https://wiki.tiffa.net/w/index.php?action=history&feed=atom&title=Translations%3AEndocrine_system%2F21%2FenTranslations:Endocrine system/21/en - Revision history2026-04-20T00:58:48ZRevision history for this page on the wikiMediaWiki 1.43.0https://wiki.tiffa.net/w/index.php?title=Translations:Endocrine_system/21/en&diff=109332&oldid=prevFuzzyBot: Importing a new version from external source2024-01-17T11:42:03Z<p>Importing a new version from external source</p>
<p><b>New page</b></p><div>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.</div>FuzzyBot