It is indisputable that metabolic syndrome (diabetes, hypertension, hyperlipidemia, polycystic ovary syndrome, sleep apnea) can soon be relieved or cured after weight loss surgery. Currently, bariatric surgery is not only used for weight loss, but more importantly for the treatment of metabolic syndrome. Often the metabolic syndrome is in remission without adequate weight loss. In our patients, polycystic ovary syndrome usually results in menstruation right after surgery; hypertension usually drops to normal 1 week after surgery; diabetes tends to recover in about a month. There is not much weight loss at this time. This indicates that weight loss surgery causes hormonal regulation changes soon after surgery, leading to a return to normal abnormal metabolism. A series of gastrointestinal hormone changes, including Ghrelin, GLP-1, GIP, Peptide YY, etc., occur after weight loss surgery, causing insulin resistance to ease and blood glucose to normalize. What causes these “downstream” hormonal changes? Current hypotheses include reduced perioperative caloric intake, anterior and posterior intestinal theory, and altered bile acids and bacterial flora. To date, however, all of these hypotheses do not provide a plausible explanation for the mechanisms by which various weight loss procedures lead to remission of the metabolic syndrome. Glycemic control usually occurs several days after bariatric surgery, before significant weight loss. The first hypothesis to emerge is an increase in hepatic insulin sensitivity due to reduced perioperative caloric intake. If this hypothesis is valid, the glycemic control effect of the three bariatric procedures: Roux-Y gastric bypass (RYGB), sleeve gastrectomy (SG) and adjustable gastric banding (LAGB) should be the same. They should be the same, however, the rate of diabetes remission is actually highest after RYGB surgery. Other GI procedures also result in reduced caloric intake during the perioperative period, but do not have glycemic control effects, but instead result in elevated blood glucose due to stress reactions. The foregut and hindgut theory is the classic hypothesis explaining the treatment of metabolic syndrome with bariatric surgery, i.e., food does not pass through the foregut and reaches the hindgut earlier after gastric diversion, thus causing a series of gastrointestinal hormonal changes that lead to rapid remission of metabolic syndrome. However, the anterior and hindgut doctrines do not plausibly explain why the other two weight loss surgical modalities, LAGB and SG, also cure the metabolic syndrome. In these two cases, the continuity of the GI tract is not interrupted and there is no problem of food stimulating the hindgut earlier or bypassing the foregut. A study by Gerhard et al. showed that fasting bile acid concentrations were higher after RYGB in patients with remission diabetes than in those with unremitting diabetes or no preoperative diabetes. Moreover, the increase in fasting bile acid concentration after RYGB was positively correlated with peak postprandial GLP-1 secretion and negatively correlated with plasma glucose concentration 2 hours after meal, which did not change after LAGB. Bile acids can regulate glucose metabolism through TGR5 receptors expressed on L cells, leading to the release of GLP-1 in the bound state. It may also induce fibroblast growth factor 19 (FGF19) synthesis and secretion from ileocytes, thereby improving insulin sensitivity and regulating glucose metabolism. However, RYGB can elevate FGF19, but LAGB does not have this effect. It is possible that intestinal flora is related to the pathology of obesity. Compared to non-obese individuals, obese individuals have an increased ratio of thick-walled bacteria/bacteroidetes and a reduced diversity of bacteria. This difference disappears with either surgery or diet control resulting in weight loss. The intestinal flora plays an important role in the extraction of energy from ingested food, and not all bacteria have this effect; post-RYGB results in altered intestinal flora, reduced ability to obtain energy from food, or unknown signals regulating energy expenditure. altered enterohepatic circulation; increased pH in the gut, leading to excessive bacterial growth; perioperative antibiotic use; and changes in energy intake or dietary patterns. Altered intestinal flora may independently affect surgical outcomes. It is also curious that only surgery involving the stomach has some effect on metabolic syndrome, while abdominal surgery such as cholecystectomy or colorectal resection does not bring down blood glucose. Lee et al. reported 360 cases of non-obese gastric cancer with diabetes mellitus who underwent gastrectomy had varying degrees of diabetes remission after surgery (mean glucose-lowering drug discontinuation rate 9.7%). The rate of diabetes remission was higher in those who underwent total gastrectomy than in those who underwent major gastrectomy and endoscopic local resection. The effect of glucose lowering also varied among different gastrointestinal reconstruction modalities. Bi-II or Roux-Y anastomosis is significantly more effective than Bi-I anastomosis in reducing glucose. The stomach is a mysterious endocrine organ with many known and unknown endocrine functions. The only way to explain the above is the gastric center hypothesis, the key link of which is in the greater curvature of the stomach. It is likely that there are some special cells in the gastric greater curvature that produce specific, as yet unknown, factors involved in mediating important metabolic processes. The greater curvature of the stomach is removed after gastric sleeve resection; food bypasses the stomach and goes directly to the small intestine after gastric diversion; and the banding effect of gastric fasciculation reduces the amount and slows the rate of food entering the stomach. All three of these surgical procedures reduce the irritation of food to the stomach. It is likely to lead to a reduction in the secretion of specific factors, which can lead to the alleviation of insulin resistance and a reduction in sympathetic tone, leading to the alleviation of metabolic diseases such as diabetes, hypertension and polycystic ovary syndrome. It is because the “upstream” part of the stomach is removed or left unattended that changes in the “downstream” gastrointestinal hormones are made. Therefore, the mechanism of bariatric surgery for metabolic syndrome should start from the greater curvature of the stomach. To find this particular cell and the hormone it secretes. By developing antagonists for this hormone, the problem of obesity and metabolic syndrome can be effectively solved. Thus, weight loss surgery treatment will become history.