Visceral Obesity Determined by CT As a Predictor of Short-term Postoperative Complications in Ovarian Cancer

Objective: To explore the association between visceral obesity and short-term postoperative complications in patients with advanced ovarian cancer undergoing cytoreductive surgery.Methods: Medical records were reviewed for patients with ovarian cancer. Visceral fat area, subcutaneous fat area and total fat area were measured on a single slice at the level of L3/4 of a preoperative CT scan. Univariable and multivariable analyses were performed to investigate the correlation between visceral obesity and short-term complications and to analyze the risk factors for complications after surgery.Results: Of the 130 patients, 53.8% (70/130) were presented visceral obesity. Patients with visceral obesity were older than those with nonvisceral obesity (58.3 years old vs. 52.3 years old, p = 0.001). The proportion of patients with hypertension was slightly higher (37.1% vs. 11.7%, p = 0.001). The total fat area and subcutaneous fat area were higher in patients with visceral obesity (296.9 ± 72.1 vs. 173.1 ± 67.3, p < 0.001; 168.8 ± 55.5 vs. 121.6 ± 54.3, p < 0.001). Compared with patients in the nonvisceral obese group, patients in the visceral obese group were more likely to have postoperative fever (21/70 30.0% vs. 8/60 1.25%, p = 0.023), leading to a longer length of hospital stay (21 days vs. 17 days, p = 0.009). Time from surgery to adjuvant chemotherapy for patients with visceral obesity has been delayed (24 days vs. 20 days, p = 0.037). Multivariate analysis showed that visceral obesity (OR 4.770, p < 0.001) and operation time (OR 1.008, p < 0.001) were independent predictors of postoperative complications. Conclusion: Visceral obesity is an important risk factor for short-term postoperative complications in patients with advanced ovarian cancer undergoing cytoreductive surgery.

Optimal Dietary Intake Composition of Choline and Betaine Is Associated with Minimized Visceral Obesity-Related Hepatic Steatosis in a Case-Control Study

Few studies on humans have comprehensively evaluated the intake composition of methyl-donor nutrients (MDNs: choline, betaine, and folate) in relation to visceral obesity (VOB)-related hepatic steatosis (HS), the hallmark of non-alcoholic fatty liver diseases. In this case–control study, we recruited 105 patients with HS and 104 without HS (controls). HS was diagnosed through ultrasound examination. VOB was measured using a whole-body analyzer. MDN intake was assessed using a validated quantitative food frequency questionnaire. After adjustment for multiple HS risk factors, total choline intake was the most significant dietary determinant of HS in patients with VOB (Beta: −0.41, p = 0.01). Low intake of choline (<6.9 mg/kg body weight), betaine (<3.1 mg/kg body weight), and folate (<8.8 μg/kg body weight) predicted increased odds ratios (ORs) of VOB-related HS (choline: OR: 22, 95% confidence interval [CI]: 6.5–80; betaine: OR: 14, 95% CI: 4.4–50; and folate: OR: 19, 95% CI: 5.2–74). Combined high intake of choline and betaine, but not folate, was associated with an 81% reduction in VOB-related HS (OR: 0.19, 95% CI: 0.05–0.69). Our data suggest that the optimal intake of choline and betaine can minimize the risk of VOB-related HS in a threshold-dependent manner.

The Roles and Associated Mechanisms of Adipokines in Development of Metabolic Syndrome

Metabolic syndrome is a cluster of metabolic indicators that increase the risk of diabetes and cardiovascular diseases. Visceral obesity and factors derived from altered adipose tissue, adipokines, play critical roles in the development of metabolic syndrome. Although the adipokines leptin and adiponectin improve insulin sensitivity, others contribute to the development of glucose intolerance, including visfatin, fetuin-A, resistin, and plasminogen activator inhibitor-1 (PAI-1). Leptin and adiponectin increase fatty acid oxidation, prevent foam cell formation, and improve lipid metabolism, while visfatin, fetuin-A, PAI-1, and resistin have pro-atherogenic properties. In this review, we briefly summarize the role of various adipokines in the development of metabolic syndrome, focusing on glucose homeostasis and lipid metabolism.

