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The fatty tissue is an endocrine organ secreting biologically active factors called adipokines that have systemic and local features. The adipokines play an important role in development of complications caused by obesity. nowadays, retinol-binding protein 4 (RBP4), one of adipokines identified recently, is considered as a connecting link between obesity and its complications. Adipokine participates in development of resistance to insulin and correlated with cardio-metabolic markers at chronic inflammatory diseases, including diabetes mellitus type II, metabolic syndrome and cardio-vascular diseases. It is considered that inflammation, produced by RBP4, induces resistance to insulin and cardio-vascular diseases. It seems that RBP4 is an adipokine that both induces resistance to insulin and participates in pathogenesis of other metabolic complications of obesity. This is confirmed by a tight relationship between RBP4 and atherogenic lipoproteins, atherosclerotic affection of vessels and cardio-vascular diseases. However, an important restriction in certain studies related to RBP4 is that they included patients who received medicinal therapy (sugar lowering and hypo-lipidemic pharmaceuticals) or had renal and hepatic insufficiency. The mentioned factors impact concentration of RBP4 in blood and hence can distort the results. In spite of that, the established potential metabolic role of RBP4 requires a further investigation. Besides further carefully planned studies are required focusing on establishing is RBP4 a molecular participator of molecular alterations or it is only a dynamically volatile "witness". The present review summarizes actual knowledge concerning the role of RBP4 under obesity, in development of dyslipidemia, insulin resistance and cardio-vascular diseases. The purpose of the study is to summarize data of studying of inflammatory and immune effects of RBP4 especially in case of cardio-vascular diseases and also establishment of perspective of applying retinol-binding protein as a potential biomarker of cardiovascular risk., Competing Interests: The authors declare no conflict of interest.

The aim of the study was to obtain a comparative evaluation of antihypertensive efficacy, tolerability and influence of combine therapy on myocardium mass, diastolic function of a left ventricle, lipid and carbohydrate exchange in patients with arterial hypertension in metabolic syndrome. Out of 40 examined cases 20 patients took enalapril and long-acting nifedipin and 20 ones--enalapril and moxonidine. All examination were been performed before administration of drugs and 6 months after the therapy. The dynamics of indices of ambulatory blood pressure monitoring, echocardiography, cycle ergometry, anthropometry, lipid, carbohydrate exchange and tolerability of conducted therapy was been evaluated. The use of this combination of the drugs may be recommended to be included in the treatment of arterial hypertension within the bounds of metabolic syndrome, as in most of cases they promote an achievement of target blood pressure level, have a cardioprotective action, high tolerability and favorable metabolic profile. The combination of enalapril and long-acting nifedipin has a more evident antihypertensive activity but a therapy with enalapril and moxonidine has a positive effect on the indices of carbohydrate exchange.

Basal and insulin-induced production of NO by monocytes significantly increased in patients with metabolic cardiovascular syndrome. Plasma insulin concentration in these patients was below the control. No intergroup differences were found in C-peptide concentration. A negative correlation was revealed between insulin-induced NO production by monocytes and C-peptide/insulin ratio in patients. The role of monocytes on the regulation of vascular tone via NO production in patients with metabolic cardiovascular syndrome is discussed.

The oxidant resistance of low-density lipoproteins was shown in patients with metabolic cardiovascular syndrome to be reduced versus healthy donors. A changing total antiradical activity of blood serum is an important factor for such reduction of the antioxidant resistance in the above pathology. The level of tocopherol in blood serum could be the most significant chain determining the mentioned activity in patients with metabolic cardiovascular syndrome.

Oxygen-dependent processes in peripheral blood monocytes were intensified in patients with metabolic cardiovascular syndrome. This was manifested in increased production of O(2)(*-) and NO. Among metabolic factors (cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triacylglycerols, glucose, etc.), products of glycosylation (fructosamine) and plasma triacylglycerols were most potent in modulating generation of O(2)(*-) and NO by monocytes.