ROLE OF ADIPOSE TISSUE AND ADIPOKINES IN CHRONIC INFLAMMATION DEVELOPMENT ON METABOLIC SYNDROME BACKGROUND

The most pressing issue that combines obesity and insulin resistance is chronic subclinical inflammation, which affects the metabolic and secretory functions of adipose tissue, and is important for the development of pathological processes. The morphological basis of inflammation is the infiltration of adipose tissue by immune competent cells. Biologically active substances specific for adipose tissue are considered to be the collagen−like protein adiponectin and the protein hormone leptin, which are secreted in adipocytes. Leptin stimulates the cellular immune response and increases the production of pro−inflammatory cytokines, and adiponectin is thought to have anti−inflammatory properties. With the development of metabolic syndrome, the concentration of adiponectin in blood decreases, and that of leptin increases. To establish the relationship between serum leptin levels with markers of systemic inflammation and spontaneous production of proinflammatory cytokines as well as mononuclear blood leukocytes, an experimental study was conducted, i.e. modeling the metabolic syndrome in white female rats WAG / GSto aged 5−6 months. The predominance of proinflammatory cytokines: interleukins − 1β, −6, −8, −10, TNF−α in supernatants of mononuclear leukocytes with increasing leptin concentration, which is consistent with the view of its ability to stimulate cell immunity and affect the production of proinflammatory cytokines. It is proven that an increase in leptin levels in metabolic syndrome is not only a symptom that characterizes the functional state of adipose tissue, but also causes spontaneous production of proinflammatory cytokines and mononuclear leukocytes in blood, that is pathogenetically interrelated with the systemic inflammatory response. It is established that the change in the cytokine profile in the serum becomes a forecast of the formation and effectiveness of treatment of metabolic syndrome on the background of obesity. Key words: obesity, metabolic syndrome, undifferentiated chronic inflammation, cytokines.