Fetal programming of the growth hormone-insulin-like growth factor axis.
Epidemiological studies have shown that small body size at birth and during infancy is associated with increased rates of chronic diseases in adulthood, including cardiovascular disease and osteoporosis. Fetal programming of the growth hormone-insulin-like growth factor (GH-IGF) axis has been proposed as a potential candidate mechanism to explain the link between low birth weight and adult disease. The IGFs and IGF-binding proteins are nutritionally regulated in the fetus and fetal growth retardation leads to abnormalities in the GH-IGF axis. There are also abnormalities in the GH-IGF axis in many of the adult diseases that are associated with low birth weight, including cardiovascular disease and osteoporosis. Finally, there are data from both animals and humans suggesting that programming of the GH-IGF axis might exist.
D000328:Adult; D000818:Animals; D001724:Birth Weight; D002318:Cardiovascular Diseases / Q000209:etiology; D005260:Female; D005317:Fetal Growth Retardation / Q000150:complications; D013006:Growth Hormone / Q000502:physiology; D019382:Human Growth Hormone / Q000502:physiology*; D006801:Humans; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D018969:Insulin-Like Growth Factor Binding Proteins / Q000502:physiology; D009747:Nutritional Physiological Phenomena; D010024:Osteoporosis / Q000209:etiology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D013002:Somatomedins / Q000502:physiology*
D018969:Insulin-Like Growth Factor Binding Proteins; D013002:Somatomedins; D019382:Human Growth Hormone; D013006:Growth Hormone