Внесок гормональних порушень у патогенез метаболічно-асоційованої стеатотичної хвороби печінки. Огляд
DOI:
https://doi.org/10.30978/MG-2024-2-26Ключові слова:
метаболічно‑асоційований стеатогепатит, метаболічно‑асоційована стеатотична хвороба печінки, глюкагоноподібний пептид, глюкагон, андрогениАнотація
Проаналізовано внесок гормонів у патогенетичні механізми метаболічно‑асоційованої стеатотичної хвороби печінки (МАСХП). Роль гормонів жирової тканини в розвитку метаболічних порушень і системних запальних реакцій доведена та добре вивчена. З прогресуванням метаболічно‑асоційованого стеатогепатиту (МАСГ) рівень лептину підвищується, а адипонектину та оментину знижується, що асоціюється з прозапальним і профібротичним станом печінки та порушенням обміну глюкози. Печінка також виробляє гормоноподібні протеїни — гепатокіни, які активно впливають на позапечінкову регуляцію метаболізму, а саме сприяють розвитку інсулінорезистентності та дисліпідемії. Одними з найперспективніших для лікування МАСХП/МАСГ вважають препарати, які діють на ендокринологічну складову патогенезу цих захворювань. Лише піоглітазон і агоністи рецепторів глюкагоноподібного пептиду (ГПП)‑1 є антигіперглікемічними препаратами, що мають докази ефективності та безпечності щодо їхнього застосування при МАСГ. Використання агоністів ГПП‑1 знижує споживання їжі, масу тіла, поліпшує контроль рівня глюкози в пацієнтів із MAСГ, зменшує стеатоз, резистентність до інсуліну і ступінь запалення в печінці. Є дані, що свідчать про перспективність застосування подвійних агоністів ГПП‑1/глюкагону та ГПП‑1 і глюкозозалежного інсулінотропного пептиду для лікування МАСХП/МАСГ. За попередніми даними, такі комбінації сприяли зниженню стеатозу та поліпшенню показників фіброзу печінки, але необхідні додаткові докази зміни гістологічних характеристик печінки. Ще однією групою гормонів, яка має важливе значення в патогенезі МАСХП, є гормони надниркових залоз (альдостерон, кортизол, андрогени), оскільки вони беруть активну участь у регуляції реакції на стрес та ліполізу. У цьому аспекті варті уваги андрогени, оскільки, по‑перше, як їхній дефіцит, так і надлишок, спричинять розвиток печінкового стеатозу, ожиріння, резистентності до інсуліну та інших ознак метаболічного синдрому, по‑друге, їхній дефіцит призведе до розвитку саркопенії, що є дуже важливим в аспекті МАСХП. Брак естрогенів у жінок також спричиняє стеатоз печінки, резистентність до інсуліну, дисліпідемію, ожиріння. Одним із чинників, які впливають на розвиток стеатозу печінки, може бути гормон росту: зниження його рівня призводить до внутрішньопечінкового накопичення жиру, що підвищує ризик розвитку МАСХП. У виникненні МАСХП можуть брати участь також гормони щитоподібної залози. Тяжкість гіпотиреозу прямо пропорційно корелює з тяжкістю МАСХП, а рівень тиреотропного гормона та вільного тироксину має асоціацію з фіброзом печінки.
Посилання
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