Metabolic sindrome: pathogenesis, prevention and treatment

In connection with a change in the lifestyle of a person, energy requirements for fats have decreased due to a decrease in physical exertion.On the contrary, there is a predominance of intellectual and operator types of activity, which are provided by the energy of glucose (the brain uses only glucose as a source of energy).This led to the development of an energy imbalance - a deficiency of one energy source (glucose) against the background of an excess of another (fat). The body is trying to ensure the functioning of the brain due to the supply of glucose with food, but at the same time an excess amount of food is supplied, which contributes to the development of obesity.Brain activity can also be achieved by increasing transport or increasing blood pressure, but this increases the risk of developing hypertension. In the liver, fat oxidation provides energy for the process of gluconeogenesis, and when there is a shortage of substrate or amino acids for gluconeogenesis (for example, during fasting or type 1 diabetes), the need for ATP energy decreases and fat oxidation during the acetyl-CoA phase is blocked.Two molecules of acetyl-CoA are condensed with the formation of acetoacetate, which is then converted into hydroxybutyrate and acetone, i.e. developing ketosis, which is a threat to life.Therefore, the body protects itself from the development of ketosis (adaptive response) through the secretion of the hormone insulin, which prevents the release of fat from the depot to the circulation. However, an increase in insulin also has an adverse effect (in particular, hypoglycemic coma), so the body protects itself against insulin through the development of insulin resistance, which leads to the development of diabetes. In response to insulin, the synthesis of fats increases and their oxidation decreases, leading to the development of dyslipidemia. This deadly quartet (obesity, hypertension, diabetes, and dyslipidemia) has been calledmetabolic syndrome (MS). For the prevention and treatment of MS, it is necessary in the phase of physical and mental activity or in the post-adsorption period to increase the body's supply of glucose energy, which can be achieved through the use of a specialized product for feeding obese individuals (Certificate of Grant of Patent GB 2496119 22 January 2014). This product also improves the interface between lipid oxidation and the process of gluconeogenesis, which prevents the development of ketogenesis. Thus, in addressing the issues of prevention and treatment of MS, it is necessary to use the metabolic approach in conjugating the processes of formation and utilization of ATP energy, which we proposed as a conceptual metabolic model developed taking into account the carbon skeleton transport during the absorptive and postabsorptive periods.