НАРУШЕНИЕ ВЫРАБОТКИ НЕЙРОМЕДИАТОРОВ В ПАТОФИЗИОЛОГИИ ДИАБЕТИЧЕСКОЙ ЭНЦЕФАЛОПАТИИ (ОБЗОР ЛИТЕРАТУРЫ)

Юрий Витальевич Быков

doi:10.56871/RBR.2024.68.38.007

Юрий Витальевич Быков Ставропольский государственный медицинский университет. 355017, г. Ставрополь, ул. Мира, 310 https://orcid.org/0000-0002-9376-7854

DOI: https://doi.org/10.56871/RBR.2024.68.38.007

Ключевые слова: диабетическая энцефалопатия, гамма-оксимасляная кислота, глютамат, дофамин, ацетилхолин, серотонин

Аннотация

В обзоре обобщены данные о нарушениях выработки нейромедиаторов в патофизиологии диабетической энцефалопатии (ДЭ). Рассмотрены основные нейромедиаторы, которые могут быть задействованы в патогенезе ДЭ: гамма-оксимасляная кислота, глутамат, дофамин, ацетилхолин, серотонин. Представлены основные патофизиологические механизмы, которые могут быть задействованы в формировании и прогрессировании ДЭ по ходу течения сахарного диабета (СД) при нарушении в выработке основных нейромедиаторов. Обоснована гиперреактивность ГАМК-эргической, глутаматергической (далее — глютамат) и дофаминергической систем, а также гипоактивность холинергической и серотонинергической систем
в патофизиологии ДЭ. Приведены данные доклинических и клинических исследований, доказывающие нарушение выработки нейромедиаторов при СД 1-го и 2-го типов, которые могут служить ранними маркерами в диагностике ДЭ.

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