Palakorn Puttaruk, Duangnate Pipatsatitpong and Pilaiwan Siripurkpong
Serum levels of soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1) reflect increases in LOX-1 receptor expression associated with inflammation and metabolic disorders.
To examine sLOX-1 levels in metabolic syndrome and association of sLOX-1 with classical risk factors, and with metabolic syndrome, a clustering of metabolic disorders associated with cardiovascular risk factors.
We selected 148 serum samples from patient participants with metabolic syndrome and 206 samples from patients with non-metabolic syndrome as controls, using the modified National Cholesterol Educational Program Adult Treatment Panel III (NCEP-ATP III) criteria.
Levels of sLOX-1 were increased significantly in participants with metabolic syndrome (P < 0.001). Serum sLOX-1 was positively associated with body mass index (BMI), blood pressure, fasting plasma glucose, triglyceride, and total cholesterol, but negatively associated with high-density lipoprotein cholesterol. Analysis of serum sLOX-1 for metabolic syndrome showed 99.03% specificity and 100% sensitivity. The area under the receiver operating characteristic curve was 0.998 (95%CI 0.996-1.001, P < 0.001). A univariate analysis showed sLOX-1 was significantly correlated with metabolic syndrome, but was not after adjustment for sex, age, blood pressure, and BMI. Multivariate regression analysis found that being overweight (82.3; 95%CI 10.7–631.9), hyperglycemia (1.1; 95%CI 1.1–1.2), and hypertriglyceridemia (1.1; 95%CI 1.0–1.1) were significantly correlated with metabolic syndrome. HDL cholesterol was a protective factor (0.96; 95%CI: 0.93–0.99).
Serum sLOX-1 is a suitable biomarker for diagnosis of metabolic syndrome. However, univariate and multivariate analysis suggested that sLOX-1 may be a modulating factor, and not an independent risk factor.
Adiponectin secreted by adipocytes plays a key role in insulin sensitivity, anti-inflammation, and antiatherosclerosis. It is involved in several conditions including obesity, type 2 diabetes mellitus, cardiovascular disease, and chronic kidney disease (CKD). Glomerular filtration rate is monitored to indicate the kidney function and CKD progression.
To assess the serum adiponectin levels in individuals with normal and mildly decreased glomerular filtration rate, analyze the association of serum adiponectin with various physical and biological parameters, and test whether serum adiponectin is the risk factor of mildly decreased glomerular filtration rate.
This cross-sectional study was conducted in 172 individuals with 35–60 years of age. Serum samples were collected and divided into two groups, based on estimated glomerular filtration rate (eGFR): 90 with normal eGFR (G1, eGFR ≥90 mL/min/1.73 m2) and 82 with mildly decreased eGFR (G2, eGFR = 60–89 mL/min/1.73 m2). Anthropometric data were recorded. Serum adiponectin was measured by enzyme-linked immunosorbent assay.
Serum adiponectin levels were significantly increased in individuals with mildly decreased eGFR (G2), compared to G1 (8.23 ± 3.26 µg/mL and 6.57 ± 3.24 µg/mL, respectively; P = 0.001). Serum adiponectin was positively associated with age and high-density lipoprotein cholesterol but negatively associated with weight, body mass index, triglyceride, and waist and hip circumferences. Univariate analysis showed that serum adiponectin was significantly correlated with mildly decreased eGFR; however, when adjusting for confounding factors, there were no correlations. Furthermore, multivariate regression analysis showed that individuals at the age of 46–55 years (4.0; 95% CI: 1.9–8.3) and > 55 years (11.4; 95% CI: 3.7–35.5) were significantly correlated with mildly decreased eGFR.
Serum adiponectin was significantly elevated in individuals with mildly decreased eGFR and may be a modulation factor, but was not an independent risk factor for mildly kidney damage. Further study is needed to clarify its potential benefits as monitoring biomarker for CKD progression.
Background: Diabetes mellitus (DM) patients lose their ability to control normal blood glucose levels, resulting in high blood glucose levels (hyperglycemia). Hyperglycemia causes DM complications. This involves responses of vascular endothelial cells (VECs) to hyperglycemia, affecting inflammatory process and platelet activity. Ecto-enzyme CD39 is expressed on VECs, catalyzing the hydrolysis of ATP and ADP to AMP and, consequently, regulating inflammatory process and platelet activation.
Objective: We studied whether high glucose concentration has an effect on CD39 expression on VECs.
Methods: Cultured human umbilical vein endothelial cells (HUVEC) were used as a model of study. HUVEC were cultured in different glucose conditions (4, 9, 24, and 34 mM) for 24 hours. Cell viability was assessed using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT)-based assay and expression of CD39 was examined by using SDS-PAGE and western blot techniques.
Results: HUVEC were cultured in normal (4 and 9 mM) or high (24 and 34 mM) glucose concentrations for short term (24 hours). The results showed that high glucose (24 and 34 mM) reduced cell viability to 89.5 ± 11.3 and 86.3 ± 13.5 (mean ± SD), compared with control (4 mM), respectively. High glucose also induced increases in CD39 expression in HUVEC.
Conclusion: High glucose decreases cell viability and increases CD39 expression in HUVEC, suggesting involvement of CD39 in cell responses to high glucose.