Pregnancy and diabetes: the maternal response.
Pregnancy places remarkable stresses on maternal carbohydrate metabolism and pancreatic insulin reserves. The normal mammal responds to pregnancy by increasing pancreatic islet size and insulin secretion. Pregnancy also causes alterations in concentrations of metabolic fuels in maternal circulation. These changes are partly attributed to gestational increases of estrogen, progesterone and human chorionic somatomammotropin, and are thought to provide a proper metabolic and hormonal incubation medium for the fetus. Conversely, the compromised pancreas of the diabetic is unable to meet the additional demands of pregnancy, and carbohydrate metabolism deteriorates. The character of these metabolic changes depends on the time of gestation and the type of diabetes mellitus.
D000818:Animals; D004967:Estrogens / Q000494:pharmacology; D005260:Female; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000473:pathology; D050356:Lipid Metabolism; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000378:metabolism* / Q000473:pathology; D011374:Progesterone / Q000494:pharmacology
D004967:Estrogens; D007328:Insulin; D011374:Progesterone; D005947:Glucose