Comments for:
Abstract
BACKGROUND Bariatric surgeries are the most effective treatments for successful and sustained weight loss, but individuals vary in treatment response. Understanding the neurobiological and behavioral mechanisms accounting for this variation could lead to the development of personalized therapeutic approaches and improve treatment outcomes. The primary objectives of this study were to investigate changes in taste preferences and taste-induced brain responses after Roux-en-Y gastric bypass (RYGB) and vertical sleeve gastrectomy (VSG) and to identify potential taste-related predictors of weight loss.METHODS Females, ages 18 to 55, with a body mass index greater than or equal to 35 kg/m2, and approved for bariatric surgery at the Johns Hopkins Center for Bariatric Surgery were recruited for participation. Demographics, anthropometrics, liking ratings, and neural responses to varying concentrations of sucrose plus fat mixtures were assessed before and after surgery via visual analog scales and functional MRI.RESULTS Bariatric surgery produced decreases in liking for sucrose-sweetened mixtures. Greater preference for sucrose-sweetened mixtures before surgery was associated with greater weight loss in RYGB, but not VSG. In the RYGB group only, individuals who showed lower taste-induced activation in the ventral tegmental area (VTA) before surgery and greater changes in taste-induced VTA activation 2 weeks following surgery experienced increased weight loss.CONCLUSION The anatomical and/or metabolic changes associated with RYGB may more effectively “reset” the neural processing of reward stimuli, thereby rescuing the blunted activation in the mesolimbic pathway found in patients with obesity. Further, these findings suggest that RYGB may be particularly effective in patients with a preference for sweet foods.FUNDING NIH K23DK100559 and Dalio Philanthropies.
Authors
Kimberly R. Smith, Afroditi Papantoni, Maria G. Veldhuizen, Vidyulata Kamath, Civonnia Harris, Timothy H. Moran, Susan Carnell, Kimberley E. Steele
Weight loss following RYGB, a result from resetting gut-brain axis and taste-related reward circuit?
Submitter: Xiaojuan Zhang | jijifaye2009@hotmail.com
Authors: Haoming Tian
Department of Endocrinology and Metabolism, West China Hospital of Sichuan University
Published July 9, 2020
Disruption in central reward circuits contributes to the pathogenesis of food overconsumption and obesity. Sustained weight loss observed in obese patients after bariatric surgery may partially due to its effects on resetting central reward circuits and therefore the hedonic control of food intake. However, the underlying mechanisms are not clear. In this issue of JCI, Smith et al. reported that taste-related reward was associated with weight loss following bariatric surgery (1). They found in their study that obese patients underwent Roux-en-Y gastric bypass (RYGB) and vertical sleeve gastrectomy (VSG) showed significant weight loss 6-month postoperatively, besides, the liking for sucrose-sweetened mixtures was decreased. Notably, greater preference for sucrose-sweetened mixture before surgery was associated with more significant weight loss in RYGB group only. What is more, lower taste-induced activation in the ventral tegmental area (VTA) of the central reward circuits prior to surgery and greater changes in taste-induced VTA activation two weeks following surgery in RYGB group but not VSG group, experienced better weight loss. These data suggest that RYGB might have an effect on resetting central reward circuits by affecting peripheral and central taste signals through anatomical and metabolic changes.
However, in this study, the authors did not provide information on diet habits and diet record before and after the surgery, which may influence the outcome. A small-scale survey shows that cutting out sugar and artificial sweeteners for 2 weeks could reset sugar preference and result in less sugar consumption (2). In a functional MRI study, glucose ingestion induced decreased signals in hypothalamus than water and artificial sweeteners (3). RYGB reduced sucrose intake in rats, preoperative sucrose exposure reduced this effect (4). Collectively, these results suggest that restricting sugar and consumption of artificial sweeteners before and after bariatric surgery might affect sugar preference and taste related central reward signals.
In a recent study published in Nature, Tan et al. showed striking results that connected gut-brain axis with sugar preference (5). They demonstrated in mice that glucose, but not artificial sweeteners, delivered directly to the gut activated neurons in the neural circuit that communicates the presence of sugar to the brain and the effects are mediated by sodium-dependent glucose transporter 1(SGLT1). SGLT1 expression was found to be upregulated after RYGB in human subjects (6), which together suggest RYGB may reset the central reward circuits by adjusting gut-brain axis as well as oral taste-related reward circuit.
Reference
1. Smith KR, Papantoni A, Veldhuizen MG, Kamath V, Harris C, Moran TH, et al. Taste-related reward is associated with weight loss following bariatric surgery. J Clin Invest. 2020.
2. Bartolotto C. Does Consuming Sugar and Artificial Sweeteners Change Taste Preferences? Perm J. 2015;19(3):81-4.
3. Smeets PA, de Graaf C, Stafleu A, van Osch MJ, van der Grond J. Functional magnetic resonance imaging of human hypothalamic responses to sweet taste and calories. Am J Clin Nutr. 2005;82(5):1011-6.
4. Bueter M, Miras AD, Chichger H, Fenske W, Ghatei MA, Bloom SR, et al. Alterations of sucrose preference after Roux-en-Y gastric bypass. Physiol Behav. 2011;104(5):709-21.
5. Tan HE, Sisti AC, Jin H, Vignovich M, Villavicencio M, Tsang KS, et al. The gut-brain axis mediates sugar preference. Nature. 2020;580(7804):511-6.
6. Nguyen NQ, Debreceni TL, Bambrick JE, Chia B, Deane AM, Wittert G, et al. Upregulation of intestinal glucose transporters after Roux-en-Y gastric bypass to prevent carbohydrate malabsorption. Obesity (Silver Spring). 2014;22(10):2164-71.
Copyright © 2024 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)