Pathogenesis of obesity in children
Last reviewed: 23.04.2024
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One of the main pathogenetic mechanisms of obesity in children - energy imbalance: energy consumption exceeds the energy expenditure. As it has been established at the present time, the pathogenesis of obesity is based not only on energy but also on nutritional imbalances. Obesity in a child progresses if the body is unable to provide oxidation of incoming fat.
The pathogenesis of obesity does not depend on its cause. The relative or absolute excess of food, especially rich in carbohydrates, leads to hyperinsulinism. The resulting hypoglycemia supports the feeling of hunger. Insulin - the main lipogenetic hormone - promotes the synthesis of triglycerides in adipose tissue, and also has an anabolic effect (growth and differentiation of fat and bone tissue).
Excessive accumulation of fat is accompanied by a secondary change in the function of the hypothalamus: increased secretion of adrenocorticotropic hormone (ACTH) and hypercorticism, a violation of the sensitivity of the ventromedial and ventro-lateral nuclei to the signals of hunger and satiety, alteration of the function of other endocrine glands, thermoregulatory centers, regulation of arterial pressure, violation of the secretion of neuropeptides and monoamines of the central nervous system, peptides of the gastrointestinal tract, etc.
Obesity in children is considered as a chronic inflammatory process, cytokines of adipose tissue play an important role in its genesis: TNF-a, interleukins (1,6,8), as well as changes in lipid composition of serum and activation of lipid peroxidation processes.
Adipocytes of adipose tissue secrete leptin, enzymes that regulate lipoprotein metabolism (lipoprotein lipase, hormone sensitive lipase), and free fatty acids. There is a feedback mechanism between the level of leptin and the production of the hypothalamic neuropeptide Y. Having penetrated the hypothalamus, leptin controls food intake through the limbic lobe and the brain stem. However, if the functional state of the system that controls body weight and the hypersensitivity of leptin receptors in the hypothalamus is disturbed, the "food center" does not respond to leptin and there is no feeling of satiety after eating. The content of leptin in the body is related to the content of insulin.
Insulin, cholecystokinin, as well as biogenic amines: noradrenaline and serotonin, which play an important role not only in regulating the actual intake of food, but also in choosing the products most preferred for this person, are involved in the regulation of the activity of hunger and saturation centers. Thyroid hormones are involved in the realization of the mechanism of food thermogenesis. Enteric hormones of the duodenum have an active regulatory effect on food behavior. At a low concentration of enteral hormones, appetite after eating does not decrease.
Increased appetite may be due to a high concentration of neuropeptide-x or endogenous opiates (endorphins).
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