Journal
OBESITY
Volume 24, Issue 3, Pages 589-596Publisher
WILEY
DOI: 10.1002/oby.21410
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Funding
- Swiss National Foundation for Science [320030-138428, 320030-135782]
- Swiss National Science Foundation (SNF) [320030_138428, 320030_135782] Funding Source: Swiss National Science Foundation (SNF)
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Objective: Fructose is partly metabolized in small bowel enterocytes, where it can be converted into glucose or fatty acids. It was therefore hypothesized that Roux-en-Y gastric bypass (RYGB) may significantly alter fructose metabolism. Methods: We performed a randomized clinical study in eight patients 12-17 months after RYGB and eight control (CM) subjects. Each participant was studied after ingestion of a protein and lipid meal (PL) and after ingestion of a protein f lipid fructose glucose meal labeled with C-13-fructose (PLFG). Postprandial blood glucose, fructose, lactate, apolipoprotein B48 (apoB48), and triglyceride (TG) concentrations, C-13-paInnitate concentrations in chylonnicron-TG and VLDL-TG, fructose oxidation ((CO2)-C-13 production), and gluconeogenesis from fructose (GNGf) were measured over 6 hours. Results: After ingestion of PLFG, postprandial plasma fructose, glucose, insulin, and lactate concentrations increased earlier and reached higher peak values in RYGB than in Ctrl. GNGf was 33% lower in RYGB than Ctrl (P = 0.041), while fructose oxidation was unchanged. Postprandial incremental areas under the curves for total TG and chylomicrons-TG were 72% and 91% lower in RYGB than Ctrl (P = 0.064 and P = 0.024, respectively). ApoB48 and C-13-paInnitate concentrations were not significantly different. Conclusions: Postprandial fructose metabolism was not grossly altered, but postprandial lipid concentrations were markedly decreased in subjects having had RYGB surgery.
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