Biological features of placental programming

Abstract

The placenta is a key organ in programming the fetus for later disease. This review outlines eight of many structural and physiological features of the placenta which are associated with adult onset chronic disease. 1) Placental efficiency relates the placental mass to the fetal mass. Ratios at the extremes are related to cardiovascular disease risk later in life. 2) Placental shape predicts a large number of disease outcomes in adults but the regulators of placental shape are not known. 3) Non-human primate studies suggest that at about mid-gestation, the placenta becomes less plastic and less able to compensate for pathological stresses. 4) Recent studies suggest that lipids have an important role in regulating placental metabolism and thus the future health of offspring. 5) Placental inflammation affects nutrient transport to the fetus and programs for later disease. 6) Placental insufficiency leads to inadequate fetal growth and elevated risks for later life disease. 7) Maternal height, fat and muscle mass are important in combination with placental size and shape in predicting adult disease. 8) The placenta makes a host of hormones that influence fetal growth and are related to offspring disease. Unfortunately, our knowledge of placental growth and function lags far behind that of other organs. An investment in understanding placental growth and function will yield enormous benefits to human health because it is a key player in the origins of the most expensive and deadly chronic diseases that humans face.

Prenatal and perinatal history in Kabuki Syndrome

“…Abnormally low levels of hCG and/or uE3 in KS pregnancies may suggest dysregulation of placental metabolism, as these substances are produced wholly or partially by the placenta. Additionally, the reduced placental weight in four term KS pregnancies also suggests impaired placental growth and function (Thornburg et al, ). Taken together, these data suggest that placental health may relate to the clinical phenotype of KS.…”

Congener-Specific Mother–Fetus Distribution, Placental Retention, and Transport of C10–13 and C14–17 Chlorinated Paraffins in Pregnant Women

“…This variation may be attributed to the differences in the pathology and physiology of the individual placentas, which might play an important role in placental differences. 58 For instance, the differences in placenta size, fat content, 59 and inflammation were reported to be important factors related to the transplacental transfer. 60 For MCCP congener groups, the R CM /R PM values decreased with increasing carbon chain length with significant differences (Table S9) (Figure 4b).…”

Normalizing adiponectin levels in obese pregnant mice prevents adverse metabolic outcomes in offspring

“…The mechanisms linking the adverse metabolic environment in maternal obesity to programming of the fetus for later disease remain poorly understood, constituting a major roadblock for the development of specific intervention strategies. One key mechanism by which maternal nutrition and metabolism influence fetal development and growth is through modulating the function of the placenta, which serves as a nutrient sensor regulating fetal growth and programming the fetus for the development of chronic disease in childhood and later in life (12)(13)(14). In mothers who are overweight or obese, there is an abundance of nutrients available, which likely results in an increased flux of nutrients across the placenta (13).…”