Patients with obstructive sleep apnea (OSA) experience insulin resistance and its clinical consequences, including hypertriglyceridemia, reduced high density lipoprotein-associated cholesterol (HDL-c), visceral adiposity, hepatic steatosis, increased epicardial fat thickness, essential hypertension, glucose intolerance, increased risk for type 2 diabetes, chronic kidney disease, subclinical vascular damage, and increased risk for cardiovascular events. Obesity is a major contributor to OSA. The prevalence of OSA is almost universal among patients with severe obesity undergoing bariatric surgery. However, insulin resistance and its clinical complications occur in OSA patients irrespective of general obesity (body mass index). In OSA patients, apnea episodes during sleep induce oxyhemoglobin desaturation and tissue hypoxia. Insulin resistance is an adaptive response to tissue hypoxia and develops in conditions with limited tissue oxygen supply, including healthy subjects exposed to hypobaric hypoxia (high altitude) and OSA patients. Indicators of oxyhemoglobin desaturation have been robustly and independently linked to insulin resistance and its clinical manifestations in patients with OSA. Insulin resistance mediates the elevated rate of type 2 diabetes, chronic kidney disease, and cardiovascular disease unexplained with traditional cardiovascular risk factors present in OSA patients. Pathophysiological processes underlying hypoxia-induced insulin resistance involve hypoxia inducible factor-1 upregulation and peroxisome proliferator-activated receptor-gamma (PPAR- γ ) downregulation. In human adipose tissue, PPAR- γ activity promotes glucose transport into adipocytes, lipid droplet biogenesis, and whole-body insulin sensitivity. Silencing of PPAR- γ in the adipose tissue reduces glucose uptake and fat accumulation into adipocytes and promotes insulin resistance. In conclusion, tissue hypoxia drives insulin resistance and its clinical consequences in patients with OSA, regardless of body mass index.

The objective of this meta-analysis was to assess the comparative efficacy of robot-assisted and laparoscopic surgery in treating gastric cancer among patients characterized by a high visceral fat area (VFA). In April 2024, we conducted a comprehensive literature review using major international databases, such as PubMed, Embase, and Google Scholar. We restricted our selection to articles written in English, excluding reviews, protocols without published data, conference abstracts, and irrelevant content. Our analysis focused on continuous data using 95% confidence intervals (CIs) and standard mean differences (SMDs), while dichotomous data were assessed with odds ratios (ORs) and 95% CIs. We set the threshold for statistical significance at P < 0.05. Data extraction included baseline characteristics, primary outcomes (such as operative time, major complications, lymph node yield, and anastomotic leakage), and secondary outcomes. The meta-analysis included three cohort studies totaling 970 patients. The robotic-assisted group demonstrated a significantly longer operative time compared to the laparoscopic group, with a weighted mean difference (WMD) of - 55.76 min (95% CI - 74.03 to - 37.50; P < 0.00001). This group also showed a reduction in major complications, with an odds ratio (OR) of 2.48 (95% CI 1.09-5.66; P = 0.03) and fewer occurrences of abdominal infections (OR 3.17, 95% CI 1.41-7.14; P = 0.005), abdominal abscesses (OR 3.83, 95% CI 1.53-9.57; P = 0.004), anastomotic leaks (OR 4.09, 95% CI 1.73-9.65; P = 0.001), and pancreatic leaks (OR 8.93, 95% CI 2.33-34.13; P = 0.001). However, no significant differences were observed between the groups regarding length of hospital stay, overall complications, estimated blood loss, or lymph node yield. Based on our findings, robot-assisted gastric cancer surgery in obese patients with visceral fat appears to be correlated with fewer major complications compared to laparoscopic surgery, while maintaining similar outcomes in other surgical aspects. However, it is important to note that robot-assisted procedures do tend to have longer operative times.

