[Maternal glucose tolerance along pregnancy (author's transl)].
The development of the foetal and placental unit induces large changes in maternal glucose tolerance along pregnancy. Oestrogen-induced hyperinsulinism is responsible for facilitated anabolism which take place during the first part of pregnancy. Accelerated catabolism occurring during the second part is due to the direct action of placental hormones, mainly of human placental lactogen. The latter is responsible for diminution of peripheral insulin activity. Hyperinsulinism, which is very important at this stage, facilitates from where nutrients can be easily removed. Glucose and amino-acide uptake by placental and foetus are greatly increased by all these changes.
D000596:Amino Acids / Q000378:metabolism; D004734:Energy Metabolism; D004967:Estrogens / Q000502:physiology; D005260:Female; D005934:Glucagon / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance; D008099:Liver / Q000378:metabolism; D008431:Maternal-Fetal Exchange; D010928:Placental Lactogen / Q000502:physiology; D011247:Pregnancy; D011261:Pregnancy Trimester, First; D011262:Pregnancy Trimester, Second; D011263:Pregnancy Trimester, Third; D011374:Progesterone / Q000502:physiology; D011972:Receptor, Insulin / Q000502:physiology
D000596:Amino Acids; D004967:Estrogens; D007328:Insulin; D011374:Progesterone; D005934:Glucagon; D010928:Placental Lactogen; D011972:Receptor, Insulin; D005947:Glucose
Tolérance glucosée de la femme enceinte.