Abstract
BackgroundGut bacteria release trimethylamine (TMA) from dietary substrates, e.g., choline, phosphatidylcholine, and L‐carnitine. TMA is absorbed and subsequently oxidized in the liver to produce trimethylamine N‐oxide (TMAO). TMAO is associated with type 2 diabetes (T2D) and increased risk of cardiovascular disease. Consumption of a high fat diet (HFD) is associated with increase in TMAO in sedentary individuals. However, whether the increase in TMAO with consumption in a HFD is observed in endurance trained individuals is unknown.MethodsHealthy, sedentary (n=17) and endurance trained (n=7) males consumed a 10‐day isocaloric lead‐in diet comprised of 55% carbohydrate, 30% total fat, <10% saturated fat prior to baseline testing. Blood samples were obtained in the fasting state and every hour during a 4‐hour high fat challenge (HFC) meal (820 kcal; 25% carbohydrate, 63% fat [21% saturated fat]) at baseline and following 5‐day HFD (30% carbohydrate, 55% total fat, 25% saturated fat). Plasma TMAO and TMA‐moieties (choline, betaine, L‐carnitine) were measured using isocratic ultraperformance liquid chromatography‐tandem mass spectrometry.ResultsAge (23±3 vs. 22±2.1 yrs) and body mass index (23.4± 3.0 vs. 23.5±2.1 kg/m2) were similar (both P>0.05) in the sedentary and endurance trained group, respectively. As expected, VO2max was significantly higher in the endurance trained compared with sedentary individuals (56.7±8.2 vs. 39.3±5.8 ml/kg/min). There were no significant differences in fasting (1.92 ± 0.8 μM vs. 2.09 ± 1.1 μM, P>0.05) or postprandial TMAO between sedentary or trained individuals, respectively, at baseline. Neither fasting (1.49± 1.2 μM vs. 2.25 ± 1.4 μM, P>0.05) or postprandial TMAO changed significantly with the HFD in the sedentary and endurance training individuals.ConclusionsNeither fasting nor postprandial TMAO changed significantly following the HFD in the endurance trained compared to sedentary individuals in the present study. Future studies are needed to identify effective interventions that target TMA‐releasing bacteria and reduce TMAO.Support or Funding InformationAmerican Diabetes Association and Translation Obesity Research Interdisciplinary Graduate Education ProgramThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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