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Prenatal adverse environment increased offspring susceptibility to multiple chronic diseases and intrauterine programming mechanisms / 中国药理学与毒理学杂志
Chinese Journal of Pharmacology and Toxicology ; (6): 12-27, 2017.
Artigo em Chinês | WPRIM | ID: wpr-508130
ABSTRACT
Epidemiological studies reveal that prenatal adverse environment could cause lower birthweight in offspring and increase the susceptibility to multiple chronic diseases (e.g. metabolic and neuropsychiatric diseases etc.) after maturity. However, the underlying mechanism remains unclarified. The hypothalamic-pituitary-adrenal (HPA) axis is a key neuroendocrine axis playing pivotal roles in systemic stress responses before and after birth. It is also an important but vulnerable fetal targeting organ. Previous studies showed that many environmental insults during pregnancy, including external environment and maternal health condition, could affect fetal development in multi-ways via maternal-placental-fetal unit, which leads to the intrauterine programming alteration of HPA axis and the in?creased susceptibility to chronic diseases in adulthood. This article reviews the latest global advances in the etiology of increased susceptibility to adult diseases induced by compromised prenatal environ?ment and the associated intrauterine programming mechanisms by incorporating our recent research findings, and proposes that the fetal over-exposure to maternal glucocorticoids (GC) could bring about the intrauterine neuroendocrine metabolic programming alteration in offspringthe core is the program?ming of GC-insulin-like growth factor 1 axis in multiple organs, and the abnormal epigenetic modification is involved in this programming.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Pharmacology and Toxicology Ano de publicação: 2017 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Journal of Pharmacology and Toxicology Ano de publicação: 2017 Tipo de documento: Artigo