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Pathogenesis of obesity in children
Last reviewed: 06.07.2025
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One of the main pathogenetic mechanisms of obesity development in children is energy imbalance: energy consumption exceeds energy expenditure. As has been established at present, the pathogenesis of obesity is based not only on energy, but also on nutrient imbalance. Obesity in a child progresses if the body is unable to ensure oxidation of incoming fat.
The pathogenesis of obesity does not depend on its cause. Relative or absolute excess of food, especially rich in carbohydrates, leads to hyperinsulinism. The resulting hypoglycemia maintains 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 adipose 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, impaired sensitivity of the ventromedial and ventrolateral nuclei to hunger and satiety signals, restructuring of the function of other endocrine glands, thermoregulation centers, regulation of blood pressure, impaired secretion of neuropeptides and monoamines of the central nervous system, gastrointestinal peptides, etc.
Obesity in children is considered a chronic inflammatory process, in whose genesis an important role is played by cytokines of adipose tissue: TNF-a, interleukins (1,6,8), as well as changes in the lipid composition of blood serum and activation of lipid peroxidation processes.
Adipocytes of adipose tissue secrete leptin, enzymes regulating 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 hypothalamic neuropeptide Y. Having penetrated the hypothalamus, leptin controls food intake through the limbic lobe and brainstem. However, if the functional state of the system controlling body weight is impaired and the sensitivity of the leptin receptors of the hypothalamus is reduced, 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 associated with the content of insulin.
Insulin, cholecystokinin, and biogenic amines: norepinephrine and serotonin, which play an important role not only in regulating food intake itself, but also in choosing the products that are most preferable for a given person, participate in regulating the activity of hunger and satiety centers. Thyroid hormones participate in the implementation of the mechanism of food thermogenesis. Enteral hormones of the duodenum have an active regulatory effect on eating behavior. With a low concentration of enteral hormones, appetite does not decrease after eating.
Increased appetite may be associated with high concentrations of neuropeptides-x or endogenous opiates (endorphins).
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