Surgery for Obesity and Related Diseases ] (2016) 00–00 Editorial comment Comment on: A β-cell pancreatic dysfunction participates in the hyperglycemic peaks observed after gastric bypass surgery of obese patients Bariatric surgery has revolutionized the management of obesity and its co-morbid diseases. As such, major physio- logic mechanisms of these procedures target metabolic pathways. Bariatric procedures have been found to induce remission or improve type 2 diabetes (T2D) by varying degrees based on the procedure performed, likely secondary to effects of changes in metabolic pathways [1,2]. Com- pared with medical management, surgery has proven more durable and cost effective [3,4], in addition to being sustainable over years [3]. Attempts to postulate the mechanism by which remission is induced have been made [5]. Weight loss, malabsorption, and release of gastrointest- inal hormones are suggested to play a role in remission [6]. Remission does not always occur in patients, however, either by means of failure at the initial therapy, by partial response only, or by recidivism. Currently, there are no established predictive risk factors for T2D-remission failure [7]. Postprandial hypo- and/or hyperglycemia have been noted in some patients after Roux en-Y gastric bypass (RYGB) [8,9]. A definite pathophysiology explaining these phenomena has not been reported. The current article attempts to offer a glimpse into these mechanisms. In this study, the authors provide an initial framework to start to explain postprandial hyperglycemic episodes in a subset of post-RYGB patients. They hypothesized that pancreatic β-cells become dysfunctional and contribute to this phenomenon. Post-RYGB patients presenting with somewhat vague symptoms, such as “malaise,” were studied. A total of 42 consecutive patients were identified. At the authors’ institution, an oral glucose tolerance test (OGTT) was performed routinely as part of the evaluation of these symptoms. The patients were divided into 2 groups based on the presence of a hyperglycemic peak, designated as PEAK (n = 18) or NOPEAK (n = 24), on the basis of the OGTT performed. Pancreatic β-cell function was evaluated by measuring insulin sensitivity, secretion, and clearance. The patients underwent continuous glucose monitoring to assess dynamic changes in glucose. At 30 minutes post-OGTT, PEAK patients were found to have high glucose and C-peptide levels and elevated insulin secretion and clearance rates. Insulin sensitivity and calculated disposition index, a measure used to reflect pancreatic β- cell function, were found to be decreased. Furthermore, the continuous glucose monitoring indicated that the PEAK group had longer periods of hyperglycemia. The hypothesis leading to the study warrants investigation. The authors decided to assess the pancreatic β-cell function through the parameters mentioned earlier. Previous studies by Jacobsen et al. and Camastra et al. have given some insight into the effect of bariatric surgery on pancreatic β-cell function [10,11]. These authors reported positive effects of RYGB on pancreatic β-cell function. In the present study, measures in relation to pancreatic β-cells function have indicated an opposite effect, which raises the question of a subtype of T2D that does not respond or at least only partially responds to RYGB [12]. It might be worthwhile for this patient population, if one truly exists, to avoid surgery and be offered another treatment modality. A major limitation of this study is its small sample size and potential for type II error. Currently, this study has limited clinical implications, yet it may serve as a basis for more clinically oriented research. Future potential areas of investigation might include a more clear focus on better understanding the metabolic aspects of bariatric surgical procedures and defining objective assessment tools to identify patients who will not go into T2D remission. Such is the current state of our evolving understanding of the metabolic aspects of bariatric surgical procedures, and how to best select the correct approach for optimal patient outcomes. Essa M. Aleassa, M.D. Matthew Kroh, M.D. Cleveland Clinic Bariatric and Metabolic Institute Cleveland, Ohio http://dx.doi.org/10.1016/j.soard.2015.11.008 1550-7289/ r 2016 American Society for Metabolic and Bariatric Surgery. All rights reserved.