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Fetal growth retardation: underlying endocrine mechanisms and postnatal consequences
Author(s) -
Gluckman PD,
Harding JE
Publication year - 1997
Publication title -
acta paediatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/j.1651-2227.1997.tb18349.x
Subject(s) - conceptus , medicine , fetus , endocrine system , pregnancy , growth retardation , gestation , fetal growth , endocrinology , fetal macrosomia , disease , physiology , gestational diabetes , biology , hormone , genetics
Considerable advance has been made in our understanding of the regulation of fetal growth and of the pathophysiology of intrauterine growth retardation. The dominant determinant of fetal growth is nutrient delivery to the conceptus, and the insulin‐like growth factors (IGFs) appear to play a central role in modulating the fetal growth response to the nutritional environment. It has also become clear that events early in gestation, or prior to conception, can be reflected in altered fetal growth and metabolism later in gestation. Intrauterine growth retardation (IUGR) may be due to identifiable genetic or toxic factors or to disordered nutrient delivery. The latter category of IUGR provides the greatest clinical concern with a high incidence of perinatal morbidity and mortality. More recently, epidemiological evidence supported by limited, but growing, experimental data suggest that the postnatal consequences of disturbed fetal growth may include metabolic disease (diabetes mellitus) and cardiovascular disease. This brief review discusses these advances with reference to data from our laboratory.