrates such as phosphatidylcholine (PC), choline, and L-carnitine. A high-fat diet is an environmental risk factor that may increase TMAO production. However, it isn’t clear if the high dietary intake of TMA is sufficient to promote increased plasma TMAO or if a high-fat intake is also required. We hypothesized that TMAO would be increased after consuming a high-fat diet and a high PC diet independently, with greater increases when consumed together. Four groups of twelve mice each were maintained on different treatments that were either low or high-fat with or without PC over two weeks. Then, a meal containing 9.99 g of corn oil and 0.75 g soybean L-α-Lecithin per 1 kg body weight was provided to all mice to indirectly observe the adaptation of the microbiota to the altered diet. The results of circulating TMAO levels showed that fat appeared to suppress TMAO production, which is against previous evidence. The microbial adaptation to the different treatments wasn’t observed in the measurement of fecal TMA levels. As a result, our hypothesis was rejected. Future work addressing the impact of gene expressions of enzymes on the gut and the liver is needed. The use of another high TMA containing substrates such as choline and rats is recommended. / Master of Science in Life Sciences / Cardiovascular disease (CVD) is heart and blood vessel diseases - many of which are caused by atherosclerosis, a condition wherein fatty materials accumulate in the artery wall, reducing blood flow. The compound trimethylamine-N-oxide (TMAO) was found to be an important biomarker of atherosclerosis. TMAO levels increase in the body when gut microbiota releases trimethylamine (TMA) moieties from dietary phosphatidylcholine (PC), choline, and L-carnitine such as eggs and meat. A high-fat intake was believed to have an impact on increased levels of TMAO. However, it wasn’t clear if the dietary intake of high TMA containing substrates such as PC, is sufficient to promote TMAO formation or if a high-fat content is also required. We hypothesized that TMAO would be increased after consuming a high-fat diet and a high PC diet independently, with greater increases when consumed together. The results would suggest new dietary strategies to avoid CVD. Four groups of twelve mice each were maintained on different treatments that were either low or high-fat with or without PC over two weeks. Then, a meal containing corn oil and PC was provided to all mice to observe the adaptation of the microbiota to the altered diet. The results showed that fat reduces circulating TMAO production, which is against previous evidence. Fecal TMA levels showed that microbiota activities weren’t observed in the colon. As a results, no significant levels of TMA and its precursors were observed in feces.
| Identifer | oai:union.ndltd.org:VTETD/oai:vtechworks.lib.vt.edu:10919/81952 |
| Date | 26 January 2018 |
| Creators | Ajlan, Reem |
| Contributors | Food Science and Technology, Neilson, Andrew P., Ponder, Monica A., Davy, Kevin P., Stewart, Amanda C. |
| Publisher | Virginia Tech |
| Source Sets | Virginia Tech Theses and Dissertation |
| Language | en_US |
| Detected Language | English |
| Type | Thesis |
| Format | ETD, application/pdf |
| Rights | In Copyright, http://rightsstatements.org/vocab/InC/1.0/ |
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