ometendoОжирение и метаболизмObesity and metabolism2071-87132306-5524Endocrinology Research Centre10.14341/2071-8713-5203ometendo-5203Research ArticleСтатьиArticlesРоль инсулиноподобного фактора роста-Iв метаболизме, регуляции клеточного обновленияи процессах старенияRol' insulinopodobnogo faktora rosta-Iv metabolizme, regulyatsii kletochnogo obnovleniyai protsessakh stareniyaGennadinikA Ggenugend@gmail.comNelaevaA Anelaeva@inbox.ru20101506201072№2 (2010)1015Copyright © Gennadinik A.G., Nelaeva A.A., 20102010Gennadinik A.G., Nelaeva A.A.Gennadinik A.G., Nelaeva A.A.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.omet-endojournals.ru/jour/article/view/5203

Резюме. Инсулиноподобный фактор роста-I (ИФР-I) является проводником биологического действия соматотропного гормона (СТГ), с другой стороны, ИФР-I имеет инсулиноподобное действие. Синтез ИРФ-I в печени увеличивается под действием СТГ и инсулина. Повышенный уровень инсулина через механизм гипогликемии способствует повышению СТГ, обладающего контринсулярным действием. СТГ в свою очередь стимулирует продукцию ИФР-I, отменяющего гипергликемическое действие гормона роста. У больных диабетом наблюдается разобщение действия СТГ и ИФР-I. При сахарном диабете 1 типа (СД1) ИФР-I снижен из-за дефицита инсулина, а СТГ относительно повышен на фоне снижения соматостатина. Так как рост-сти- мулирующий эффект СТГ опосредуется ИФР-I, больные СД1 отстают в физическом и половом развитии. При сахарном диабете 2 типа (СД2) гиперинсулинемия обусловливает увеличение продукции ИРФ-I, тогда как СТГ снижен из-за увеличения уровня соматостатина и лептинорезистентности, что способствует ожирению, гипогонадизму, нарушению репродукции. Сахароснижающее действие ИФР-I утрачивается из-за резистентности рецепторов мышечной ткани. СД2 сопряжен с повышенным риском злокачественных новообразований, поскольку ИФР-I стимулирует пролиферацию, а метаболические нарушения, связанные со снижением СТГ и гипергликемией, уменьшают способность клеток к репарации и супрессивную функцию иммунной системы. Resume. IGF-I is a conductor of biological action of somatotropic hormone (SH), on the other hand IGF-I has insulin-like action. IGF-I synthesis in a liver is increased by SH and insulin action. The elevated insulin level through the hypoglycemic mechanism promotes the SH increase. Also SH stimulates production of IGF-I, cancelling hyperglycemiс action of SH. Dysbalanced action of SH and IGF-I was observed in patients with diabetes. In patients with diabetes mellitus type I IGF-I is lowered because of insulin deficiency, but SH is relatively increased in case of decrease of somatostatin. As growth-stimulating effect of SH is mediated by IGF-I, patients with diabetes mellitus type I have a retardation of physical and sexual development. In patients with diabetes mellitus type II hyperinsulinemia causes an increase of production of IGF-I, whereas SH is relatively lowered because of the increase of somatostatin level and resistance of receptors to leptin, that promotes obesity, hypogonadism, reproduction disturbanses. IGF-I ability to reduce glycemia is lost because of resistency of a muscular receptors. Diabetes mellitus type II is associated with the high risk of malignant neoplasms, because IGF-I stimulates cell proliferation, but the metabolic abnormalities connected with hyperglycemia and SH decrease reduce the ability of cells to a reparation and suppression functions of the immune system.

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