235-LB: Postprandial Short-Chain Fatty Acid Concentrations in the Intestinal Lumen and Plasma

2020 
Obesity continues to be a global health risk affecting over 650 million adults worldwide. Fiber intake is negatively correlated with obesity, and increased fiber intake is associated with weight loss. Fiber is digested by the gut microbiota to produce short chain fatty acids (SCFA), which may have a beneficial effect on metabolic disease. While it is well known that SCFAs are mostly utilized by enterocytes as a fuel source, the timing of postprandial production and absorption of SCFAs from a meal, as well as the effect of high-fat feeding, has yet to be characterized. In the present study, we aimed to determine the levels of acetate, butyrate, and propionate, the major SCFAs, after a meal in rats maintained for 4wks on a chow, high-fat diet (45% kcal from fat; HFD) or HFD with 10% oligofructose (OFS), a well-studied prebiotic known to induce weight loss. SCFA levels were measured in the distal small intestine, cecum, and colon of rats, as well as the portal vein and vena cava at 0, 2, 4, 6, and 8 hours following consumption of an isocaloric meal of the maintenance diet. Chow rats had significantly increased levels of SCFAs as early as 2h postprandially, in the cecum, colon, portal vein, and vena cava compared to baseline levels, whereas HFD-fed rats displayed minimal increases in SCFAs. Addition of OFS rescued SCFA production, peaking at 4h postprandial; however, concentrations were not rescued to chow values at all timepoints. Increased body weight and adiposity was not associated with baseline SCFA levels in any compartment, but was negatively associated with postprandial SCFA levels in the cecum, colon, and portal vein. Overall, this study demonstrates that SCFAs exhibit a post-prandial rise similar to ingested macronutrients, and that baseline fasting levels of SCFAs may be an inaccurate indication of SCFA production in rodents. These data lay the groundwork for future studies to examine how rises in SCFA levels from breakdown of non-digestible carbohydrates can contribute to improve metabolic disease. Disclosure R. Meyer: None. A.I.L. Lane: None. A. Kangath: None. S.N. Weninger: None. T. Martinez: None. F. Duca: None.
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