Human obestatin level and its correlations with metabolic syndrome components in non-diabetic obese patients

Human obestatin level and its correlations with metabolic syndrome components in non-diabetic obese patients

e250 Abstracts / Atherosclerosis 263 (2017) e111ee282 PO457. ROLE OF BROWN ADIPOSE TISSUE IN THE PATHOGENESIS OF METABOLIC SYNDROME PO459. LIPOCALI...

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e250

Abstracts / Atherosclerosis 263 (2017) e111ee282

PO457. ROLE OF BROWN ADIPOSE TISSUE IN THE PATHOGENESIS OF METABOLIC SYNDROME

PO459. LIPOCALIN 2 MAY BE A POTENTIAL BIOMARKER OF ATHEROSCLEROTIC COMPLICATIONS IN OBESE NON-DIABETIC INDIVIDUALS

Vojtech Skop, Jaroslava Trnovska, Martina Hüttl, Olena Oliyarnyk, Irena Markova, Hana Malinska, Ludmila Kazdova. Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic

Peter Fulop, Ildiko Seres, Hajnalka Lorincz, Sandor Somodi, Mariann Harangi, Gyorgy Paragh. University of Debrecen Faculty of Medicine, Debrecen, Hungary

Aim: Recent studies dealing with metabolic syndrome (MS) and related complications has been focused on brown adipose tissue (BAT), because depots of this tissue has been lately found in adult humans and because of its ability to degrade energetic substrates. However, the exact role of BAT in the pathogenesis of MS remains unclear. Here we study age-related changes of interscapular BAT (iBAT) activity of non-obese model of dyslipidemia and metabolic syndrome - hereditary hypertriglyceridemic rats (HHTg) in comparison with control rats Wistar. We further analyzed the effect iBAT extirpation on metabolic syndrome-related disorders. Methods: Metabolic parameters and iBAT activity (14C-glucose and 14Cpalmitate utilization) were analyzed in two and twelve-month-old rats. In another experiment iBAT was extirpated from five-weeks and eighteenmonth-old rats and metabolic parameters were analyzed one week and three weeks after operation. Results: Higher age in both rat strains was associated with reduced BAT weight and activity and with impaired MS-related parameters, especially insulin sensitivity. Compare to Wistar controls, HHTg rats had higher plasma level of triglycerides, non-esterified fatty acids, increased ectopic lipid deposition and reduced insulin sensitivity. However, HHTg rats had strongly higher BAT activity and they were less obese in old age than Wistar rats. To test the hypothesis that reduced obesity was associated with higher BAT activity, we analyzed effect of iBAT extirpation. Nevertheless, this intervention had not significant effect on metabolism. Conclusions: Results show that BAT activity is reduced in older age, however, it likely does not play a significant role in the pathogenesis of metabolic syndrome. Funding:GACR P301/13-04420S.

PO458. HUMAN OBESTATIN LEVEL AND ITS CORRELATIONS WITH METABOLIC SYNDROME COMPONENTS IN NON-DIABETIC OBESE PATIENTS Anita Szentpeteri, Hajnalka Lorincz, Sandor Somodi, Viktoria Evelin Varga, Ildiko Seres, Gyorgy Paragh, Mariann Harangi. University of Debrecen Faculty of Medicine, Debrecen, Hungary Aim: Obestatin is a ghrelin-associated peptide, derived from preproghrelin. Although many of its effects is unclear, accumulating evidence supports positive actions on both metabolism and cardiovascular function. Human circulating obestatin levels generally demonstrate an inverse association with obesity and diabetes. To date, level of obestatin and its correlations to the components of metabolic syndrome and lipid subfractions in non-diabetic obese (NDO) patients have not been investigated. Methods: Fifty NDO patients (BMI: 41.96±8.6 kg/m2) and thirty-two normal-weight, age- and gender-matched healthy controls (BMI: 24.16±3.3 kg/m2) were enrolled into our study. Obestatin level was measured by ELISA. Low-density lipoprotein (LDL) and high-density lipoprotein (HDL) subfractions were detected by nongradient polyacrylamide gel electrophoresis (Lipoprint). Results: Serum level of obestatin was significantly lower in NDO patients compared to controls (3.01±0.5 vs. 3.29±0.6 ug/ml, p<0.05). We found significant negative correlations between the level of obestatin and BMI (r¼-0.33; p<0.001), level of serum glucose (r¼-0.27, p<0.05), HbA1c (r¼0.38; p<0.001) and insulin (r¼-0.34; p<0.05). Significant positive correlation was found between obestatin level and the levels of ApoA1 (r¼0.25; p<0.05) and large HDL subfractions (r¼0.24; p<0.05), and mean LDL size (r¼0.25; p<0.05). Conclusions: Decreased level of obestatin may contributes to the development of metabolic syndrome in obese patients even without disturbed insulin sensitivity.

