Department of Obstetrics and Gynecology, University of Medicine and Dentistry of New Jersey, Stratford, NJ 08084
The interest of Jessica Long (1) in our paper (2) is appreciated. In her letter, Long raised a question about whether "variations of glucose levels across ethnic boundaries are a result or cause of low birth weights" (1, p. 1229). Lower glucose levels are found not only among pregnant African Americans but also in African-Americans girls and women who are not pregnant and therefore do not have a placenta (3). This implies that the lower glucose in this ethnic group probably is not consequent to placental growth hormone.
Long hypothesized that it is placental growth hormone that gives rise to ethnic differences in restricted fetal growth. It is well known that maternal-fetal nutrient transport is essential for fetal growth; glucose is one of the most important of these nutrients. Maternal glucose levels are regulated by a number of hormones, especially insulin, insulin growth factor 1, and insulin antagonists such as the placental hormones that include placental growth hormone. This hormone is produced by the placenta and substitutes for pituitary human growth hormone during pregnancy. As far as we are aware, whether or not African Americans or any other ethnic group has different levels of placental growth hormone has never been studied. Placental growth hormone is thought to be regulated by maternal glucose levels via the synctrophoblast, which expresses the glucose transporter Glut1 (4). Placental growth hormone is not detectable in the fetal circulation, and its effect on the fetus seems to be an indirect one (4). Placental growth hormone stimulates gluconeogenesis and lipolysis to increase nutrient availability to the fetoplacental unit (4). Placental growth hormone is lower in growth-restricted fetuses because their placentas are smaller and because of other reasons (placental pathology, abnormal regulation of placental growth hormone synthesis) (4). Thus, it seems that, while placental growth hormone may have the potential to be one of a number of markers for in utero growth retardation, it seems an unlikely candidate to "explain" why African-American women have smaller babies.
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