Effects of roux‐en‐Y gastric bypass surgery on postprandial fructose metabolism

Abstract

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 (Ctrl) subjects. Each participant was studied after ingestion of a protein and lipid meal (PL) and after ingestion of a protein1lipid1fructose1glucose meal labeled with 13 C-fructose (PLFG). Postprandial blood glucose, fructose, lactate, apolipoprotein B48 (apoB48), and triglyceride (TG) concentrations, 13 C-palmitate concentrations in chylomicron-TG and VLDL-TG, fructose oxidation ( 13 CO 2 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 5 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 5 0.064 and P 5 0.024, respectively). ApoB48 and 13 C-palmitate 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.

Role of the Enterocyte in Fructose-Induced Hypertriglyceridaemia

“…The study again demonstrated the capacity for DNL from fructose within human enterocytes [57]. In control subjects, the reported incremental area under the curve values (iAUC) for CM-[ 13 C]-palmitate were almost 2-fold greater than the VLDL-[ 13 C]-palmitate iAUC, suggesting enterocytes contributed more de novo palmitate to the overall circulating TRL-TG pool than hepatocytes.…”

“…Emerging evidence from rodents and humans indicates that enterocytes may make a more meaningful contribution to fructose metabolism than previously thought [42,57]. This appears to include disposal of fructose carbons via DNL, providing de novo FA to the circulation.…”

“…The aforementioned studies of Theytaz et al (2014) [56] and Surowska et al (2016) [57] provide some of the only available results to date regarding the effect of fructose on CM-TG levels, although they did not isolate specific CM and VLDL fractions as described above, but used the concentration of TG in the Sf > 400 fraction as a marker of CM-TG [56,57]. In the latter study, control subjects (no RYGB surgery) that consumed Fr + G in addition to ProLip tended to show an increased Sf > 400-TG response, with a larger delayed peak and higher iAUC over the 360 min time course, although these differences were not significant, perhaps owing to the low statistical power of the study and high inter-individual variation.…”

Dietary Fructose and Glucose: The Multifacetted Aspects of Their Metabolism and Implication for Human Health

“…The aforementioned studies of [56] and Surowska et al (2016) [57] provide some of the only available results to date regarding the effect of fructose on CM-TG levels, although they did not isolate specific CM and VLDL fractions as described above, but used the concentration of TG in the Sf > 400 fraction as a marker of CM-TG [56,57]. In the latter study, control subjects (no RYGB surgery) that consumed Fr + G in addition to ProLip tended to show an increased Sf > 400-TG response, with a larger delayed peak and higher iAUC over the 360 min time course, although these differences were not significant, perhaps owing to the low statistical power of the study and high inter-individual variation.…”

More pieces of the fructose puzzle

“…Interestingly, Intralipid plus glucose also increased the fractional clearance rate of TRP‐apo48. The group of Luc Tappy tracked the incorporation of 13 C into chylomicron and VLDL1 over 6 h in young normal weight and older overweight men who consumed meals consisting of 13 C‐labelled fructose, and unlabelled glucose, lipids and protein. The concentration of 13 C‐palmitate in chylomicron‐ and VLDL‐TG increased progressively after ingestion of 13 C‐fructose labelled meals in both groups of subjects, indicating that both intestinal and hepatic DNL contributed to the disposal of fructose carbons .…”