Novel mechanism causing restricted fetal growth: does maternal homocysteine impair placental amino acid transport?

Abstract

Determining the physiological mechanisms regulating fetal growth is critical for a better understanding of normal fetal development and the pathophysiology of abnormal fetal growth. Intrauterine growth restriction (IUGR) occurs when the fetus fails to reach its genetically determined growth potential. IUGR babies have a markedly increased perinatal morbidity, higher incidence of neuro-developmental impairment and increased risk of adult disease such as diabetes and cardiovascular disease (Hales et al. 1991; Barker et al. 1993). The primary determinant of fetal growth is the availability of nutrients, which is directly dependent on the transport functions of the placenta. The aetiology of human IUGR is complex, but a common theme in many cases of IUGR is an impaired placental nutrient transport. In a recent issue of The Journal of Physiology, Tsitsiou et al. (2009) reported experimental evidence for a novel mechanism by which placental amino acid transport may be reduced by elevated maternal homocysteine levels leading to IUGR.