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4th INTERNATIONAL CONSENSUS SUMMIT FOR SLEEVE GASTRECTOMY II: Mechanisms of Action Is GLP-1 the Culprit of the Effects of Sleeve Gastrectomy on Glucose Tolerance? by JOSEP VIDAL, MD, and ANTONIO LACY, MD Bariatric Times. 2013;10(5 Suppl A):A7–A8 AUTHOR AFFILIATIONS: Dr. Vidal is from the Obesity Unit and Endocrinology and Nutrition Department, Hospital Clinic, University of Barcelona, Barcelona, Spain. Dr. Lacy is from the Obesity Unit and Gastrointestinal Surgery Department, Hospital Clinic, University of Barcelona, Barcelona, Spain. ADDRESS FOR CORRESPONDENCE: Dr. Josep Vidal, Obesity Unit, Endocrinology and Nutrition Department, Hospital Clínic Universitari, Villarroel 170, 08036 Barcelona, Spain; Phone: 34 932279846; Fax: 34 934516638; E-mail: jovidal@clinic.ub.es FUNDING AND DISCLOSURES: No funding was provided. The authors report no conflicts of interest relevant to the content of this article. KEY POINTS • Sleeve gastrectomy is associated with similar improvement of T2DM as gastric bypass. • The GLP-1 response to nutrient intake is enlarged following SG. • GLP-1 is not a critical for the improvement of glucose homeostasis following SG. O bservational and randomized clinical trials have shown that sleeve gastrectomy (SG) and gastric bypass (GBP) are associated with comparable beneficial effects on glucose tolerance in subjects with type 2 diabetes mellitus (T2DM).1,2 It has been proposed that an enhanced GLP1 response to meal intake following GBP underpins the amelioration of glucose tolerance following GBP.3 Thus, we and others have addressed the question of whether glucagon-like peptide-1 (GLP-1) plays a role in mediating the favorable metabolic effects of SG. SG has traditionally been considered a restrictive bariatric procedure. Accordingly, it has been hypothesized that the post-SG changes in gastrointestinal hormones would be negligible recapitulating the hormonal changes observed following adjustable gastric banding. In sharp contrast, studies evaluating the GLP-1 response to a meal challenge have consistently shown an enlarged gastrointestinal hormonal response following SG.2,4–6 The post-SG enlarged GLP-1 response has been reported in subjects with or without T2DM prior to surgery and at short- and long-term after the operation.2, 4–6 The mechanisms underlying this observation are not well understood. By comparing the GLP-1 response in subjects that had lost a comparable amount of weight following a dietary intervention or SG, Valderas et al6 demonstrated that the enlarged GLP-1 as a result of SG is independent of weight loss. The potential roles of accelerated gastric emptying, neural and/or hormonal mechanisms, or the presence of a sufficient number of L-cells in the proximal gut to account for the enlarged incretin secretion after SG have yet to be elucidated. Undoubtedly, the parallel occurrence of an enlarged hormonal response along with the resolution of T2DM following SG strongly suggest GLP-1 as mediator.2 However, acceptance of the hypothesis should not rely merely on the data summarized up to this point. To further evaluate the role of GLP1 in mediating the glucose-lowering effects of SG, we first performed a cross-sectional study including individuals with morbid obesity who presented with T2DM prior to SG but differed in the long-term post-surgical outcome (≥24-months) of T2DM.7 Onethird of the body mass index (BMI)-, gender-, and age-matched cohort did not present with remission of T2DM following SG, one-third of the participants presented with sustained partial remission, and the remainder presented with relapse of T2DM following an initial period of remission lasting for at least 12 months. We hypothesized that if GLP-1 was critical May 2013 • Supplement A • Bariatric Times A7