ometendoОжирение и метаболизмObesity and metabolism2071-87132306-5524Endocrinology Research Centre10.14341/2071-8713-5280ometendo-5280Research ArticleСтатьиArticlesОсобенности жирового обмена при болезниИценко-КушингаOsobennosti zhirovogo obmena pri bolezniItsenko-KushingaDzeranovaL Kmetabol@endocrincentr.ruParamonovV Mvalery.paramonov@gmail.comRozhinskayaL Yarozh@endocrincentr.ruPleshchevaA Vnastia040883@yandex.ruManchenkoO Vo-manchenco@yandex.ruVorontsovA Vmr2005@mail.ruKolesnikovaG Shorm@endocrincentr.ruGrigor'evA Yu-PigarovaE Akpigarova@gmail.com20101503201071№1 (2010)5862Copyright © Dzeranova L.K., Paramonov V.M., Rozhinskaya L.Y., Pleshcheva A.V., Manchenko O.V., Vorontsov A.V., Kolesnikova G.S., Grigor'ev A.Y., Pigarova E.A., 20102010Dzeranova L.K., Paramonov V.M., Rozhinskaya L.Y., Pleshcheva A.V., Manchenko O.V., Vorontsov A.V., Kolesnikova G.S., Grigor'ev A.Y., Pigarova E.A.Dzeranova L.K., Paramonov V.M., Rozhinskaya L.Y., Pleshcheva A.V., Manchenko O.V., Vorontsov A.V., Kolesnikova G.S., Grigor'ev A.Y., Pigarova E.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/5280

На примере описанного в статье клинического случая представлены особенности липидного обмена и распределения жировой ткани при гиперкортицизме. Предположительные причины увеличения массы жировой ткани в организме при избытке глюкокортикостероидов (ГКС), ее своеобразного «кушингоидного» перераспределения, роль рецепторов к ГКС и 11-β гидроксистероиддегидрогеназы 1 типа (11β-HSD1), обратимость специфических изменений после нормализации уровня кортизола в организме рассматриваются в контексте физиологических и патофизиологических аспектов действия ГКС.

The reported clinical case represents an example of characteristic traits in lipid metabolism and fat tissue deposition in hypercorticosolism. Probable causes for fat mass expansion in glucocorticosteroid excess, its distinctive cushingoid distribution, role of 11β-HSD1 and glucocorticoid receptors and reversibility of specific abnormalities after correction of hypercortisolism are discussed in the context of physiological and pathological aspects of glucocorticosteroid action.

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The authors declare that there are no conflicts of interest present.