UNASSIGNED: Numberous studies have heatedly discussed whether obesity is a risk factor for anastomotic leakage (AL) because of the increasing number of colorectal cancer (CRC) cases and high incidence of CRC in patients with obesity.
UNASSIGNED: We aimed to explore the relationship between visceral obesity(VO) and AL after CRC surgery. The databases of Pubmed, Embase, and the Cochrane Library were searched for relevant data and articles published until November 1, 2022. We identified the difference in the incidence of AL after CRC surgery between patients with and without VO. The quality of included studies was evaluated using the Newcastle- Ottawa Scale, and odds ratio (OR) and 95% CI were used to assess the association between VO and AL.
UNASSIGNED: This meta-analysis included 7 studies with 2,136 patients. The OR of patients with VO versus those without VO was 2.15 (95%CIs = 1.46-3.15, test for heterogeneity: P = 0.29, I2 = 18%) based on the fixed-effect model in seven studies. Notably, the difference between the two groups was statistically significant (Z = 3.91 P < 0.0001). Patients with VO in the colon cancer group exhibited a higher incidence of AL (OR = 2.88, 95% CIs = 1.38-5.99, test for heterogeneity: P = 0.27, I2 = 20%) than those in the rectal cancer group (OR = 2.74, 95% CIs = 1.13-6.65, test for heterogeneity: P = 0.20, I2 = 38%). In the studies in the relevant literature, heterogeneity was low. Regarding patients with VO, four Asian studies reported increased morbidity due to AL (OR = 2.79, 95% CIs = 1.35-5.78, test for heterogeneity: P = 0.35, I2 = 9%) compared with three non-Asian studies.
UNASSIGNED: Our findings confirmed the significant relationship between VO and AL. Thus, VO could be considered a reliable risk factor of surgery for colon cancer.

BACKGROUND: Computed tomography (CT)-defined fat quantification has been an emergent field of research in oncology. It was shown that this parameter is predictive and prognostic of several clinically relevant factors in several tumor entities.
OBJECTIVE: Our aim was to establish the effect of visceral (VFA) and subcutaneous fat areas (SFA) on overall survival (OS), disease-free survival (DFS), and postoperative complications in gastric cancer patients based on a large patient sample.
METHODS: MEDLINE library, EMBASE, and SCOPUS databases were screened for the associations between VFA and SFA defined by CT images and OS, DFS, and postoperative complications in gastric cancer patients up to August 2022. The primary endpoint of the systematic review was the hazard ratio for the outcome parameters. High VFA was, in most studies, defined by the threshold value of 100 cm2. In total, 9 studies were suitable for the analysis and included in the present study.
RESULTS: The included studies comprised 3,713 patients. The identified frequency of visceral obesity was 44.9%. The pooled hazard ratio for the effect of high VFA on OS was 1.28 (95% CI 1.09-1.49, p = 0.002). For SFA, it was 1.87 (95% CI 1.45-2.42, p < 0.0001). The pooled hazard ratio for the influence of high VFA on DFS was 1.17 (95% CI 0.95-1.43, p = 0.14). The pooled odds ratio for the associations between VFA and postoperative complications was 1.36 (95% CI 1.09-1.69, p = 0.006).
CONCLUSIONS: CT-defined VFA and SFA influence OS in patients with gastric cancer. VFA also influences the occurrence of postoperative complications. Therefore, assessment of fat areas should be included in clinical routine in patients with gastric cancer.

The association between obesity, cancer and cardiovascular disease (CVD) has been demonstrated in animal and epidemiological studies. However, the specific role of visceral obesity on cancer and CVD remains unclear. Visceral adipose tissue (VAT) is a complex and metabolically active tissue, that can produce different adipokines and hormones, responsible for endocrine-metabolic comorbidities. This review explores the potential mechanisms related to VAT that may also be involved in cancer and CVD. In addition, we discuss the shared pharmacological treatments which may reduce the risk of both diseases. This review highlights that chronic inflammation, molecular aspects, metabolic syndrome, secretion of hormones and adiponectin associated to VAT may have synergistic effects and should be further studied in relation to cancer and CVD. Reductions in abdominal and visceral adiposity improve insulin sensitivity, lipid profile and cytokines, which consequently reduce the risk of CVD and some cancers. Several medications have shown to reduce visceral and/or subcutaneous fat. Further research is needed to investigate the pathophysiological mechanisms by which visceral obesity may cause both cancer and CVD. The role of visceral fat in cancer and CVD is an important area to advance. Public health policies to increase public awareness about VAT\'s role and ways to manage or prevent it are needed.

