1.Diabetes and obesity epidemic. Diabetes and obesity have become 2 major global health problems. According to statistics, there are about 1, 7.1 billion people suffering from diabetes worldwide, and it is expected to reach 3, 6.6 billion in 2030; Chinese diabetic patients have exceeded 20 million, and it is expected to exceed 42 million by 2030, of which more than 90% are type 2 diabetes. Weight gain and obesity lead to insulin resistance and impaired beta cell function, which are closely related to type 2 diabetes. The risk ratio (odds ratio, OD) for diabetes in adults who are morbidly obese (BMI ≥ 40) is 7, 73 compared to those who are growing in weight [2]. In the United States, the vast majority of diagnosed type 2 diabetic patients are overweight, half are obese (BMI ≥ 30), and 9% are morbidly obese (BMI ≥ 40). And 30% of morbidly obese individuals who undergo bariatric surgery have type 2 diabetes. Therefore, obesity-related diabetes becomes “Diabesity”, that is, diabetes – obesity. 2, the surgical treatment of diabetes A large number of domestic and foreign research proves that, for morbid obesity combined with diabetes patients, surgery is the only long-term effective treatment, and in reducing weight at the same time, can effectively relieve the symptoms of diabetes. The results showed that after bariatric surgery, 86.6% of patients with diabetes were relieved or recovered, and 78.1% of patients were cured. Various types of bariatric surgery have different effects in the treatment of diabetes. The main bariatric surgery procedures include Laparoscopic Adjustable Gastric Banding (LAGB), Sleeve Gastrectomy (SG), Roux-en-Y gastric bypass (RYGB) and biliopancreatic diversion with duodenal switch (BPD/DS). BPD/DS provided the most significant relief, followed by RYGB and LAGB. after surgery, rapid blood glucose levels returned to normal before significant weight loss. Patients treated with insulin preoperatively had a significant reduction in insulin dosage postoperatively, and the vast majority of patients were able to suspend insulin use at six weeks postoperatively. Insulin resistance and glycated hemoglobin HbA1c were also significantly lower than before surgery. Diabetes control after bariatric surgery can remain effective in the long term. The rationale for performing bariatric surgery in diabetic patients with low BMI is still insufficient. Because a large proportion of diabetic patients with low BMI have type 1 diabetes, which occurs mainly with autoimmune beta-cell destruction, bariatric surgery in this group is much less effective than in type 2 diabetes. In addition, numerous studies have shown that bariatric surgery has a preventive effect on diabetes. In a longitudinal study, LAGB was shown to significantly improve insulin resistance and metabolic syndrome in obese individuals, and Long et al. reported a 30-fold reduction in the risk of type 2 diabetes after RYGB surgery in patients with high preoperative glucose [13]. Also the incidence of metabolic syndrome was significantly lower after surgery. In contrast, patients who underwent BPD surgery achieved normal insulin levels 6 months after surgery. 3. influencing factors and underlying mechanisms Diabetes remission after bariatric surgery is related to several factors such as the degree of postoperative weight loss, reduced food intake and the duration of diabetes. However, a growing number of studies have found that the mechanisms involved are concurrently so simple that postoperative changes in the anatomy of the gastrointestinal tract and a series of intestinal endocrine hormonal changes also play a key role. 3.1 Weight loss and reduced food intake Surgery-induced reduction in food intake and absorption and weight loss play an important role in the improvement of postoperative glycemic control. Intake and weight loss can reduce the concentration of sugar and free fatty acids in the body, thus reducing the toxic effects on islet cells, improving insulin resistance and increasing insulin secretion. However, an increasing number of studies have demonstrated that weight loss and reduced absorption concurrently cause the underlying cause of diabetes remission during RYBG and BPD surgery, and that patients’ blood glucose and insulin levels return to normal within a few days after RYBG and BPD surgery, well before significant weight loss. Compared to the first two, the therapeutic effect of LAGB on diabetes is relatively weak and does not become apparent until after significant postoperative weight loss. A large retrospective analysis showed an average excess weight loss of 47.5% and diabetes remission of 47.9% in patients undergoing volume restriction surgery alone, compared to 61.6%, 83.7% and 70.1%, 98.9% with RYGB, respectively. If the effect of LAGB on glycemic control depends mainly on the degree of weight loss correlation, the therapeutic effect of RYBG and BPD surgery on diabetes is not only explained by reduced food intake and absorption and weight loss. In one study, diabetic patients were subjected to strict food and energy intake restrictions according to post-RYGB criteria. However, it was found that the patients failed to achieve significant relief of diabetic symptoms. This suggests that other mechanisms besides institutional reduction and reduced intake are playing an important role. 3.2 Duration of diabetes The study found a strong relationship between diabetes remission after bariatric surgery and preoperative diabetic condition. Patients with a diabetic disease duration of >10 years showed less significant improvement in diabetic symptoms after surgery [16]. Disease duration >3 years showed significant improvement in glycemic control after surgery [17]. The lesser the preoperative β-cell function destruction, the stronger the effect of postoperative gut hormones to promote insulin secretion from β-cells. 3.3 Gastrointestinal hormone alterations Gastrointestinal hormones mainly include: intestinal insulin (Incretin), peptide YY (PYY), and growth hormone-releasing peptide (Ghrelin). Glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are also included. These hormones constitute the Enteroinsular Axis (EIA), which is involved in the regulation of insulin release by the intestine [18]. GLP-1 is secreted by terminal ileal L cells and acts on pancreatic β cells to increase glucose-dependent insulin secretion, while inhibiting glucagon secretion by α cells. It also slows gastric emptying and delays food absorption and postprandial blood glucose levels. It also acts on the central nervous system to produce a feeling of satiety and reduce appetite. In addition, GLP increases insulin sensitivity by increasing hepatocyte and skeletal muscle gluconeogenesis and adipose tissue lipogenesis.GIP is secreted by K cells in the upper duodenum and jejunum. The effect is similar to that of GLP-1, but the effect is slightly weaker. PYY, like GLP-1, is secreted by terminal L cells of the ileum. It mainly acts on the corresponding receptors on the peripheral and central nervous system to achieve the function of slowing down gastric emptying and reducing appetite. Ghrelin is mainly secreted by the gastric fundic cells and acts on the hypothalamus to promote appetite, while inhibiting energy consumption and lipolysis. It inhibits insulin secretion from pancreatic islet cells by paracrine means. Serum Ghrelin levels are inversely proportional to body weight. Under normal conditions, the gastrointestinal mucosa secretes GLP-1, GIP and PYY after direct stimulation by food, and the vagus nerve is involved in regulating the secretion of these hormones. ghrelin increases before meals and decreases after meals. In diabetic patients, the islet cell response to GIP is reduced, while GLP-1 secretion is decreased. Basal and postprandial levels of PYY and Ghrelin are reduced in obese individuals, and even lower in diabetic patients. The deficiency of these hormones then leads to reduced insulin secretion. Bariatric surgery, mainly RYGB and BPD surgery, can increase the levels of these gastrointestinal hormones to achieve the corresponding endocrine effects, improve insulin resistance and increase insulin secretion. In contrast, the endocrine effect of gastric restriction surgery alone is not significant. Numerous studies have demonstrated that postprandial and oral glucose tolerance test (OGTT) GLP-1 levels increased significantly in diabetic patients after RYGB and BPD surgery [19].PYY levels increased significantly after bariatric surgery [15]. Although Ghrelin levels theoretically increase with weight loss, some studies have found that Ghrelin levels do not increase significantly after RYGB surgery, but rather decrease [19-20]. There are relatively few studies on GIP, and the results are not uniform and remain to be studied.