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EPIGENETIC PROGRAMMING AND FETAL GROWTH RESTRICTIONS

Published online by Cambridge University Press:  03 June 2010

JOSE CARLOS FERREIRA
Affiliation:
Program in Genetics and Genome Biology, Hospital for Sick Children Research Institute, Toronto, ON, Canada University of Toronto, Toronto, ON, Canada
SANAA CHOUFANI
Affiliation:
Program in Genetics and Genome Biology, Hospital for Sick Children Research Institute, Toronto, ON, Canada
JOHN KINGDOM
Affiliation:
Maternal–Fetal Medicine Division, Department of Obstetrics and Gynecology, Mount Sinai Hospital, Toronto, ON, Canada University of Toronto, Toronto, ON, Canada
ROSANNA WEKSBERG*
Affiliation:
Program in Genetics and Genome Biology, Hospital for Sick Children Research Institute, Toronto, ON, Canada Division of Clinical and Metabolic Genetics, Hospital for Sick Children, Toronto, ON, Canada University of Toronto, Toronto, ON, Canada
*
Rosanna Weksberg, Hospital for Sick Children, Division of Clinical and Metabolic Genetics, 525 University Avenue, Suite 940, 9th Floor, Toronto, Ontario M5G 1X8Canada. Email address: [email protected]

Extract

Normal fetal growth and development depends on multiple molecular mechanisms that coordinate both placental and fetal development. Efforts to better understand fetal/placental growth dysregulation and fetal growth restriction (FGR) are now being driven by several findings that highlight the longterm impact of FGR on susceptibility to disease. The association of poor fetal growth to perinatal medical complications is well accepted but more recent data also show that FGR is linked to common, serious adult health problems. Several large-scale human epidemiological studies from diverse countries have shown that conditions such as coronary heart disease, hypertension, stroke, type 2 diabetes mellitus, adiposity, insulin resistance and osteoporosis are more prevalent in individuals with a history of low birthweight.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2010

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