Developmental exposure to endocrine-disrupting chemicals programs for reproductive tract alterations and obesity later in life.
Many chemicals in the environment, especially those with estrogenic activity, are able to disrupt the programming of endocrine signaling pathways established during development; these chemicals are referred to as endocrine-disrupting chemicals. Altered programming can result in numerous adverse cons...
| Publicado en: | American Journal of Clinical Nutrition Vol. 94; no. 6S; pp. 1939S - 1940 |
|---|---|
| Autor principal: | |
| Formato: | review Journal Article |
| Publicado: |
Elsevier B.V.
Dec2011 Supplement
|
| Acceso en línea: | Ver este registro en EBSCOhost |
| fields | @attributes: recordID: 1 pdfLink: plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=108207305&site=ehost-live header: @attributes: shortDbName: ccm uiTerm: 108207305 longDbName: CINAHL Complete uiTag: AN controlInfo: bkinfo: dissinfo: jinfo: jid: 00029165 AJC jtl: American Journal of Clinical Nutrition issn: 00029165 maglogo: N pubinfo: dt: Dec2011 Supplement vid: 94 iid: 6S pid: 467 pub: Elsevier B.V. place: New York, New York artinfo: ui: 108207305 2011386378 10.3945/ajcn.110.001057 NLM22089436 108207305 ppf: 1939S ppct: 1 formats: tig: atl: Developmental exposure to endocrine-disrupting chemicals programs for reproductive tract alterations and obesity later in life. aug: au: Newbold, Retha R affil: National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC. sug: subj: Endocrine System Drug Effects Maternal Exposure Obesity Risk Factors Reproductive Health In Adulthood Adult Diethylstilbestrol Environmental Exposure Estrogens Female Fetus Infant Infant, Newborn Pregnancy Prenatal Exposure Delayed Effects Thalidomide Adult: 19-44 years Fetus, conception to birth Infant: 1-23 months Infant, Newborn: birth-1 month Female ab: Many chemicals in the environment, especially those with estrogenic activity, are able to disrupt the programming of endocrine signaling pathways established during development; these chemicals are referred to as endocrine-disrupting chemicals. Altered programming can result in numerous adverse consequences in estrogen-target tissues, some of which may not be apparent until later in life. For example, a wide variety of structural, functional, and cellular effects have been identified in reproductive tract tissues. In addition to well-documented reproductive changes, obesity and diabetes have joined the list of adverse effects that have been associated with developmental exposure to environmental estrogens and other endocrine-disrupting chemicals. Obesity is a significant public health problem reaching epidemic proportions worldwide. Experimental animal studies document an association of developmental exposure to environmental estrogens and obesity. For example, a murine model of perinatal exposure to diethylstilbestrol has proven useful in studying mechanisms involved in abnormal programming of differentiating estrogen-target tissues, including reproductive tract tissues and adipocytes. Other environmental estrogens, including the environmental contaminant bisphenol A, have also been linked to reproductive problems and obesity later in life. Epidemiology studies support similar findings in humans, as do studies of cells in culture. Together, these findings suggest new targets for abnormal programming by estrogenic chemicals and provide evidence supporting the scientific concept termed the developmental origins of adult disease. Furthermore, the association of environmental estrogens with obesity and diabetes expands the focus on these diseases from intervention or treatment to include prevention or avoidance of chemical modifiers, especially during critical windows of development. pubtype: Academic Journal doctype: review Journal Article ougenre: Article language: English refInfo: holdings: @attributes: islocal: N |
|---|