Fetal origins of cardiovascular disease.
Several epidemiologic studies have shown that intrauterine growth retardation is a risk factor for the development of cardiovascular disease in later life. In this review, we discuss these epidemiologic studies and animal models that have been developed to investigate the pathophysiology of this phenomenon. We discuss data suggesting that intrauterine growth retardation leads to fetal exposure to maternal glucocorticoids. In addition, we present other data showing that fetal exposure of glucocorticoids during specific times of fetal development results in focal and segmental glomerulosclerosis, a reduced number of nephrons, hypertension, and diabetes. These studies suggest that at critical times during fetal development fetal injury programs the development of cardiovascular disease and diabetes in later life.
Baum
Michel
M
Department of Pediatrics, The University of Texas Southwestern Medical Center, Dallas, Texas 75235-9063, USA. Michel.Baum@UTSouthwestern.edu
Ortiz
Luis
L
Quan
Albert
A
D000818:Animals; D002318:Cardiovascular Diseases / Q000196:embryology* / Q000453:epidemiology / Q000503:physiopathology; D003907:Dexamethasone / Q000009:adverse effects; D003920:Diabetes Mellitus / Q000196:embryology / Q000453:epidemiology / Q000503:physiopathology; D004044:Dietary Proteins / Q000008:administration & dosage; D005314:Embryonic and Fetal Development; D005260:Female; D005317:Fetal Growth Retardation / Q000453:epidemiology; D005938:Glucocorticoids / Q000009:adverse effects; D006801:Humans; D023421:Models, Animal; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012307:Risk Factors
D004044:Dietary Proteins; D005938:Glucocorticoids; D003907:Dexamethasone