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PMID: 12367816 Published · ppublish English Journal Article Review

Fetal programming of coronary heart disease.

Trends in endocrinology and metabolism: TEM ·Vol. 13 ·No. 9 ·2002-11-00 ·Pages 364-8

Barker DJ

Abstract

People who develop coronary heart disease grow differently from other people both in utero and during childhood. Slow growth during fetal life and infancy is followed by accelerated weight gain in childhood. Two disorders that predispose to coronary heart disease, type 2 diabetes and hypertension, are preceded by similar paths of growth. Mechanisms underlying this are thought to include the development of insulin resistance in utero, reduced numbers of nephrons associated with small body size at birth and altered programming of the micro-architecture and function of the liver. Slow fetal growth might also heighten the body's stress responses and increase vulnerability to poor living conditions in later life. Coronary heart disease appears to be a developmental disorder that originates through two widespread biological phenomena, developmental plasticity and compensatory growth.

MeSH Terms
Birth Weight Body Mass Index Child Coronary Disease/epidemiology,etiology Diabetes Mellitus, Type 2/epidemiology Embryonic and Fetal Development Female Fetal Growth Retardation/complications,physiopathology Humans Hypertension/epidemiology Infant Infant, Low Birth Weight Infant, Newborn Male Poverty Pregnancy Prenatal Exposure Delayed Effects Weight Gain
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Barker David J P
MRC Environmental Epidemiology Unit, University of Southampton, Southampton General Hospital, SO16 6YD, Southampton, UK. djpb@mrc.soton.ac.uk
Article Info
Journal
Trends in endocrinology and metabolism: TEM
Abbr.
Trends Endocrinol Metab
ISSN
1043-2760
Published
2002-11-00
Pages
364-8
Language
English
Region
United States
NLM ID
9001516
Subset
IM
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