Editing Endocrine system (section)

===Pancreas===
The human fetal [[pancreas]] begins to develop by the fourth week of gestation. Five weeks later, the pancreatic [[Alpha cell|alpha]] and [[beta cell]]s have begun to emerge. Reaching eight to ten weeks into development, the pancreas starts producing [[insulin]], [[glucagon]], [[somatostatin]], and [[pancreatic polypeptide]]. During the early stages of fetal development, the number of pancreatic alpha cells outnumbers the number of [[Pancreatic beta cell function|pancreatic beta cells]]. The alpha cells reach their peak in the middle stage of gestation. From the middle stage until term, the beta cells continue to increase in number until they reach an approximate 1:1 ratio with the alpha cells. The [[insulin]] concentration within the fetal pancreas is 3.6 pmol/g at seven to ten weeks, which rises to 30 pmol/g at 16–25 weeks of gestation. Near term, the insulin concentration increases to 93 pmol/g. The endocrine cells have dispersed throughout the body within 10 weeks. At 31 weeks of development, the [[islets of Langerhans]] have differentiated.

While the fetal pancreas has functional beta cells by 14 to 24 weeks of gestation, the amount of insulin that is released into the bloodstream is relatively low. In a study of pregnant women carrying fetuses in the mid-gestation and near term stages of development, the fetuses did not have an increase in plasma insulin levels in response to injections of high levels of glucose. In contrast to insulin, the fetal plasma glucagon levels are relatively high and continue to increase during development. At the mid-stage of gestation, the glucagon concentration is 6 μg/g, compared to 2 μg/g in adult humans. Just like insulin, fetal glucagon plasma levels do not change in response to an infusion of glucose. However, a study of an infusion of alanine into pregnant women was shown to increase the cord blood and maternal glucagon concentrations, demonstrating a fetal response to amino acid exposure.

As such, while the fetal pancreatic alpha and beta islet cells have fully developed and are capable of hormone synthesis during the remaining fetal maturation, the islet cells are relatively immature in their capacity to produce glucagon and insulin. This is thought to be a result of the relatively stable levels of fetal [[Blood sugar|serum glucose]] concentrations achieved via maternal transfer of glucose through the placenta. On the other hand, the stable fetal serum glucose levels could be attributed to the absence of pancreatic signaling initiated by incretins during feeding. In addition, the fetal pancreatic islets cells are unable to sufficiently produce [[Cyclic adenosine monophosphate|cAMP]] and rapidly degrade cAMP by [[phosphodiesterase]] necessary to secrete glucagon and insulin.

During fetal development, the storage of glycogen is controlled by fetal [[glucocorticoid]]s and [[Human placental lactogen|placental lactogen]]. Fetal insulin is responsible for increasing glucose uptake and [[lipogenesis]] during the stages leading up to birth. Fetal cells contain a higher amount of insulin receptors in comparison to adults cells and fetal insulin receptors are not downregulated in cases of [[hyperinsulinemia]]. In comparison, fetal haptic glucagon receptors are lowered in comparison to adult cells and the glycemic effect of glucagon is blunted. This temporary physiological change aids the increased rate of fetal development during the final trimester. Poorly managed maternal [[diabetes mellitus]] is linked to [[Large for gestational age|fetal macrosomia]], increased risk of miscarriage, and defects in fetal development. Maternal hyperglycemia is also linked to increased insulin levels and beta cell hyperplasia in the post-term infant. Children of diabetic mothers are at an increased risk for conditions such as: [[polycythemia]], [[renal vein thrombosis]], [[hypocalcemia]], [[Infant respiratory distress syndrome|respiratory distress syndrome]], [[jaundice]], [[cardiomyopathy]], [[Congenital heart defect|congenital heart disease]], and improper organ development.