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What causes diabetes mellitus in children?
Last reviewed: 04.07.2025
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Causes of Diabetes in Children
It is assumed that both genetic predisposition and environmental factors play a role in the development of diabetes mellitus. Hereditary predisposition to type 1 diabetes mellitus is associated with an unfavorable combination of normal genes located in different loci on different chromosomes, most of which control various links in the body's autoimmune processes. More than 95% of patients with type 1 diabetes mellitus have the HLA-DR3, -DR4 or -DR3/DR4 alleles. A high degree of predisposition to type 1 diabetes mellitus is carried by combinations of certain allelic variants of the HLA-DQh DR genes.
In addition, various environmental factors are involved in the pathogenesis of diabetes mellitus. Most of these factors are unknown, but viral infections (enterovirus, rubella virus) and nutritional factors (e.g., cow's milk in early childhood) can become trigger factors that initiate the autoimmune process in predisposed individuals. The immunological process leading to the manifestation of type 1 diabetes mellitus begins years before the onset of clinical symptoms of the disease. During this prediabetic period, elevated titers of various autoantibodies to islet cells (ICA) and insulin (IAA) or to a protein found in islet cells - GAD (glutamate decarboxylase) can be detected in the blood of patients.
Pathogenesis of diabetes mellitus
There are six stages in the development of the disease.
- Stage I - genetic predisposition associated with HLA.
- Stage II - exposure to a factor that provokes autoimmune insulitis.
- Stage III - chronic autoimmune insulitis.
- Stage IV - partial destruction of beta cells. Reduced insulin secretion in response to glucose administration while maintaining basal glycemia (on an empty stomach).
- Stage V - clinical manifestation of the disease with residual insulin secretion.
- Stage VI - complete destruction of beta cells, absolute insulin deficiency.
Insulin deficiency leads to a decrease in glucose transport to liver cells, fat and muscle tissue, and an increase in hyperglycemia. To compensate for energy deficiency, mechanisms for the formation of endogenous glucose in the liver are activated.
Under the influence of "counterinsular" hormones (glucagon, adrenaline, GCS) glycogenolysis, gluconeogenesis, proteolysis, lipolysis are activated. Hyperglycemia increases, the content of amino acids, cholesterol, free fatty acids in the blood increases, energy deficiency worsens. At the level of glycemia above 9 mmol/l, glucosuria appears. osmotic diuresis develops, which in turn leads to polyuria, dehydration and polydipsia. Insulin deficiency and hyperglucagonemia promote the conversion of fatty acids into ketones. The accumulation of ketones leads to metabolic acidosis. Ketones, excreted in the urine together with cations, increase the loss of water and electrolytes. Growing dehydration, acidosis, hyperosmolality and oxygen deficiency lead to the development of diabetic coma.