Superoxide dismutase isoenzymes gene expression in peripheral blood mononuclear cells in patients with coronary artery disease

Summary Background The purpose of the study was to determine oxidative stress-related plasma thiol/disulphide, ischemia-modified albumin (IMA) levels and ferroxidase activity among women with obesity in insulin-resistant and non-insulin-resistant groups in comparison with an overweight group. Methods We compared plasma thiol/disulphide, IMA levels, and ferroxidase activity between the study groups. We analyzed plasma thiol/disulphide homeostasis with a newly developed automated measurement method; IMA with Albumin Cobalt Binding Test and ferroxidase (ceruloplasmin) levels with an automated, colourimetric method. Results There were no significant differences between insulin-resistant and non-insulin-resistant women with obesity in terms of plasma native thiol, total thiol, disulphide, disulphide/native thiol ratio, disulphide/total thiol or native thiol/total thiol values. Ferroxidase activity was higher in insulin-resistant than in non-insulin-resistant women with obesity and higher in the total women with obesity group than in the overweight subjects (p<0.001, and p=0.014, respectively). IMA was lower in the insulin-resistant group than in the non-insulin-resistant group and overweight groups (p=0.011, and p=0.042, respectively). Conclusions The significantly greater increase in ferroxidase activity in insulin-resistant subjects with obesity may reflect its role as a positive acute phase protein. These findings may be related to the pathogenesis of the disease. Changes in oxidative status occur in women with obesity, and partially in overweight subjects. The ferroxidase activity of ceruloplasmin plays a crucial role in iron homeostasis and lowers oxidative stress by reducing the detrimental effects of iron.

Section: Introductionmentioning

confidence: 99%

Thiol/Disulphide homeostasis, ischemia modified albumin, and ferroxidase as oxidative stress markers in women with obesity with insulin resistance

Ateş¹,

Set²,

Karahan³

et al. 2019

“…It is now recognized that adipose tissue is not only depot of fat, but an endocrine organ and that it is probably an important link between increased fat mass and insulin resistance. It also produces several inflammatory products that lead to atherogenesis (30). CRP is related to various type of atherosclerosis (31).…”

Section: Discussionmentioning

confidence: 99%

Association of overweight and obesity with cardiovascular risk factors in patients with atherosclerotic diseases

Maksimović¹,

Vlajinac²,

Radak³

et al. 2019

Summary Background The aim of this study was to compare demographic, clinical and biochemical characteristics, including inflammatory markers, according to the nutritional status of patients with verified atherosclerotic disease. Methods This cross-sectional study involved 1045 consecutive patients with verified carotid disease or peripheral arterial disease (PAD). Anthropometric parameters and data on cardiovascular risk factors and therapy for hypertension and hyperlipidemia were collected for all participants. Results Carotid disease was positively and PAD was negatively associated with body mass index (BMI). Negative association between obesity and PAD was significant only in former smokers, not in current smokers or in patients who never smoked. Overweight and general obesity were significantly related to metabolic syndrome (p < 0.001), lower values of high – density lipoprotein cholesterol (p < 0.001), increased triglycerides (p < 0.001), hyperglycemia (p < 0.001), self-reported diabetes (p < 0.001), hypertension (p < 0.001), high serum uric acid (p < 0.001), increased high sensitivity C-reactive protein (p = 0.020) and former smoking (p = 0.005) after adjustment for age, gender and type of disease. Antihypertensive therapy seems to be less effective in patients who are overweight and obese. Conclusions In conclusion, overweight and general obesity were significantly related to several cardiovascular risk factors.

“…Endocan is highly expressed in endothelial cell injury (1) with its up-regulation observed in the presence of proangiogenic molecules and proinflammatory cytokines (2). The pathological accumulation of lipids in NAFLD triggers inflam mation (10), which can lead to hepatocytes dysfunction. Additionally, paralell with the liver fibrosis and with the processes of its repairment, increased production of extracellular matrix proteins occurs (11).…”

Section: Discussionmentioning

confidence: 99%

“…The NAFLD is the most frequent manifestation of hepatic disorders (9). It represents the increased accumulation of lipids which can trigger inflammation (10), and lesions of hepatocytes, that can consequently progress into fibrosis (11). Even more, if not treated fibrosis can further progress into cirrhosis and hepatocellular carcinoma (11).…”

Section: Introductionmentioning

confidence: 99%

Is endocan a novel potential biomarker of liver steatosis and fibrosis?

Klisić

Kavarić

Abenavoli

et al. 2019

Summary Background Studies that evaluated endocan levels in nonalcoholic fatty liver disease (NAFLD) and liver fibrosis are scarce. We aimed to explore endocan levels in relation to different stages of liver diseases, such as NAFLD, as determined with fatty liver index (FLI) and liver fibrosis, as assessed with BARD score. Methods A total of 147 participants with FLI≥60 were compared with 64 participants with FLI <30. An FLI score was calculated using waist circumference, body mass index, gamma-glutamyl transferase and triglycerides. Patients with FLI≥60 were further divided into those with no/mild fibrosis (BARD score 0–1 point; n=23) and advanced fibrosis (BARD score 2–4 points; n=124). BARD score was calculated as follows: diabetes mellitus (1 point) + body mass index≥28 kg/m2 (1 point) + aspartate amino transferase/alanine aminotransferase ratio≥0.8 (2 points). Results Endocan was independent predictor for FLI and BARD score, both in univariate [OR=1.255 (95% CI= 1.104–1.426), P=0.001; OR=1.208 (95% CI=1.029– 1.419), P=0.021, respectively] and multivariate binary logistic regression analysis [OR=1.287 (95% CI=1.055– 1.570), P=0.013; OR=1.226 (95% CI=1.022–1.470), P=0.028, respectively]. Endocan as a single predictor showed poor discriminatory capability for steatosis/fibrosis [AUC=0.648; (95% CI=0.568–0.727), P=0.002; AUC= 0.667 (95% CI=0.555–0.778), P=0.013, respectively], whereas in a Model, endocan showed an excellent clinical accuracy [AUC=0.930; (95% CI=0.886–0.975), P<0.001, AUC=0.840 (95% CI=0.763–0.918), P<0.001, respectively]. Conclusions Endocan independently correlated with both FLI and BARD score. However, when tested in models (with other biomarkers), endocan showed better discriminatory ability for liver steatosis/fibrosis, instead of its usage as a single biomarker.