When the BMI is above 35, and there are chronic comorbidities like diabetes or hypertension, or when the BMI is above 40 for the treatment of clinically severe obesity, bariatric surgery, also known as bariatric surgery, may be performed. Laparoscopic sleeve gastrectomy is a surgical procedure that is frequently performed due to its benefits, which include reducing comorbidities, providing effective weight loss, not requiring anastomosis, not resulting in mesenteric defects, maintaining the continuity of the pylorus and digestive system, reducing ghrelin production, and not altering the absorption of foods, minerals, vitamins, and medications [14, 15].
In both men and women, obesity appears to be the primary contributor to insulin resistance (IR). The release of proinflammatory cytokines and adipokines is one of the symptoms of obesity, which is also known as a chronic inflammatory condition [16–18]. Even in adipocytes, it has been demonstrated to cause a localized increase in IR [17, 19]. IR stands for relative insensitivity to the effects of the insulin hormone in peripheral tissues like muscles, the liver, and adipose tissue. The development and progression of cardiometabolic risk factors linked to metabolic syndrome in conjunction with obesity are significantly influenced by IR. According to studies, obesity may exacerbate the pathological role of inflammation in IR and metabolic syndrome. On the other hand, it has been suggested that obesity may have an impact on inflammation [20–23].
There is only weak evidence for a direct link between UII and obesity or dyslipidemia. However, UII (Urotensin II) may play a role in the development of metabolic syndrome or its components, such as hypertension, insulin resistance, hyperglycemia, and inflammation. It is thought that UII influences digestive function and contributes to inflammation. The Renin-Angiotensin-Aldosterone system is crucial for many cardiovascular processes, and UII and angiotensin II can interact synergistically, particularly in conditions characterized by endothelial dysfunction, such as metabolic syndrome [8].
Regardless of whether a patient has proteinuria or not, elevated plasma UII levels have been observed in diabetic patients [24]. The increase is not influenced by fasting plasma glucose or glycated hemoglobin levels, indicating that UII release or production is not solely reliant on hyperglycemia. There was no correlation between glucose levels and serum UII levels in our study's PREOP, POSTOP, and C groups when glucose and UII levels were measured. In the PREOP group, glucose levels were higher, but in the POSTOP group, they fell even lower than in the C group. Additionally, there were a statistically significant drop in serum UII levels between the PREOP and POSTOP groups. HbA1c levels were discovered to be high in a study done on kids with obesity [25]. In our study, the POSTOP group's HbA1c levels also dropped and eventually reached levels comparable to those of the C group.
Studies on experimental animals have demonstrated that the expression of UII is present in epididymal fat but not in abdominal or perirenal fat. It is thought that UII may contribute to abdominal obesity, which is thought to be a critical factor in the development of metabolic syndrome if similar effects on lipid metabolism and feeding behavior are seen in humans. Plasma UII levels and body weight have been shown to correlate positively in studies done in the Hong Kong Chinese population [24–27].
Obese mice were used to examine the effects of UR blockade on various aspects of metabolic syndrome in a study to ascertain the role of UII in the pathogenesis of the condition. Compared to wild-type mice, obese mice treated with the UII receptor antagonist SB657510 experienced less weight gain and significant reductions in blood pressure, hyperlipidemia, and glucose levels [28]. According to the results of a study done on obese kids, those who had a family history of high blood pressure had serum UII levels that were significantly higher than those in the control group [25]. In our study, weight loss was accompanied by a parallel decline in blood pressure and serum UII levels. These results support the idea that, in the event of a decline in UII system activity, the UII system may be crucial in the fight against obesity and metabolic syndrome.
In a study, it was found that among 12 phenotypes related to adipose accumulation and fatty acid composition, the UII gene is significantly associated with the amount of saturated fatty acids in skeletal muscles, while the UII receptor gene has significant effects on the levels of saturated and monounsaturated fatty acids. This study offers the first proof that the UII and UII receptor genes control the adipose accumulation and fatty acid metabolism in skeletal muscle, highlighting their potential pathological roles in type 2 diabetes mellitus and obesity in humans [29]. In our study, serum UII levels and PREOP adipose tissue levels were both found to be elevated. The adipose tissue and serum UII levels of Group C, whose BMI was within normal ranges, showed comparable parallelism. As a result, with weight loss, adipose tissue UII levels drop. The literature is supported by our findings.
A different study that compared vitamin B12 levels in patients who had undergone sleeve gastrectomy found that post-operatively low B12 levels were more typical in women [30]. POSTOP vitamin B12 levels decreased in our study, but deficiency has not yet materialized. After surgery, inconsistency in the general biochemical profile was seen in earlier studies, particularly in the levels of albumin, uric acid, creatinine, AST, and ALT, and it has been hypothesized that this inconsistency is more pronounced in men [31]. Uric acid levels decreased in a study where biochemical evaluations were carried out a year after obesity surgery [32]. Similar results were found in our study, where uric acid levels dropped, and statistically significant differences were found six months after the operation.
One year after sleeve gastrectomy, patients who underwent the procedure had normal serum levels of calcium and albumin, according to another study [33]. However, it was found in our study that although there was no statistically significant difference, albumin levels were higher after six months of surgery compared to the control group. Six months after sleeve surgery, some researchers claim that there were no appreciable changes in the levels of serum glucose, albumin, BUN, creatinine, or GFR [34]. However, in our study, there were statistically significant variations in glucose and urea levels between the preoperative and postoperative groups.
Studies have shown that sleeve gastrectomy has regulatory effects on lipid markers [35]. While some studies have claimed that there was a significant increase in HDL and cholesterol serum levels following sleeve gastrectomy, other studies have asserted that there was no such significant increase [36]. Even studies have suggested that men and women have different total cholesterol and HDL cholesterol levels [37]. Given the significance of this issue, it is acknowledged that additional research is required to define the connection between gender and post-sleeve gastrectomy comorbidities.
It has been suggested that serum UII levels correlated positively with systolic blood pressure, diastolic blood pressure, and uric acid and negatively with creatinine, BUN, and nitric oxide when correlation analyses were done with the UII levels [38, 39]. However, the findings of our study were consistent with previous research, with negative correlations between serum UII levels and creatinine, AST, and GGT. Additionally, tissue UII levels showed negative correlations with GGT and total bilirubin levels while showing positive correlations with uric acid, sodium, and potassium levels. Additionally, our study showed that tissue and serum UII levels rose with increasing BMI, adding significant new data to the literature.