Maternal adaptations to store and transfer nutrients to the fetus are discussed in Chapter 4 and summarized here. Three major maternal storage depots are the liver, muscle, and adipose tissue. These maternal depots and the storage hormone insulin are intimately involved in the metabolism of the nutrients absorbed from the gut. Maternal insulin secretion is sustained by increased serum levels of glucose and amino acids. he net efect is maternal storage of glucose as glycogen primarily in liver and muscle, retention of some amino acids as protein, and storage of the excess as fat. Storage of maternal fat peaks in the second trimester and then declines as fetal energy demands rise in the third trimester (Pipe, 1979). Interestingly, the placenta appears to act as a nutrient sensor, altering transport based on the maternal supply and environmental stimuli (Fowden, 2006; Jansson, 2006b).
During times of fasting, glucose is released from glycogen, but maternal glycogen stores cannot provide an adequate amount of glucose to meet requirements for maternal energy and fetal growth. Augmentation is provided by cleavage of triacylglycerols, stored in adipose tissue, which result in free fatty acids and activation of lipolysis.
Although dependent on the mother for nutrition, the fetus also actively participates in providing its own nutrition. At midpregnancy, fetal glucose concentration is independent of maternallevels and may exceed them (Bozzetti, 1988). Glucose is the major nutrient for fetal growth and energy. Logically, mechanisms exist during pregnancy to minimize maternal glucose use so that the limited maternal supply is available to the fetus. Human placental lactogen (hPL), a hormone normally abundant in the mother bur not the fetus, has an insulin antagonist efect. It blocks the peripheral uptake and use of glucose, while promoting mobilization and use of free fatty acids by maternal tissues (Chap. 5, p. 100). his hormone is also diabetogenic as discussed in Chapter 57 (p. 1107).
he transfer of D-glucose across cell membranes is accomplished by a carrier-mediated, stereospecific, nonconcentrating process of facilitated difusion. There are 14 glucose transport proteins (GLUTs) encoded by the SLC2A gene family and characterized by tissue-speciic distribution (Leonce, 2006). GLUT-1 and GLUT -3 primarily facilitate glucose uptake by the placenta and are located in the plasma membrane of the syncytiotrophoblast microvilli (Acosta, 2015). DNA methylation regulates expression of placental GLUT genes, with epigenetic modiication across gestation (Novakovic, 2013). It increases as pregnancy advances and is induced by almost all growth factors (Frolova, 2011). GLUT-3 expression is up regulated with fetal growth restriction a anzen, 2013).
Lactate is a product of glucose metabolism and transported across the placenta also by facilitated difusion. By way of cotransport with hydrogen ions, lactate is probably transported as lactic acid.