Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy (SG) have been shown to cause remarkable improvement in type 2 diabetes, often with complete remission within days after surgery and before any significant weight loss (1). The mechanisms explaining the benefit on glycemic control independent of weight loss are still not entirely clear, but enhanced postprandial insulin secretion induced by exaggerated secretion of glucagon-like peptide 1 (GLP-1) has been suggested to be an important contributor (1). Indeed, several studies have highlighted the crucial role of GLP-1 in the improvement of β-cell function after RYGB (2–7). GLP-1 is an incretin hormone that is released into the bloodstream postprandially from the intestine (8). Among its multiple actions, GLP-1 stimulates insulin secretion and decreases appetite (8). Type 2 diabetic patients have severely impaired incretin effect, which improves after surgery (5). In the current issue of Diabetes , this view is challenged. In the article by Jimenez et al. (9), the GLP-1 receptor was pharmacologically blocked with exendin (9–39) in patients who had undergone SG and presented with long-term type 2 diabetes remission. The blockade of the GLP-1 system resulted in impaired insulin secretion but limited deterioration of glucose tolerance. In another protocol, subjects with type 2 diabetes antedating SG but with different long-term (>2 years) outcomes (remission, relapse, or lack of remission) had a comparable GLP-1 response to a mixed-meal, which was observed regardless of outcome (9). Not surprisingly, the β-cell function was most impaired in the nonremitting patients. In a previous study of long-term remission after RYGB, the same group of researchers concluded that the enhanced GLP-1 secretion after surgery is neither sufficient nor critical …
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