Progressive rise in gut hormone levels after Roux-en-Y gastric bypass suggests gut adaptation and explains altered satiety

CM Borg, CW Le Roux, MA Ghatei… - Journal of British …, 2006 - academic.oup.com
CM Borg, CW Le Roux, MA Ghatei, SR Bloom, AG Patel, SJB Aylwin
Journal of British Surgery, 2006academic.oup.com
Background Bariatric surgery is the most effective treatment for achieving long-term weight
loss in morbidly obese patients. This study investigated prospective changes in gut
hormones and metabolic indices after Roux-en-ϒ gastric bypass (RYGB). Methods Six
patients were seen before, and at 1, 3 and 6 months after operation. Blood was collected
after a 12-h fast and at regular intervals after a mixed 420-kcal meal. Hormonal responses
were determined, and comparisons between basal levels and areas under the curve were …
Background
Bariatric surgery is the most effective treatment for achieving long-term weight loss in morbidly obese patients. This study investigated prospective changes in gut hormones and metabolic indices after Roux-en-ϒ gastric bypass (RYGB).
Methods
Six patients were seen before, and at 1, 3 and 6 months after operation. Blood was collected after a 12-h fast and at regular intervals after a mixed 420-kcal meal. Hormonal responses were determined, and comparisons between basal levels and areas under the curve were made. Visual analogue scores were used to assess satiety, hunger and nausea.
Results
Mean body mass index decreased from 48·3 kg/m2 before surgery to 36·4 kg/m2 6 months after RYGB. This was accompanied by a decrease in fasting leptin (P < 0·001) and insulin (P = 0·021) levels. At 1, 3 and 6 months after operation, progressively increasing peptide YY (P < 0·001), enteroglucagon (P = 0·045) and glucagon-like peptide 1 (P = 0·042) responses were observed. There was no change in fasting ghrelin levels (P = 0·144). Postprandial satiety was significantly increased by 1 month after surgery and this was maintained until the end of the study (P < 0·001).
Conclusion
RYGB resulted in substantial weight loss with enhanced postprandial satiety, a sustained weight plateau, and proportionate reduction in fasting insulin and leptin levels. Lack of the expected increase in appetite and food intake as components of a counter-regulatory response may be explained by gut adaptation and the consequent graded rise in the levels of gut hormones that promote satiety.
Oxford University Press