Genes & CellsGenes & CellsГены и КлеткиGenes and Cells2313-18292500-2562Human Stem Cells Institute69905810.17816/gc699058ReviewsНаучные обзорыMolecular mechanisms of stress-induced changes in metabolism and neuroregulationМолекулярные механизмы стресс-индуцированных изменений в метаболизме и нейрорегуляцииhttps://orcid.org/0000-0002-1688-40458046-1515KarabanovSergeyКарабановСергей Юрьевич
Russian Federation

Candidate of Veterinary Sciences, Researcher of Experimental clinic and research laboratory for bioactive substances of animal origin

кандидат ветеринарных наук, научный сотрудник экспериментальной Клиники-лаборатории биологически активных веществ животного происхождения

karabans89@gmail.comhttps://orcid.org/0000-0003-3573-930X4079-2394FedulovaLiliyaФедуловаЛилия Вячеславовна
Russian Federation

Doctor of Technical Sciences, Professor of RAS, Head of the Experimental clinic and research laboratory for bioactive substances of animal origin

доктор технических наук, профессор РАН, заведующий Клиникой-лабораторией биологически активных веществ животного происхождения

l.fedulova@fncps.ruhttps://orcid.org/0000-0002-4752-39398668-7770VasilevskayaEkaterinaВасилевскаяЕкатерина Романовна
Russian Federation

Candidate of Technical Sciences, Researcher of Experimental clinic and research laboratory for bioactive substances of animal origin

кандидат технических наук, научный сотрудник экспериментальной Клиники-лаборатории биологически активных веществ животного происхождения

e.vasilevskaya@fncps.ruhttps://orcid.org/0000-0001-6934-73427063-6360KibitkinaAnastasiyaКибиткинаАнастасия Анатольевна
Russian Federation

Research assistant of Experimental clinic and research laboratory for bioactive substances of animal origin

младший научный сотрудник экспериментальной Клиники-лаборатории биологически активных веществ животного происхождения

a.kibitkina@fncps.ruV.M. Gorbatov Federal Research Center for Food Systems«Федеральный научный центр пищевых систем им. В.М. Горбатова» РАН300420262122212202503042026Copyright ©; , Eco-VectorCopyright ©; , Эко-ВекторEco-VectorЭко-Векторhttps://eco-vector.com/for_authors.php#07https://genescells.ru/2313-1829/article/view/699058

Chronic stress elicits a broad spectrum of molecular alterations affecting nearly all levels of metabolic regulation. The primary initiating mechanism involves activation of the hypothalamic-pituitary-adrenal axis by a stressor, resulting in sustained glucocorticoid release. This, in turn, drives a systemic reprogramming of energy metabolism, fosters low-grade chronic inflammation and oxidative stress, and instigates persistent epigenetic modifications. These pathological processes are characterized by a severe imbalance in pro- and antioxidant systems, significant shifts in adipose and muscle tissue metabolism including induced lipolysis and gluconeogenesis and impaired leptin and insulin signalling. Consequently, they elevate the risk for abdominal obesity, metabolic syndrome, type 2 diabetes, and related comorbidities. Of particular significance are stress-induced epigenetic changes, such as DNA methylation, which can serve to entrench a pathological metabolic phenotype over the long term. This review, therefore, aims to systematise and analyses current knowledge on the complex molecular mechanisms underpinning stress-induced dysfunction in metabolism and neuroendocrine regulation in mammals.

Хронический стресс способен вызывать широкий спектр молекулярных изменений, которые затрагивают практически все уровни регуляции обмена веществ. Ключевым пусковым механизмом является активация гипоталамо-гипофизарно-надпочечниковой оси в ответ на стрессовый стимул и последующий устойчивый выброс глюкокортикоидных гормонов, что приводит к системной перестройке энергетического обмена веществ, развитию хронического воспаления низкой степени активности, окислительного стресса, а также к устойчивым эпигенетическим модификациям. Данные процессы сопровождаются глубоким нарушением баланса между про- и антиоксидантными системами организма, значительными изменениями метаболизма жировой и мышечной тканей, включая индукцию липолиза и глюконеогенеза, а также дисфункцией лептиновой и инсулиновой сигнализации. В результате чего повышается риск развития абдоминального ожирения, метаболического синдрома, сахарного диабета 2-го типа, а также других сопутствующих заболеваний. Особую роль играют индуцированные стрессом эпигенетические изменения, такие как метилирование ДНК, способные закрепить патологический метаболический фенотип на длительный срок. Таким образом, целью данного обзора является систематизация и анализ современных представлений о комплексных молекулярных механизмах, лежащих в основе стресс-индуцированных изменений метаболизма и нейроэндокринной регуляции у млекопитающих.

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