Low birth weight and endocrine dysfunction in postnatal life.
Small size at birth has long been recognized as a factor increasing neonatal morbidity and mortality. During the last decade, reduced growth in early life has also been strongly linked with a number of endocrine dysfunctions. Included among the most important alterations are insulin insensitivity, gonadal and somatotropic axis abnormalities and premature adrenarche. These have been associated with an escalating prevalence of T2DM and CHD abnormal gonads and genitalia, growth hormone resistance and decreased growth as well as early puberty. The usual hypothesis proposed to explain the development of these long term alterations relates to the thrifty phenotype as an adaptive response to in utero malnutrition and modifications thereof; called "Fetal Origins" and updated to "Developmental Origins" which include the additional contributions of the patterns of growth in infancy and childhood. In this paper the factors that participate in the programming of the fetus and infants that lead to endocrine dysfunction in postnatal life is reviewed.
Mericq
Veronica
V
Institute of Maternal and Child Research, Faculty of Medicine, University of Chile, Santiago. vmericq@med.uchile.cl
D000311:Adrenal Glands / Q000503:physiopathology; D000818:Animals; D000831:Animals, Newborn; D004700:Endocrine System Diseases / Q000209:etiology* / Q000503:physiopathology; D047109:Fetal Development / Q000502:physiology*; D042341:Gonadal Hormones / Q000502:physiology; D013006:Growth Hormone / Q000502:physiology; D006801:Humans; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D007236:Infant, Small for Gestational Age; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000235:genetics; D008954:Models, Biological; D015398:Signal Transduction
D042341:Gonadal Hormones; D007328:Insulin; D013006:Growth Hormone