Bariatric surgery operations were designed to promote weight loss. However, it was soon realized that these operations were also associated with impressive and sustained improvements in type 2 diabetes mellitus (T2DM). In fact, it has recently been recognized by the American Diabetes Association that bariatric surgery has the potential to offer complete remission of a T2DM. Certainly, weight loss plays an important role in the amelioration of T2DM following bariatric surgery. Nonetheless, mounting evidence shows that certain intestinal diversionary operations improve T2DM through mechanisms beyond weight loss and reduced caloric intake. Although the precise weight-independent mechanisms mediating T2DM remission are not yet clear, it has been proposed that changes in the secretion of gastrointestinal hormones secondary to the rearrangement of the gastrointestinal tract anatomy could be involved. In that respect, two different theories have been put forward. According to the hindgut hypothesis, the bypass of the proximal gut results in an expedited delivery of ingested nutrients to the lower bowel accentuating the secretion of GLP-1. Consequently, glucose tolerance would be enhanced shortly after surgery by virtue of the stimulatory effects of GLP-1 on insulin secretion, and its inhibitory effects on glucagon secretion. In the long run, GLP-1 would also enhance glucose tolerance by increasing the pancreatic beta cell mass. In contrast, the foregut hypothesis proposes that it is the exclusion of the duodenum from contact with ingested nutrients what exerts direct antidiabetes effects. The absence of nutrient contact with the duodenum and proximal jejunum would preclude the secretion of an unidentified pro-diabetogenic factor (anti-incretin). Several studies have now demonstrated that gastric bypass surgery is associated with a marked increase in the GLP-1 secretory response to peroral nutrient stimulation in non-diabetic and diabetic subjects. It has been shown that the exaggerated GLP-1 response is independent of weight loss, and is associated with remission of T2DM. Interestingly, we have shown that GLP-1 could also be involved in the resolution of T2DM following sleeve gastrectomy. Therefore, there is compelling data to suggest that GLP-1 could be a contributing factor accounting for the early resolution of T2DM independent of the bypass of the proximal intestine. The long-term effects of the increased GLP-1 secretion following bariatric surgery in human subjects are yet to be clarified. Elucidating the mechanisms underlying the metabolic benefits of bariatric surgery could be critical to identify novel anti-diabetic therapeutic targets and/or to propose safer modalities of metabolic surgery.