Presented work aimed at preparing literature review that could describe the contribution of Glucocorticoids (GC) and stress to pathogeny of diabetes mellitus and related disorders: Metabolic syndrome and obesity. This review includes the following topics: Effects of GC and stress on glucose metabolism, the role of GC and stress in pathogenetic mechanisms of clinical and experimental diabetes, the importance of catecholamines and other stress hormones in mechanisms of hypo and hyperglycemia, interactions of GC with high-fat diet, contribution of GC to comorbidity of metabolic and neuropsychiatric disorders, metabolic consequences of prolonged GC treatment, the role of GC in programming/imprinting phenomena, the importance of stress proteins in pathogeny of metabolic disorders and modes of counteracting stress and GC in diabetes and related diseases. The conclusion is made about the necessity of more detailed evaluation of the effects of hormones having antistress properties, as applied to metabolic disorders.
The mini-review is presented, including both early and recent investigations, on growth inhibition induced by glucocorticoids. These data are discussed, together with current concepts of growth regulation, involving tissue streaming and some evidence, as referred to stem and progenitor cells. It is outlined that future studies on cultures of induced pluripotent stem cells may open translational perspective for such area, important for endocrine aspects of pediatrics and perinatology
The review is presented about contribution of glucocorticoids and stress to programming / imprinting phenomena. After their definition, possible mechanisms of such phenomena are described, including the role of glucocorticoids in ontopathogenic model, as well as the ways of diminishing adverse effects of these hormones. It is outlined that health professionals should participate in educational campaigns for decreasing adverse actions of stress and glucocorticoids, especially in perinatal period. Moreover, DOHaD concept should be introduced to the contents of university courses in biomedical sciences.
Введение и методология Концепция "онтогенетической природы здоровья и болезней" (Developmental Origins of Health and Disease, DOHaD) получила развитие за последние 25-30 лет, начиная с основополагающих работ английского эпидемиолога David J.P. Barker и его коллег в конце прошлого века [1]. Один из главных аспектов такой концепции-это явления импринтинга/программирования, которые характеризуются отдаленными последствиями влияния некоторых факторов в критических периодах развития, включая и перинатальный период, с увеличением риска кардиометаболических расстройств и других болезней уже во взрослом состоянии и даже в старости [2]. На экспериментальных моделях лабораторных жи-вотных было показано, что глюкокортикоиды (ГК) играют существенную роль в механизмах явлений импринтинга/программирования [3]. В наших предыдущих работах мы также поддержали важность этого аспекта [4, 5]. Однако в регуляции постнатального развития и роста ГК взаимодействуют со многими другими биорегуляторами, особенно тиреоидными гормонами (ТГ): L-тироксином (T 4) и L-трийодотиронином (T 3) [6], учитывая то, что рецепторы как ГК, так и ТГ являются внутриклеточными факторами, регулирующими транскрипцию генов, зависящими от связывания соответствующих лигандов и относящимися к одному и тому же семейству рецепторных белков [7, 8].
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