Study of type 1 vascular adhesion molecules in patients with acute myocardial infarction with ST segment elevation at different body weights

Objective: to study the level of adhesion molecules in patients with STEMI with different BMI at the hospital stage and 12 months after the index event.Materials and methods: the study included 126 people with STEMI who had undergone PCI and 27 people in the control group. The analysis of the level of svcam‑1 in peripheral blood at the beginning of the disease and after 12 months was carried out, BMI and waist volume were measured. An assessment of the nature and frequency of complications after STEMI was performed.Results: the levels of biomarkers of the vascular endothelial adhesion molecule type 1 increase during the acute period of stemi, statistically signifi tly decrease, but remain increased by 3.5 times 12 months after the index event compared with the initial values. There was no association of VCAM‑1 with visceral obesity in the groups of our patients. Vascular endothelial adhesion molecules of type 1 increase in patients with a fatal outcome, as well as with an increase in the severity of OSN and CHF. Thus, VCAM 1 can be a predictor of an unfavorable outcome of AMI.Conclusions: the article presents the study of a marker of systemic inflammation VCAM‑11 in patients with STEMI with various types of obesity or BMI at the stage of hospitalization and outpatient follow‑up during the year. The determination of the VCAM‑1 level can be used to assess the intensity of the inflammatory process and the risk of adverse outcomes.

The role of non-alcoholic fatty liver disease in the development of vascular rigidity and cardiovascular risk in patients with arterial hypertension

Purpose. To assess the parameters of lipid and carbohydrate metabolism, insulin resistance, chronic low-intensity systemic inflammation, structural and functional parameters of the liver in patients with hypertension (AH) and non-alcoholic fatty liver disease (NAFLD) compared with patients with isolated AH, as well as the impact of changes in these parameters on reducing the elasticity of the main arteries and increasing the risk of cardiovascular complications in patients with comorbid pathology.Material and methods. A comparative cross-sectional study was carried out, which included 120 patients, aged 45 to 65, with AH grade I-II, stages 1-2 (with (FLI≥60) and without NAFLD). During the initial examination, a clinical examination was carried out, the parameters of lipid, carbohydrate and structural-functional parameters of the liver were assessed. The severity of chronic systemic inflammation and insulin resistance were also assessed. Pulse wave velocity (PWV), central aortic pressure (CAP), vascular age and total cardiovascular risk were measured according to the SCORE scale.Results. The data obtained indicate a more pronounced insulin resistance, chronic systemic inflammation, as well as significantly higher lipid metabolism in patients with AH and NAFLD in comparison with patients with isolated AH. In addition, in patients of this group, the indicators of PWV and CAP were significantly higher, and patients with AH and NAFLD had a higher 10-year fatal risk (p=0.013). The performed ROC analysis showed that at FLI≥60, a high risk of PWVm>10m/s is predicted. Multiple regression analysis found that an increase in VLDL cholesterol leads to an increase in the values of both PWVe (p<0.001) and PWVb (p=0.048). The 10-year fatal risk (SCORE) in patients with AH and NAFLD increased with an increase in PWVe (p=0.021), FLI (p=0.013), and visceral obesity (p<0.001).Conclusion. The study shows that in patients with AH and NAFLD, compared with patients with isolated AH, the indicators of insulin resistance and chronic low-intensity systemic inflammation are significantly higher, the highly atherogenic type of hyperlipidemia and visceral obesity are more often found. Also, in comorbid patients with AH, statistically significant higher values of CAP and augmentation index are determined. Stiffness indices of the great arteries were also significantly higher in patients with comorbid pathology. The ROC analysis showed that at FLI≥60, a high risk of PWVm>10 m/s was predicted, which is associated with the development of cardiovascular complications. Also, multiple regression analysis showed that the increase in PWVe and PWVm was mainly due to an increase in VLDL cholesterol, and the 10-year fatal cardiovascular risk of complications had the greatest increase with an increase in the values of PWVe, FLI and visceral obesity.

