**Table 1.**

*Mean cytokine levels (pg/mL) in obese patients.*

The glycoprotein OPG, which belongs to the tumor necrosis factor receptor superfamily, was initially identified as an inhibitor of bone resorption, however other important regulatory functions of OPG have been later identified. The OPG/RANKL (NF-κB ligand receptor) axis has been shown to play a significant regulatory role in the skeletal, immune, and vascular systems, including vascular calcification that accompanies atherosclerosis. Elevated OPG levels are associated with the incidence and prevalence of coronary heart disease. Moreover, increased OPG is considered as an independent risk factor for overall vascular mortality in obese adults and IR (insulin resistant) [4]. Our data showed that the OPG level was the most sensitive proinflammatory cytokine. This is confirmed by other authors. Kotanidou et al. (2018) reported that obese individuals show an increase in serum OPG already during puberty, and a key factor in the regulation of OPG is IR, which accompanies even the initial metabolic disorders on the background of excessive body weight [5].

We also investigated the levels of some hormones, which we believe play a key role in the regulation of appetite, neurophysiological relationships between the gut-brain axis and muscles, and physical activity (**Table 2**).

The most significant changes were observed in insulin and leptin. Hyperinsulinemia as a consequence of insulin resistance and hyperleptinemia are the most common hormonal disorders in the background of being overweight. These data are confirmed by numerous studies. Leptin is one of the most well-known adipose tissue hormones; it is very sensitive to energy consumption, especially in energy-deficient conditions. It has been shown that a reduction in the serum leptin was observed before fat loss even after 2–3 days of a low-calorie diet. Decreased leptin levels can cause a number of biological and hormonal responses, including the decreased activity of the sympathetic nervous system, hypothalamic gonadotropinreleasing hormones, IGF-I (insulin growth factor I), GH (increased production of growth hormone), and ACTH (adrenocorticotropic hormone). Conversely, hyperleptinemia, which is common in overweight people, is associated with leptin resistance. At night, the leptin level is 30% higher [4]. In the presence of obesity, the level of leptin is increased many times, and a 10% decrease in body weight decreases its blood content by 50%. According to modern ideas, leptin sends a signal to the hypothalamus by activating specific leptin receptors, which are located in different parts of the brain – hypothalamus, cerebellum, cortex, hippocampus, thalamus, and vascular plexus of the cerebral capillary endothelium [6].

An important regulator of leptin secretion is hyperinsulinemia. Adipocytes produce leptin in response to increased postprandial insulin levels in healthy people and patients with metabolic syndrome. Based on numerous studies, we can conclude that the feedback mechanism between the level of insulin secretion by β-cells and fat and muscle cells utilizing glucose depends only on leptin action because leptin receptors are present in the islets of Langerhans of the pancreas, so there is a direct relationship between the concentration of insulin and its effect on the secretion of hormones by adipocytes. Normally, due to the increase in insulin secretion, production of leptin increases that inhibits the secretion and release of insulin by the feedback mechanism [7].

It should be noted that in our study we did not find a significant difference in cortisol levels between patients with normal body weight and obesity. However, it is well known that over time, elevated glucocorticoid levels can lead to increased skeletal muscle protein breakdown, adipose tissue lipolysis, and hepatic gluconeogenesis accompanied by decreased glucose utilization. These effects increase circulating blood glucose levels, thus contributing to insulin resistance and hyperinsulinemia.

*Personalized Strategy of Obesity Prevention and Management Based on the Analysis… DOI: http://dx.doi.org/10.5772/intechopen.105094*

