Special Issue "Nutrition, Taste, Reward and Bariatric Surgery"

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Public Health".

Deadline for manuscript submissions: 31 July 2023 | Viewed by 1081

Special Issue Editors

Department of Neural and Behavioral Sciences, College of Medicine, The Pennsylvania State University, Hershey, PA 17033, USA
Interests: bariatric surgery; animal models of obesity; food reward; taste; addiction
Department of Surgery, Division of Minimally Invasive Surgery/Bariatrics, College of Medicine, The Pennsylvania State University, Hershey, PA 17033, USA
Interests: bariatric surgery; weight management; obesity; minimally invasive surgery
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Special Issue Information

Dear Colleagues,

Bariatric surgery is the most effective and lasting treatment for severe obesity and associated metabolic disorders, but various procedures have differential outcomes with individual differences with respect to durability of weight loss, in addition to potentially conferring increased risk for substance use. The neural and hormonal mechanisms underlying decreased high calorie food intake and altered nutrient and taste preferences with the potential of reward transfer to non-food substances after bariatric surgery remain largely unexplored. Thus, this Special Issue solicits original studies and reviews on the recent progress in the field in order to promote a better understanding of pre-surgical and post-surgical factors contributing to metabolic surgery’s long-term success as well as individual differences in quality-of-life outcomes. We invite submissions from studies in human and animal models with a broad area of focus including but not limited to nutrient preferences, individual taste and reward reactivity, metabolic, gut-and-brain hormonal and neural (e.g., vagal) mechanisms, as well as the contribution of changes in gut microbial–host metabolic crosstalk, and inflammatory processes.   

Prof. Dr. Andras Hajnal
Prof. Dr. Ann M Rogers
Guest Editors

Manuscript Submission Information

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Keywords

  • bariatric surgery
  • high-calorie diets
  • post-operative nutrition
  • food reward
  • food preferences
  • taste
  • substance use disorders
  • gut–brain signaling
  • gut microbiota
  • gut–neuroimmune system

Published Papers (1 paper)

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Research

Article
Reduction of Plasma BCAAs following Roux-en-Y Gastric Bypass Surgery Is Primarily Mediated by FGF21
Nutrients 2023, 15(7), 1713; https://doi.org/10.3390/nu15071713 - 31 Mar 2023
Viewed by 871
Abstract
Type 2 diabetes (T2D) is a challenging health concern worldwide. A lifestyle intervention to treat T2D is difficult to adhere, and the effectiveness of approved medications such as metformin, thiazolidinediones (TZDs), and sulfonylureas are suboptimal. On the other hand, bariatric procedures such as [...] Read more.
Type 2 diabetes (T2D) is a challenging health concern worldwide. A lifestyle intervention to treat T2D is difficult to adhere, and the effectiveness of approved medications such as metformin, thiazolidinediones (TZDs), and sulfonylureas are suboptimal. On the other hand, bariatric procedures such as Roux-en-Y gastric bypass (RYGB) are being recognized for their remarkable ability to achieve diabetes remission, although the underlying mechanism is not clear. Recent evidence points to branched-chain amino acids (BCAAs) as a potential contributor to glucose impairment and insulin resistance. RYGB has been shown to effectively lower plasma BCAAs in insulin-resistant or T2D patients that may help improve glycemic control, but the underlying mechanism for BCAA reduction is not understood. Hence, we attempted to explore the mechanism by which RYGB reduces BCAAs. To this end, we randomized diet-induced obese (DIO) mice into three groups that underwent either sham or RYGB surgery or food restriction to match the weight of RYGB mice. We also included regular chow-diet-fed healthy mice as an additional control group. Here, we show that compared to sham surgery, RYGB in DIO mice markedly lowered serum BCAAs most likely by rescuing BCAA breakdown in both liver and white adipose tissues. Importantly, the restored BCAA metabolism following RYGB was independent of caloric intake. Fasting insulin and HOMA-IR were decreased as expected, and serum valine was strongly associated with insulin resistance. While gut hormones such as glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) are postulated to mediate various surgery-induced metabolic benefits, mice lacking these hormonal signals (GLP-1R/Y2R double KO) were still able to effectively lower plasma BCAAs and improve glucose tolerance, similar to mice with intact GLP-1 and PYY signaling. On the other hand, mice deficient in fibroblast growth factor 21 (FGF21), another candidate hormone implicated in enhanced glucoregulatory action following RYGB, failed to decrease plasma BCAAs and normalize hepatic BCAA degradation following surgery. This is the first study using an animal model to successfully recapitulate the RYGB-led reduction of circulating BCAAs observed in humans. Our findings unmasked a critical role of FGF21 in mediating the rescue of BCAA metabolism following surgery. It would be interesting to explore the possibility of whether RYGB-induced improvement in glucose homeostasis is partly through decreased BCAAs. Full article
(This article belongs to the Special Issue Nutrition, Taste, Reward and Bariatric Surgery)
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