BACKGROUND: With the rising prevalence of obesity, there is a plethora of literature discussing the relationship between obesity and acute pancreatitis (AP). Evidence has shown a possible correlation between visceral adipose tissue (VAT) and AP incidence and severity. This systematic review explores these associations.
METHODS: Eligible articles were searched and retrieved using Medline and Embase databases. Clinical studies evaluating the impact of VAT as a risk factor for AP and the association of the severity of AP and VAT were included.
RESULTS: Eleven studies, with a total of 2529 individuals were reviewed. Nine studies showed a statistically significant association between VAT and the severity of AP. Only four studies found VAT to be a risk factor for acute pancreatitis. Two studies showed VAT to be associated with an increased risk of local complications and two studies showed a correlation between VAT and mortality.
CONCLUSIONS: This is the first systematic review conducted to study the association between VAT and AP. The existing body of evidence demonstrates that VAT has a clinically relevant impact and is an important prognostic indicator of the severity of AP. However, it has not shown to be an independent risk factor to the risk of developing AP. The impact of VAT on the course and outcome of AP needs to be profoundly explored to confirm these findings which may fuel earlier management and better define the prognosis of patients with AP. VAT may need to be incorporated into prognostic scores of AP to improve accuracy.

There is strong evidence suggesting that excessive fat distribution, for example, in the bowel mesentery or a reduction in lean body mass (sarcopenia) can influence short-, mid-, and long-term outcomes from patients undergoing various types of surgery. Body composition (BC) analysis aims to measure and quantify this into a parameter that can be used to assess patients being treated for abdominal wall hernia (AWH). This study aims to review the evidence linking quantification of BC with short- and long-term abdominal wall hernia repair outcomes.
A systematic review was performed according to the PRISMA guidelines. The literature search was performed on all studies that included BC analysis in patients undergoing treatment for AWH using Medline, Google Scholar and Cochrane databases by two independent reviewers. Outcomes of interest included short-term recovery, recurrence outcomes, and long-term data.
201 studies were identified, of which 4 met the inclusion criteria. None of the studies were randomized controlled trials and all were cohort studies. There was considerable variability in the landmark axial levels and skeletal muscle(s) chosen for analysis, alongside the methods of measuring the cross-sectional area and the parameters used to define sarcopenia. Only two studies identified an increased risk of postoperative complications associated with the presence of sarcopenia. This included an increased risk of hernia recurrence, postoperative ileus and prolonged hospitalisation.
There is some evidence to suggest that BC techniques could be used to help predict surgical outcomes and allow early optimisation in AWH patients. However, the lack of consistency in chosen methodology, combined with the outdated definitions of sarcopenia, makes drawing any conclusions difficult. Whether body composition modification can be used to improve outcomes remains to be determined.

Perceived stress has been proposed as a risk factor of metabolic syndrome. However, correlations between perceived stress and parameters of the metabolic syndrome have not been properly analyzed despite extensive research data on the topic. Our current meta-analysis aimed to examine the mutual association between perceived stress of patients and parameters of metabolic syndrome.
This systematic review has been registered on the PROSPERO database (registration number CRD42017055293). Eligible studies divided participants based on their stress level or on the presence of metabolic syndrome. They reported at least one parameter of the metabolic syndrome or the stress level of the participants measured with some stress scale. Data from 17 articles met the eligibility criteria and were included. Random effects model with the DerSimonian and Laird weighting methods was applied. I-squared indicator and Q test were performed to assess heterogeneity.
Although the majority of individual studies failed to demonstrate correlations between stress and their analyzed parameters of metabolic syndrome, our meta-analysis showed a significant association between stress and BMI [average effect size (ES) with 95% confidence interval (95%CI), ES = 0.65, 95%CI 0.16, 1.14), waist circumference (ES = 1.84 cm, 95%CI 0.79, 2.89) and serum triglyceride level (ES = 7.52 mg/dl, 95%CI 0.07, 14.96). Additional analysis confirmed effects of stress on serum HDL (ES = - 1.699 mg/dl, 95%CI -2.966, -0.432) and diastolic blood pressure (ES = 1.04 mmHg, 95%CI 0.18, 1.89). No correlations were found for fasting glucose or systolic blood pressure. No association between metabolic syndrome and stress level of patients was detected either.
The potentially key role of visceral obesity in the association between perceived stress and dyslipidemia or diastolic blood pressure are discussed together with potential moderators (e.g. gender-differences, variations in stress assessment and metabolic syndrome criteria) that may explain the inconsistent, contradictory results of the individual studies.