The mechanism by which type 2 diabetes can be remitted or even cured after weight loss surgery has been investigated at home and abroad: a. Weight loss and reduced food intake after weight loss surgery: The reduction in food intake and absorption and weight loss due to surgery play an important role in improving glycemic control after surgery. However, a growing body of evidence suggests that weight loss and reduced food digestion and absorption after bariatric surgery may not be the underlying cause of diabetes remission. In many cases, patients’ blood glucose and insulin levels gradually return to normal within a few days after bariatric surgery, well before the significant weight loss. The remission of diabetes after surgery does not directly correlate with weight loss, suggesting that there are other important mechanisms at play besides weight loss and reduced absorption. Second, the gastrointestinal hormonal changes after bariatric surgery: these hormones mainly include glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic hormone (GIP), peptide YY (PYY), growth hormone-releasing peptide (Ghrelin), etc., which together constitute the “intestine-insulin axis “They are involved in the regulation of insulin release by the intestine. After bariatric surgery, especially after Roux-en-Y bypass surgery, biliopancreatic open-heart surgery and duodenal diversion, the levels of these gastrointestinal hormones can be significantly improved to achieve the corresponding endocrine effects, improve insulin resistance, increase insulin secretion, and finally achieve the effect of improving blood glucose. Third, the “anterior small intestine hypothesis” and “hindgut hypothesis”: Rubino, a famous scholar, believes that in the “anterior small intestine” (i.e., duodenum and proximal jejunum), there are anti-intestinal pro-insulin factors, which play a role in the development of blood glucose. It is hypothesized that the development of type 2 diabetes is due to an imbalance caused by the relatively overactive anti-intestinal insulin factor, resulting in a delayed insulin response to absorbed carbohydrates and a glucose intolerance response. Some bariatric surgery (such as gastric short-circuit surgery) can directly treat diabetes after the “anterior small intestine” is excluded from the intestinal insulin axis, and this is the “anterior small intestine hypothesis”. In contrast, the “hindgut hypothesis” believes that after gastric short-circuiting surgery, food reaches the distal small intestine earlier than normal, and the feedback from the intestinal insulin axis plays a role in controlling blood glucose balance. mini-gastrointestinal short-circuiting surgery also means that the duodenum and the proximal jejunum are left open, and after the surgery, in addition to weight loss, the patient’s original combined diabetes is significantly relieved. In addition to weight loss, the patient experienced significant remission of the combined diabetes. Since the remission of diabetes after bariatric surgery may be related to the opening of the duodenum and proximal jejunum, and there is no direct causal link with the weight loss of the patient, it is inevitable to wonder whether surgery is also effective in the treatment of diabetes in non-obese patients. The preliminary results of our multicenter “Clinical Study on the Effect of Gastrointestinal Surgery on Glucose Metabolism in Patients with Type 2 Diabetes” showed that patients who used the surgery without food passing through the duodenum had significant improvement or even cure of diabetes after surgery, while patients who had food passing through the duodenum had little or no significant change in blood glucose after surgery. The study is still continuing. After the gastrointestinal reconstruction with food not passing through the duodenum in our department for six patients with gastric cancer combined with type 2 diabetes, four of them had normal blood glucose.