Why the study?
In animal models, RYGB is associated with increased Roux limb intestinal glucose uptake that may contribute to early metabolic benefits, but prospective clinical studies are lacking.
Does Roux-en-Y gastric bypass increase intestinal glucose uptake in patients undergoing the procedure?
Does Roux-en-Y gastric bypass increase intestinal glucose uptake in patients undergoing the procedure?
In humans, Roux-en-Y gastric bypass increases glucose uptake in the colon rather than the Roux limb, highlighting a physiological difference from rodent models.
RYGB may increase colonic glucose uptake in humans; hypothesis-generating for mechanisms differing from rodent models.
Context In animal models, Roux-en-Y gastric bypass (RYGB) is associated with increased Roux limb intestinal glucose uptake that may contribute to early metabolic benefits, though prospective clinical studies are lacking. Objective The present study aimed to test the hypothesis that Roux limb glucose uptake would increase relative to baseline in a cohort of patients undergoing RYGB. Methods RYGB patients underwent preoperative baseline, and 3- and 6-month positron emission tomography/computed tomography postoperative imaging. Maximum and mean standardized uptake values (SUV) were measured from the following predefined regions of interest: cecum, hepatic flexure, splenic flexure, sigmoid colon, duodenal bulb, Roux limb, and common channel. SUV ratios were normalized to the spleen for assessment of longitudinal change. Results Despite significant weight loss in all patients, no changes in Roux limb glucose uptake were observed relative to baseline; however, marked increases in glucose uptake were detected in the colon (cecum, hepatic flexure, and sigmoid colon) by 3 months that were maintained at 6 months (P < .05). Conclusion RYGB is associated with increased intestinal glucose uptake in humans, but this increase appears limited to the colon in the early postoperative period up to 6 months. While the marked increases in Roux limb glucose uptake may contribute to weight loss in rodent models, this mechanism does not appear to translate to human physiology. Unexpected increases in colonic glucose uptake warrant dedicated mechanistic studies to determine the clinical significance of these changes.
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Corpodean et al. (2025) studied this question.
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