The physiology and pathophysiology of intrauterine growth retardation.
Insulin-like growth factor I (IGF-I) is the primary hormone influencing fetal growth in later gestation. The regulation of fetal IGF-I in utero is primarily influenced by placental glucose transfer, which regulates fetal insulin release. Furthermore, insulin has direct adipogenic effects on the fetus; fetal growth hormone (GH) may also have additional modes of action on fetal growth. Swallowed amniotic fluid contains IGF-I and may influence gastrointestinal maturation and fetal growth. Furthermore, both fetal and maternal IGF-I can influence placental metabolism. Experimentally, the maternal administration of GH and IGF-I can affect placental function and thus influence fetal growth; this may suggest therapeutic approaches to the treatment of intrauterine growth retardation (IUGR) in utero. Both experimental and clinical evidence support our hypothesis that IUGR is a multihormone relative resistance syndrome; relative resistance to insulin, IGF-I and GH can be demonstrated. Such resistance may be the basis of altered programming by which fetal growth retardation is associated with postnatal growth failure and a greater propensity to develop cardiovascular and metabolic disease in later life.
Gluckman
P D
PD
Research Centre for Developmental Medicine and Biology, University of Auckland, New Zealand.
Harding
J E
JE
D000818:Animals; D004351:Drug Resistance; D005314:Embryonic and Fetal Development / Q000502:physiology; D005260:Female; D005317:Fetal Growth Retardation / Q000503:physiopathology* / Q000628:therapy; D006801:Humans; D007334:Insulin-Like Growth Factor I; D010920:Placenta / Q000503:physiopathology; D011247:Pregnancy
D007334:Insulin-Like Growth Factor I