title: Endocrine regulation in asymmetric intrauterine fetal growth retardation.
abstract: OBJECTIVE
  The ponderal index (PI) is a widely accepted measure of disproportionate growth or asymmetrical growth retardation by pediatricians worldwide. Identification of disproportionately grown small for gestational age (SGA) neonates by using the ponderal index as a measure of the nutritional status at birth, is important because they constitute a high-risk group among SGA neonates. Poor nutritional status of the mother could have a direct effect on the organs of the developing fetus and/or affect the endocrine milieu in the maternal feto-placental unit resulting in an increased incidence of intrauterine growth-retarded (IUGR)/SGA births. IUGR is a significant risk factor for adult disease. In this study, we have investigated the endocrine adaptation by the fetus to overcome the growth disadvantage caused due to poor nutritional status of the mother.
  
  
  METHODS
  We examined the quantitative variations in hormonal and growth factor profiles in paired maternal and cord blood samples obtained from mothers and their neonates who were classified based on their growth status into SGA and appropriate for gestational age (AGA).
  
  
  RESULTS
  (1) A total of 24.7% neonates had a PI < 2, indicating a high incidence of asymmetric IUGR in the population studied. (2) Anthropometric parameters measured in the mothers indicate that the mothers giving birth to neonates with a PI < 2 had poor nutritional status, both prior to and during pregnancy. (3) We observed increased levels of placental lactogen and prolactin and decreased levels of insulin in the cord blood of neonates with PI < 2, while lower levels of insulin-like growth factor 1 (IGF-1) and higher levels of epidermal growth factor (EGF) were observed in their mothers.
  
  
  CONCLUSIONS
  Poor maternal nutritional status results in fetal adaptation to a growth restricted environment via the modulation of the pituitary-thyroid axis thereby altering the endocrine milieu, thus affecting fetal growth.
authors.affiliation: Department of Endocrinology & Metabolism, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India, 110029. smahajan@buffalo.edu
authors.forename: S D
authors.initials: SD
authors.lastname: Mahajan
authors.forename: R
authors.initials: R
authors.lastname: Aalinkeel
authors.forename: S
authors.initials: S
authors.lastname: Singh
authors.forename: P
authors.initials: P
authors.lastname: Shah
authors.forename: N
authors.initials: N
authors.lastname: Gupta
authors.forename: N
authors.initials: N
authors.lastname: Kochupillai
mesh_terms: D000328:Adult; D005260:Female; D005312:Fetal Blood / Q000378:metabolism*; D005317:Fetal Growth Retardation / Q000097:blood* / Q000378:metabolism*; D006801:Humans; D007231:Infant, Newborn; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood*; D039382:Maternal Nutritional Physiological Phenomena; D011247:Pregnancy; D013963:Thyroid Hormones / Q000097:blood*
chemical_list: D036341:Intercellular Signaling Peptides and Proteins; D013963:Thyroid Hormones