Homocysteine is the confounding factor of metabolic syndrome-confirmed by siMS score.

BACKGROUND: Abdominal adiposity has a central role in developing insulin resistance (IR) by releasing pro-inflammatory cytokines. Patients with metabolic syndrome (MS) have higher values of homocysteine. Hyperhomocysteinemia correlates with IR, increasing the oxidative stress. Oxidative stress causes endothelial dysfunction, hypertension and atherosclerosis. The objective of the study was to examine the correlation of homocysteine with siMS score and siMS risk score and with other MS co-founding factors. METHODS: The study included 69 obese individuals (age over 30, body mass index [BMI] >25 kg/m2), classified into two groups: I-with MS (33 patients); II-without MS (36 patients). Measurements included: anthropometric parameters, lipids, glucose regulation parameters and inflammation parameters. IR was determined by homeostatic model assessment for insulin resistance (HOMA-IR). ATP III classification was applied for diagnosing MS. SiMS score was used as continuous measure of metabolic syndrome. RESULTS: A significant difference between groups was found for C-reactive protein (CRP) (p<0.01) apolipoprotein (Apo) B, HOMA-IR and acidum uricum (p<0.05). siMS risk score showed a positive correlation with homocysteine (p=0.023), while siMS score correlated positively with fibrinogen (p=0.013), CRP and acidum uricum (p=0.000) and homocysteine (p=0.08). Homocysteine correlated positively with ApoB (p=0.036), HbA1c (p=0.047), HOMA-IR (p=0.008) and negatively with ApoE (p=0.042). CONCLUSIONS: Correlation of siMS score with homocysteine, fibrinogen, CRP and acidum uricum indicates that they are co-founding factors of MS. siMS risk score correlation with homocysteine indicates that hyperhomocysteinemia increases with age. Hyperhomocysteinemia is linked with genetic factors and family nutritional scheme, increasing the risk for atherosclerosis.

Homocysteine is a marker for metabolic syndrome and atherosclerosis.

BACKGROUND: It has been documented that patients with metabolic syndrome (MS) and vascular complications have higher homocysteine levels. Hyperhomocysteinemia correlates with IR, increasing oxidative stress, which causes lesions of vascular endothelium leading to endothelial dysfunction, hypertension and atherosclerosis. OBJECTIVE: The objectives of the study were to examine homocysteine values, along with cardiovascular risk factors (lipid and apolipoprotein status, CRP, blood pressure), indicators of renal function (microalbuminuria/24h), glucose regulation and insulin resistance (glucose and insulin level, HbA1c, HOMA-IR, uric acid) and anthropometric parameters (BMI, WC, HC, WHR) in patients with and without MS as a correlation between homocysteine and MS factors. METHODS: The study included obese and overweight individuals, aged of 30-75 yrs. classified into two groups: with MS (n=35) and without MS (n=41). RESULTS: Patients with MS had increased WC, BMI, BP, glycaemia, HOMA-IR, TG, CRP, microalbuminuria, homocysteine and decreased HDL-C (p<0.05). Statistically significant difference between groups was found for WC, BMI, sBP and dBP, TG, HDL-C (p<0.01) and glycaemia, CRP, Apo B, HOMA-IR (p<0.05). Significant positive correlations were found between homocysteine and sBP (p=0.036), dBP (p=0.04), Apo B (p=0.038) and hyperlipoproteinemia (type IIa, type IIb and type IV) (p=0.04). CONCLUSION: Patients with MS had increased abdominal obesity, hypertension, hypertriglyceridemia, inflammation factors, IR, homocysteine and microalbuminuria as markers of endothelial dysfunction. A correlation between homocysteine and hypertension and hyperlipoproteinemia showed that homocysteine could be used as a potential marker for atherosclerosis progression.

Liver function test changes in centrally obese youth with metabolic syndrome in a Serbian population.

OBJECTIVE: The aim of this study was to investigate the association between metabolic syndrome and liver enzymes in overweight and obese adolescents and young adults. METHODS: A total of 126 overweight and obese adolescents and young adults (age, 15-26 years), 55 (43.6%) with metabolic syndrome and 71 (56.4%) without metabolic syndrome, were studied. RESULTS: Patients with metabolic syndrome had significantly higher alanine aminotransferase (ALT), γ-glutamyl transpeptidase (GGT), and alkaline phosphatase (ALP) levels compared to patients without metabolic syndrome [36.5±22.2 vs. 29.4±17.8 IU/L (P=0.043), 33.8±17.8 vs. 26.9±18.4 IU/L (P=0.002), and 84.3±32.2 vs. 75.7±29.5 IU/L (P=0.063)]. Aspartate aminotransferase (AST) levels were similar in both groups (24.1±9.8 vs. 23.3±9.0 IU/L, P=0.674). Elevated AST, ALT, GGT, and ALP levels were observed in 6, 15, 18, and 5 patients (11%, 27%, 14%, and 9%) with metabolic syndrome compared to 6, 17, 6, and 4 (8%, 24%, 8% and 5%) patients without metabolic syndrome (P=0.872, P=0.826, P<0.001, and P=0.035). In multivariate regression models adjusted for age and gender, metabolic syndrome was not a significant predictor of ALT (P=0.967), GGT (P=0.526), and ALP levels (P=0.221), but insulin resistance was a significant predictor for ALT and GGT levels (P=0.001, P=0.028). CONCLUSION: Changes in liver function tests were observed in obese patients with metabolic syndrome, compared to patients without metabolic syndrome, especially in ALT and GGT levels. Insulin resistance is an independent pathogenic mechanism in liver function test changes regardless of metabolic syndrome in nondiabetic centrally obese youth.

Prothrombogenic factors and reduced antioxidative defense in children and adolescents with pre-metabolic and metabolic syndrome.

BACKGROUND: The aim of this study was to examine prothrombogenic factors and antioxidative defense in obese children and adolescents with pre-metabolic and metabolic syndrome, and to analyze insulin secretion and resistance, early glycoregulation disorders and lipid status. METHODS: Insulin sensitivity was determined using the homeostasis model assessment for insulin resistance (HOMA-IR), while insulin secretion was determined using the homeostasis model assessment beta (HOMA-beta). Prothrombogenic factors analyzed were plasma plasminogen activator inhibitor-1 (PAI-1) and fibrinogen. Superoxide dismutase and glutathione peroxidase were measured as markers of antioxidative defense. RESULTS: Patients with metabolic syndrome were characterized with increased body mass index (BMI), waist circumference, and HOMA-IR and HOMA-beta levels, and all had increased blood pressure and triglyceride levels, low high-density lipoprotein cholesterol levels, increased PAI-1 levels and reduced antioxidative defense levels. Patients with pre-metabolic syndrome had higher levels of basal and mean insulinemia during an oral glucose tolerance test, higher levels of HOMA-beta and lower levels of antioxidative defense compared to patients with metabolic syndrome. CONCLUSIONS: Negative correlations between antioxidative defense parameters and BMI, abdominal obesity, insulin secretion, systolic blood pressure and atherogenic lipid factors, as well as correlations between PAI-1 and insulin resistance and basal glycemia in the metabolic syndrome group contribute to accelerated atherosclerosis. Positive correlations between PAI-1 and waist circumference and BMI, and negative correlations between BMI and antioxidative defense in the pre-metabolic syndrome patients show that this early stage preceding the metabolic syndrome is also characterized by atherosclerotic complication risks and evident hyperinsulinism and insulin resistance.