A Hypercaloric Diet Induces Early Podocyte Damage in Aged, Non-Diabetic Rats

Background/Aims: The number of patients of older age with metabolic syndrome, obesity, and associated kidney disease, which is characterized by podocyte damage, glomerular hypertrophy, and focal segmental glomerulosclerosis (FSGS), is increasing worldwide. Animal models that would reflect the development of such kidney diseases could facilitate the testing of drugs. We investigated the renal effects of a long-term high caloric diet in aged rats and the potential effects of drugs used to treat metabolic syndrome. Methods: We analyzed nine-month-old male and female Sprague Dawley rats fed five months with a normal diet (control group) or high-fat-high-carbohydrate diet (HFHCD group). Two additional groups were fed with HFHCD and treated with drugs used in patients with metabolic syndrome, i.e., the glucagon-like peptide receptor 1 agonist liraglutide (HFHCD+liraglutide group) or metformin (HFHCD+metformin group). Results: Except an increase of waist circumference as a sign of visceral obesity, the HFHCD diet did not induce metabolic syndrome or obesity. There were no significant changes in kidney function and all groups showed similar indices of glomerular injury, i.e., no differences in glomerular size or the number of glomeruli with FSGS or with FSGS-precursor lesions quantified by CD44 expression as a marker of parietal epithelial cell (PEC) activation. Analysis of ultrastructural morphology revealed mild podocyte stress and a decrease of glomerular nestin expression in the HFHCD group, whereas podocin and desmin were not altered. HFHCD did not promote fibrogenesis, however, treatment with liraglutide led to a slightly increased tubulointerstitial damage, immune cell infiltration, and collagen IV expression compared to the control and HFHCD groups. Conclusion: A five-month feeding with HFHCD in aged rats induced mild podocyte injury and microinflammation, which was not alleviated by liraglutide or metformin.

Comparison of Visceral Fat Lipolysis Adaptation to High-Intensity Interval Training in Obesity-Prone and Obesity-Resistant Rats

Background/objectives: Visceral obesity is one of the key features of metabolic syndrome. High-intensity interval training (HIIT) could effectively reduce visceral fat but its effects show strong heterogeneity in populations with different obesity degree. The mechanism may be related to the differential adaptation to training between obesity phenotypes, namely obesity prone (OP) and obesity resistant (OR). The aim of the present study was to compare adaptive changes of visceral adipose lipolysis adaptation to HIIT between OP and OR animals and further explore the upstream pathway.Methods: OP and OR Sprague Dawley rats were established after feeding a high-fat diet for 6 weeks; they were then divided into HIIT (H-OP and H-OR) and control (C-OP and C-OR) groups. After 12 weeks of HIIT or a sedentary lifestyle, animals were fasted for 12 h and then sacrificed for histology as well as gene and protein analysis. Visceral adipocytes were isolated without fasting for catecholamine stimulation and β3-adrenergic receptor (β3-AR) blockade in vitro to evaluate the role of upstream pathways.Results: After training, there were no differences in weight loss or food intake between OP and OR rats (P > 0.05). However, the visceral fat mass, adipocyte volume and liver lipid of OP rats decreased more than that of OR rats (P < 0.05). Meanwhile, the cell lipolytic capacity and the increase in the expression of β3-AR was higher in the OP compared with OR groups (P < 0.05). Although training did not increase sympathetic nervous system activity (P > 0.05), the cell sensitivity to catecholamine increased significantly in the OP compared with OR groups (P < 0.05). After blocking β3-AR, the increased sensitivity disappeared.Conclusion: With HIIT, OP rats lost more visceral fat than OR rats, which was related to stronger adaptive changes in lipolysis. Increased β3-AR expression, rather than altered sympathetic nerve activity, mediated this adaption.