In Utero Fetal Programming and Its Impact on Health in Adulthood
Adverse events during intrauterine life may program organ growth and favor disease later in life. This is the usually called 'Barker's hypothesis'. Increasing evidence suggests that conditions like vascular disease, hypertension, metabolic syndrome, and type 2 diabetes mellitus are pr...
- Autores:
- Tipo de recurso:
- Fecha de publicación:
- 2012
- Institución:
- Universidad del Rosario
- Repositorio:
- Repositorio EdocUR - U. Rosario
- Idioma:
- eng
- OAI Identifier:
- oai:repository.urosario.edu.co:10336/23925
- Acceso en línea:
- https://doi.org/10.1016/j.endonu.2012.02.002
https://repository.urosario.edu.co/handle/10336/23925
- Palabra clave:
- Adulthood
Cell function
Diseases
Endothelium cell
Fetus development
Health status
Human
Insulin resistance
Mitochondrion
Non communicable disease
Oxidative stress
Prevalence
Short survey
Adult
Birth weight
Blood vessels
Chronic disease
Fetal development
Humans
Insulin resistance
Metabolism
Mitochondria
Coronary heart disease
Fetal growth retardation
Insulin resistance
Maternal nutrition
- Rights
- License
- Abierto (Texto Completo)
Summary: | Adverse events during intrauterine life may program organ growth and favor disease later in life. This is the usually called 'Barker's hypothesis'. Increasing evidence suggests that conditions like vascular disease, hypertension, metabolic syndrome, and type 2 diabetes mellitus are programmed during the early stages of fetal development and become manifest in late stages of life, when there is an added impact of lifestyle and other conventional acquired environmental risk factors that interact with genetic factors. The aim of this review was to provide additional, updated evidence to support the association between intrauterine fetal health and increased prevalence of chronic non-communicable diseases in adulthood. Various potential cellular and molecular mechanisms proposed to be related to the above hypothesis are discussed, including endothelial function, oxidative stress, insulin resistance, and mitochondrial function. © 2011 SEEN. |
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