Is fetal XXXX in adequately controlled @entity6 @entity1 the result of a placental defect?--a hypothesis.

@entity1 @entity6 @entity2690 @entity1365 @entity22408 @entity3190 @entity8455 @entity4854 @entity413
@entity8455 may occur even in adequately controlled @entity6 mothers. This may reflect the problem of using maternal glycemia as an indicator of fetal glycemia, because the placenta interposed between both compartments has its own @entity413 metabolism. Here, we propose a model by which the placenta protects the fetus at moderate levels of maternal @entity4854 . One characteristic feature of the @entity1 placenta in @entity6 is the increased deposition of glycogen. Neither @entity4854 nor @entity3190 increase the glycogen content in the trophoblast. Since the glycogen increments in @entity6 are predominantly located around fetoplacental vessels, it is tempting to assume a fetal origin of @entity413 making up the glycogen deposits. In fact, @entity413 can be transported back from the fetus into the placenta and this reflux is increased in @entity6 . Therefore, in conditions of fetal @entity413 levels exceeding the demand for sustaining fetal growth and metabolism, @entity413 can be stored in the liver and other fetal tissues. Once these stores are saturated, @entity413 is extracted from the fetal circulation by the @entity413 transporters @entity1365 and @entity22408 on cells surrounding the fetoplacental vasculature and stored therein, again in the form of glycogen. These processes might be under the control of fetal @entity2690 , because @entity2690 injected into the fetal circulation increases placental glycogen stores. @entity8455 would then occur only when fetal @entity4854 exceeds the placental capacity to store excess fetal @entity413 . Thus, the placental failure to protect the fetus would cause the 'unexplained' phenotypic changes occasionally found in fetuses born to well-controlled @entity6 @entity1 .
