Bariatric surgery, including the Roux-en-Y gastric bypass (RYGB), is currently the only effective long-term treatment for morbid obesity. Contrary to the traditional classification of RYGB as a restrictive and malabsorptive procedure, these factors seem to play a minor role. Increasing evidence suggests that changes in gut hormone levels, such as glucagon-like peptide-1 (GLP-1), may account for the majority of the effects.
One major side effect of RYGB surgery is a decrease in bone density. In a longitudinal study in rats, we showed that bone mineral density decreased early after RYGB surgery and coincided with intestinal calcium malabsorption. Although intestinal calcium absorption normalized between two and seven weeks after surgery, there was no restoration of bone mass; this was potentially caused by chronic lactic acidosis. The RYGB-induced changes in bone metabolism occurred independent of weight loss.
Previous studies have shown that the compensatory decrease in energy expenditure in response to body weight loss is attenuated in RYGB rats. Since increased GLP-1 levels contribute to the reduced caloric intake after RYGB surgery, we hypothesized that they may also be involved in the reported alterations in energy expenditure; however, we did not find any effect of acute GLP-1 agonism or antagonism on energy expenditure. We were further able to show that the altered energy expenditure in RYGB rats was not caused by differences in body composition or by a shift in the thermoneutral zone.