Fetal bowel contents consist of various products of secretion, such as glycerophospholipids from the lung, desquamated fetal cells, lanugo, scalp hair, and vernix. It also contains undigested debris from swallowed amnionic fluid. The dark greenish-black color forms from bile pigments, especially biliverdin. Meconium can pass from normal bowel peristalsis in the mature fetus or from vagal stimulation. It can also pass when hypoxia stimulates arginine vasopressin (A VP) release from the fetal pituitary gland. A VP stimulates colonic smooth muscle to contract, resulting in intraamnionic defecation (deVane, 1982; Rosenfeld, 1985). Meconium is toxic to the respiratory system, and its inhalation can result in meconium aspiration syndrome (Chap. 33, p. 620).
The hepatic diverticulum is an outgrowth of the endodermal lining of the foregut. Epithelial liver cords and primordial cells diferentiate into hepatic parenchyma. Serum liver enzyme levels increase with gestational age. Still, the fetal liver has a gestational-age-related diminished capacity for converting free unconjugated bilirubin to conjugated bilirubin (Morioka, 2015). Because of hepatic immaturity, the preterm newborn is at particular risk for hyperbilirubinemia (Chap. 33, p. 626). And because the life span of normal fetal macrocytic erythrocytes is shorter than that of the adult, relatively more unconjugated bilirubin is produced. As just noted, the fetal liver conjugates only a small fraction, and this is excreted into the intestine and ultimately oxidized to biliverdin. Most of the unconjugated bilirubin is excreted into the amnionic luid after 12 weeks and transferred across the placenta (Bashore, 1969).
Importantly, placental bilirubin transfer is bidirectional. Thus, a woman with severe hemolysis from any cause has excess unconjugated bilirubin that readily passes to the fetus and then into the amnionic fluid. Conversely, conjugated bilirubin is not exchanged to any significant degree between mother and fetus.
Most fetal cholesterol derives from hepatic synthesis, which satisies the large demand for low-density lipoprotein (LDL) cholesterol by the fetal adrenal glands. Hepatic glycogen is present in low concentration during the second trimester, but near term, levels rise rapidly and markedly to reach concentrations that are two-to threefold higher than those in the adult liver. After birth, glycogen content falls precipitously.
from the endoderm of the foregut. Gene regulation of its development was recently reviewed Qennings, 2015). Insu lin-containing granules can be identiied by 9 to 10 weeks, and insulin is detectable in fetal plasma at 12 weeks (Adam, 1969). The pancreas responds to hyperglycemia by secreting insulin (Obenshain, 1970). Glucagon has been identified in the fetal pancreas at 8 weeks. Although hypoglycemia does not cause an increase in fetal glucagon levels, similar stimuli do so by 12 hours after birth (Chez, 1975). At the same time, however, fetal pancreatic a cells do respond to L-dopa infu sions (Epstein, 1977). Therefore, unresponsiveness to hypo glycemia is likely the consequence of failed glucagon release rather than inadequate production. This is consistent with developmental expression of pancreatic genes in the fetus (Mally, 1994).