Mericq Veronica
Institute of Maternal and Child Research, Faculty of Medicine, University of Chile, Santiago.
Pediatr Endocrinol Rev. 2006 Sep;4(1):3-14.
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.
出生时体型小长期以来一直被认为是增加新生儿发病率和死亡率的一个因素。在过去十年中，生命早期生长减缓也与多种内分泌功能障碍密切相关。其中最重要的改变包括胰岛素不敏感、性腺和生长激素轴异常以及肾上腺早现。这些改变与2型糖尿病和冠心病患病率不断上升、性腺和生殖器异常、生长激素抵抗、生长发育迟缓以及青春期提前有关。通常提出的解释这些长期改变发展的假说是节俭表型，这是对子宫内营养不良及其改变的一种适应性反应；称为“胎儿起源”，并更新为“发育起源”，其中包括婴儿期和儿童期生长模式的额外影响。本文综述了参与胎儿和婴儿编程并导致出生后内分泌功能障碍的因素。