Aim: Lipocalin 2 (Lcn2) is an adipokine that promotes insulin resistance and inflammation, hence enhances atherosclerosis. This process is also regulated by other adipokines as well as lipoproteins and antioxidant factors. Imbalance between adipokine concentrations and subsequent increase in pro-inflammatory and/or pro-oxidant processes may lead to early cardiovascular complications in obese patients. Therefore, we aimed to analyze the associations between Lcn2 and markers of inflammation and oxidant status in such patients. Methods: Enrolling fifty obese patients with undisturbed insulin sensitivity, we measured levels of serum lipoproteins, Lcn2, hsCRP and various adipokines as well as paraoxonase-1 (PON1) activities in fifty obese nondiabetic patients and compared their data with thirty-eight lean subjects matched in age and gender. Adipokine levels were measured by ELISA, whereas PON1 activities was determined by spectrophotometry. Results: Lcn2 levels tended to be higher in the obese group; however, the difference was not significant. Lcn2 concentrations correlated positively with BMI and with the levels of lipoprotein(a) [Lp(a)], hsCRP and serum amyloid A. Additionally, Lcn2 levels showed significant positive associations with the concentrations of pro-inflammatory adipokines including leptin, chemerin, IL-6 and pigment epithelium-derived factor (PEDF); while Lcn2 levels correlated negatively with PON1 paraoxonase and arylesterase activities, respectively. Conclusions: Our results suggest that lipocalin 2 promotes pro-inflammatory mechanisms in obese non-diabetic patients and may serve as an early biomarker of atherosclerotic complications even in the absence of manifest insulin resistance.

PO460. HORMONAL AND ADIPOSITY STATE OF WOMEN WITH POLYCYSTIC OVARY SYNDROME: IMPLICATION OF ADIPOCYTOKINES Zafirova Ivanovska2, Sasha Aleksandra Atanasova Boshku1, Beti Jovanovska Mishevsk3. 1 University Clinic of Obstetrics and Gynecology, Medical Faculty, Ss Cyril and Methodius University, Skopje, Republic of Macedonia; 2 Institute of Epidemiology and Biostatistics with Medical Informatics, Medical Faculty, Ss Cyril and Methodius University, Skopje, Republic of Macedonia; 3 University Clinic of Endocrinology and Metabolic Disorders, Ss Cyril and Methodius University, Skopje, Republic of Macedonia Aim: Obesity and insulin resistance are frequently seen comorbidities affecting already disturbed metabolism of patients with polycystic ovary syndrome. Adiponectin and leptin disturbed secretion can be one of contributing factors of obesity and insulin resistance in PCOS. The aim this study was to determine levels of adiponectin and leptin as well as their association with other components of the syndrome. Methods: A cross esectional study of clinical hormonal, biochemical markers,adiponectin and leptin in of 61 women with PCOS 56 controls was conducted. Results: There was statistically significant difference of adiponectin and leptin between the groups (p>0.001). Significant negative correlation of adiponectin with BMI as well as with waist circumference (r¼ -0.478; -0.452, p<0.001), and negative correlation with testosterone, FAI, insulin and HOMA e IR were observed. Positive correlation of adiponectin and SHGB and fasting glucose levels were presented. Correlation analysis of leptin with other metabolic parameters has shown positive correlation with BMI, WC, insulin and HOMA-IR. Significant inverse correlation was presented between leptin and SHGB. In conclusion, adiponectin and leptin may serve as a potential biomarkers of insulin resistance. Determining levels of adiponectin and leptin in the early course of this syndrome may