Bariatric surgery is the most effective treatment for obesity and also greatly improves glycaemic control, often within days after surgery, independently of weight loss. Laparoscopic adjustable gastric banding (LAGB) was designed as a purely restrictive procedure, whereas vertical sleeve gastrectomy (VSG) and Roux-en-Y gastric bypass (RYGB) induce changes in appetite through regulation of gut hormones, resulting in decreased hunger and increased satiation. Thus, VSG and RYBG more frequently result in remission of type 2 diabetes than does LAGB. With all three of these procedures, remission of diabetes is associated with early increases in insulin sensitivity in the liver and later in peripheral tissues; VSG and RYBG are also associated with improved insulin secretion and an exaggerated postprandial rise in glucagon-like peptide 1. The vagal pathway could have a role in the neurohumoral regulatory pathways that control appetite and glucose metabolism after bariatric surgery. Recent research suggests that changes in bile acid concentrations in the blood and altered intestinal microbiota might contribute to metabolic changes after surgery, but the mechanisms are unclear. In this Series paper, we explore the possible mechanisms underlying the effects on glucose metabolism and bodyweight of LAGB, VSG, and RYGB surgery. Elucidation of these mechanisms is providing knowledge about bodyweight regulation and the pathophysiology of type 2 diabetes, and could help to identify new drug targets and improved surgical techniques.
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