Bariatric Times

NOV 2017

A peer-reviewed, evidence-based journal that promotes clinical development and metabolic insights in total bariatric patient care for the healthcare professional

Issue link:

Contents of this Issue


Page 12 of 32

12 Review Bariatric Times • November 2017 w eight lost within the first year. 6 Currently available evidence on weight loss-induced changes in appetite-regulating hormones supports a physiological-based r ationale for why weight maintenance after a period of acute weight loss is so challenging. The disruption of gut hormones persists following acute weight loss, and levels of some key p eptides never return back to pre- weight loss baseline even after one year. 11 Given leptin's release from adipose tissue, it is not surprising that r eduction in body weight and fat mass result in decreased levels of leptin. Profound reduction in circulating leptin levels following acute diet- i nduced weight loss can cause an increase in appetite and a decrease in energy expenditure. Sumithran et al 11 followed 50 patients with obesity through a 10-week diet-intensive w eight loss program and then for one additional year. They found that after a sharp decrease in leptin levels during the 10-week diet phase, consistently decreased leptin levels w ere strongly correlated with weight regain over the one-year follow-up period. Levels of anorexigenic gut hormones, such as GLP-1, PYY, and C CK, are all decreased from baseline following a period of diet-induced weight loss (Table 1). Reductions in these hormones can persist up to one y ear after diet-induced weight loss, which promotes increased appetite and decreased satiety, eventually leading to weight regain. 7 Higher fasting levels of ghrelin compared to b aseline are observed after a period of diet-induced weight loss, increasing the desire to overeat. It appears the body tries to defend its original set point by increasing orexigenic p eptides and decreasing anorexigenic peptides following a period of non- surgical-induced weight loss. This homeostatic imbalance might explain why there seems to be a limit to the a mount of weight that can be lost via lifestyle modification alone and why maintaining the weight loss is so challenging. Medications and gene t herapies directed toward moderating optimal levels of these peptides are currently available, and more are being investigated. The role of gut-brain axis peptides i n explaining the failure of diet alone to preserve weight loss compared to the persistent weight loss seen in bariatric surgery patients has been applicably explored. In contrast to d iet alone, today's most commonly performed bariatric surgery procedures (sleeve gastrectomy [SG] and Roux-en-Y gastric bypass [RYGB]) are associated with sustained r eductions in orexigenic hormones and increases in anorexigenic hormones up to one year postoperatively. 17 Leptin levels are reduced after all t ypes of bariatric surgery, presumably because of the drop in body fat mass. Adipocyte reduction might not be the only mechanism of leptin reduction since a drop in leptin levels can be s een as soon as one week after SG and RYGB, prior to notable weight loss. 18 Leptin is also produced in the gastric fundus. Limited interaction of nutrients with the limited remaining gastric fundus after SG and RYGB could explain the early reduction in leptin levels. Not all bariatric procedures have the same impact on these gut-derived appetite-regulating hormones. Much like diet-induced weight loss, adjustable gastric banding (AGB) was associated with increased ghrelin levels versus decreased levels seen after SG and RYGB. Favorable increases in anorexigenic hormones, such as GLP-1, PYY, and post-prandial insulin, are more pronounced in RYGB versus AGB subjects and seem to be similarly significant in RYGB and SG patients 8,12,19-20 . Compared to SG, RYGB patients exhibit higher post-prandial levels of GLP-1 and PYY, most likely because of earlier delivery of nutrients to the ileum 15 . Table 1 illustrates the advantageous impact of RYGB and SG on appetite- influencing gut peptides and how bariatric surgery enhances gut-brain circuitry to promote weight loss. This is in contrast to the adversarial neurohormonal environment created by diet-induced weight loss, which seems to put the body into a state of defending its original weight set point. CONCLUSION Physiological research on obesity has resulted in tremendous developments, and one of the most influential advances is the delineation of neurohormonal factors that interplay along the gut brain axis to control appetite, gastric emptying, satiety, and overall adiposity. Weight loss induced by diet alone is difficult to maintain, in part because of the increase in ghrelin and decrease in anorexigenic gut peptides, such as GLP-1, PYY, CCK, and amylin, produced by this method of weight

Articles in this issue

Links on this page

Archives of this issue

view archives of Bariatric Times - NOV 2017