## 4 Discussion
The significance of insulin resistance in weight regulation is further substantiated by several studies, which demonstrate that hyperinsu-linemia or insulin resistance may potentially augment the probability of substantial weight reduction by up to threefold [17]. The underlying mechanism by which our findings were observed may be related to the role of insulin resistance in promoting weight gain. Insulin exerts its suppressive effect on lipolysis under typical conditions; however, in individuals with insulin resistance, the presence of hyperinsulinemia activates lipoprotein lipase on fat cell membranes and enhances the synthesis of fatty acid-binding proteins, thereby promoting the accumulation of free fatty acids (FFAs) within adipocytes [18]. Consequently, the development of insulin resistance can contribute to weight gain. Bariatric surgery has been shown to reduce both weight and insulin resistance [19]. The findings of this study suggest that patients with higher preoperative HOMA2-IR or basal insulin levels may experience more pronounced weight loss after surgery due to the greater reduction in insulin resistance postoperatively. HOMA2-B is a metric that reflects the insulin secretion capacity of pancreatic \(\beta\)-cells. The findings of this study indicate a correlation between preoperative insulin secretion and postoperative weight change, which is consistent with the conclusions of several previous studies. Retrospective research has demonstrated a negative relationship between HOMA-B and the percentage of total body weight loss (TBWL) at 2, 3, and 4 years post-surgery [20]. Furthermore, a study comparing patients who achieved complete remission (CR) of type 2 diabetes mellitus (T2 DM) after bariatric surgery with those who did not (non-CR) found that CR was associated with postoperative weight change, and preoperative HOMA2-B was a key predictor of remission [21]. One hypothesis to elucidate the association between preoperative \(\beta\)-cell function and postoperative weight loss is that patients with low insulin secretion before surgery may continue to experience limited insulin secretion postoperatively, even if insulin resistance improves [22]. Consequently, insufficient insulin secretion might limit the extent of weight loss [23], probably because of the lack of anabolic function of insulin. Another hypothesis is the normalization of adipokine secretion from adipocytes following weight loss. Adiponectin, a type of adipokine, plays a role in protecting pancreatic beta cells to maintain insulin secretion capacity [24;25]. Adiponectin activates AMP-activated protein kinase (AMPK), increasing energy expenditure and promoting the oxidation of glucose and fatty acids, thereby facilitating weight loss [26]. Individuals with reduced insulin secretion capacity may have decreased adiponectin levels. It has been demonstrated that weight reduction can lead to the normalization of adiponectin secretion [27;28]. Consequently, individuals with impaired insulin secretion capacity may experience enhanced weight loss as a consequence of the normalization of adiponectin levels. This study identified vitamin B12 as a significant predictor of postoperative weight change. Vitamin B12, a water-soluble vitamin, is obtained through dietary intake and synthesized by the gut microbiome. It plays essential roles in cellular metabolism, DNA synthesis, epigenetic regulation, and mitochondrial metabolism. The findings of this study agree with those of previous research, which demonstrated an inverse relationship between B12 levels and BMI [29] and between B12 levels and adiposity in children [30]. According to another study [31], maternal rats fed a diet deficient in B12 not only exhibited increases in body fat and alterations in their lipid profile but also transmitted these effects to their offspring, which demonstrated significantly elevated visceral fat at three months and developed dyslipidemia by twelve months of age.