Effect of maternal malnutrition and anemia on the endocrine regulation of fetal growth.
Fetal growth retardation is a result of a complex pathology caused by multiple factors of fetal, placental, and maternal origin. Hormones and growth factors released as a result of maternal-fetal physiological interactions play an importance role in fetal well being and fetal outcome. Intrauterine Growth Retardation (IUGR) is associated with significant perinatal and childhood morbidity. It is estimated that 13.7 million infants are born annually with IUGR, comprising 11% of all births in developing countries. Both maternal malnutrition and anemia are associated with various degrees of fetal growth retardation. The relationship between decreasing birth weight percentiles and increasing fetal morbidity and mortality has been demonstrated by several investigators and epidemiological studies suggest that IUGR is a significant risk factor for the subsequent development of chronic hypertension, ischemic heart disease, diabetes, and obstructive lung disease in adult life (Barker's Hypothesis). Maternal anemia and/or malnutrition are recognized to be the most frequent cause of IUGR and SGA birth in developing countries like India. In order to investigate adaptive mechanisms by the fetus to overcome the growth disadvantage caused due to maternal nutritional limitations, we examined the quantitative variations in hormonal and growth factor profiles in paired cord blood and maternal samples obtained from neonates born to malnourished and/or anemic mothers. The results of our study show that: 1) The percentage of small for gestational age (SGA) neonates born to malnourished and anemic mothers was significantly higher than those born to mothers who were either malnourished or anemic; 2) Significantly higher levels of GH, PRL, HPL and IGF-1 were observed in the cord blood of neonates born to malnourished and anemic mothers indicative of an adaptive response on part of the fetus to over come an in-utero growth disadvantage; 3) The anoxemia-related fetal perturbations may have unique features that make them distinct from nutrient deficiency-related IUGR. Thus, these novel observations are relevant to the context of the ongoing scientific debate on Barker's hypothesis.
Department of Endocrinology and Metabolism, All India Institute of Medical Sciences, New Delhi, India. smahajan@buffalo.edu
Supriya D
SD
Mahajan
S
S
Singh
P
P
Shah
N
N
Gupta
N
N
Kochupillai
D000328:Adult; D000740:Anemia / Q000150:complications* / Q000503:physiopathology*; D004702:Endocrine Glands / Q000503:physiopathology*; D005260:Female; D005312:Fetal Blood; D047109:Fetal Development; D005317:Fetal Growth Retardation / Q000209:etiology*; D019382:Human Growth Hormone / Q000097:blood; D006801:Humans; D007231:Infant, Newborn; D007236:Infant, Small for Gestational Age; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D044342:Malnutrition / Q000150:complications* / Q000503:physiopathology*; D010928:Placental Lactogen / Q000097:blood; D011247:Pregnancy; D011248:Pregnancy Complications; D011388:Prolactin / Q000097:blood
D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D011388:Prolactin; D010928:Placental Lactogen