Adipose tissue is recognized as a rich source of proinflammatory mediators that may directly contribute to vascular injury, insulin resistance, and atherogenesis. Many studies have shown that adiponectin has antiatherogenic and anti-inflammatory properties. Adiponectin acts not only as a factor increasing insulin sensitivity, and the protective effect may result from its ability to suppress production of proinflammatory cytokines. It negatively regulates the expression of TNF-alpha and C-reactive protein (CRP) in adipose tissue; reduces expression of vascular and intracellular adhesion molecules (VCAM-1, ICAM-1), E-selectin, interleukin-8 (IL-8). Hyperleptinemia has been linked with the development of hypertension and endothelial dysfunction/atherosclerosis, two main pathophysiological conditions associated with cardiovascular disease development. Leptin-mediated increases in sympathetic nervous system activity may be among the principal mechanisms evoking obesity related hypertension. Leptin stimulates the secretion of proinflammatory cytokines, and increases the release of endothelin-1 (ET-1), which may promote hypertension. Increased serum levels of asymmetric dimethylarginine (ADMA), a physiological regulator of the biosynthesis of nitric oxide (NO), promote the process of atherosclerosis, leading to the occurrence of endothelial dysfunction and cardiovascular disease.

ATANASSOVA P., HRISCHEV P., ORBETZOVA M., NIKOLOV P., NIKOLOVA J., GEORGIEVA E. 2014. Expression of leptin, NGF and adiponectin in metabolic syndrome. Folia Biologica (Kraków) $ : 301-306. Adipose tissue secretes a variety of adipokines involved in the regulation of energy metabolism and insulin resistance. Metabolic syndrome corresponds to a clinical condition in which white adipose tissue is characterized by an increased production and secretion of inflammatory molecules which may have local effects on adipose tissue physiology but also systemic effects on other organs. The aim of this study was to assess the expression of leptin, NGF and adiponectin in women with metabolic syndrome compared to healthy controls. Plasma leptin, NGF and adiponectin levels were measured by the ELISA method. Leptin and NGF immunohistochemical expression was analyzed in subcutaneous adipose tissue. The results indicated that in women with metabolic syndrome waist circumference, body mass index, HOMA index, glucose, total cholesterol and triglyceride levels were significantly increased in parallel with over-expressed plasma levels of leptin and NGF and decreased adiponectin. The immunohistochemical expression of leptin and NGF was very strong. In conclusion, this is the first study demonstrating a complex of immunochemical and immunohistochemical expression of the key adipokines including leptin, NGF and adiponectin in women with metabolic syndrome. Locally-produced pro-inflammatory adipokines probably contribute to the ethiopathogenic mechanisms of metabolic syndrome.

The AIM of the study was to compare the levels of certain adipose tissue hormones in women with the two main morphological types of obesity - android and gynoid obesity. MATERIALS AND METHODS: The study included 2 groups of age- and weight-matched women with android (n = 32) and gynoid (n = 27) type of obesity, and a group of age-matched healthy women (n = 24) with normal weight and body constitution. Leptin, resistin, tumour necrosis factor α (TNFα), neuropeptide Y (NPY), glucose and insulin were measured.HOMA index was calculated. RESULTS: Leptin levels in the women with gynoid obesity did not differ significantly from those in the controls and the women with android obesity. The controls had significantly lower leptin levels compared with the android obesity women. NPY was significantly higher in the control women compared to the women with android obesity and did not differ significantly between the two groups of obese women. TNFα levels in all groups were very similar. Resistin did not show significant differences between all groups but tended to have the lowest levels in the controls. In the women with android obesity, insulin was significantly higher than that in the women with gynoid obesity and the controls. Insulin resistance was found in the women with android obesity only. Basal insulin and HOMA index in the women with gynoid obesity did not differ significantly from the values in the control group. CONCLUSION: The results from this study contribute to understanding the association of adipose tissue hormones and insulin resistance in obesity. When adipose tissue is predominantly distributed in the abdominal area at similar amount and percentage of body fats, leptin production is higher and insulin resistance develops. In the gynoid type of adipose tissue predisposition, overt insulin resistance is not found, leptin levels does not differ significantly from those in the control group.

Insulin resistant PCOS women were at higher atherogenic risk compared to non-insulin resistant group. sVCAM-1 data confirms the necessity of further investigations for clarifying its role in IR.

Pre-hypertension is a precursor of hypertension. Endothelial dysfunction is the key element for early prediction of cardiovascular events. We investigated whether flow mediated dilation, a non-invasive method for assessment of endothelial function, is decreased and if there is a parallel with some biomarkers of endothelial dysfunction. 103 patients with pre-hypertension at the age 43,5±6 years, were enrolled. Weight, body surface area, waist, total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, plasma glucose were followed up for each patient, indicating statistically higher values in the pre-hypertensive subjects. Flow mediated dilation was reduced when compared to our control data from healthy volunteers. It was in parallel with ADMA and sVCAM-1. There were no significant differences in sICAM-1. Pre-hypertension objects demonstrated reduced flow mediated dilation and significantly changed ADMA and sVCAM-1. Intima-media thickness didn't show any significant differences between pre-hypertensive and healthy objects. In conclusion, there is a correlation between clinical chemical biomarkers, flow mediated dilation, endothelial dysfunction and pre-hypertension which confirms their role as a predictor of pre-hypertention and cardiovascular disorders and as a challenge for primary prevention.