Fetal carbohydrate metabolism: its clinical importance.
A basic understanding of fetal nutrition and metabolism is essential in the clinical management of the obstetric patient. The fetus depends upon a constant infusion of glucose for energy production and growth. Maternal glucose is the prime source of this nutrient. Alterations in maternal carbohydrate homeostasis will lead to changes in fetal metabolism. In diabetes mellitus, hyperglycemia may produce hyperinsulinemia and macrosomia. The growth-retarded fetus may have a decreased supply of maternal glucose and reduced amounts of hepatic glycogen and adipose tissue. The fetus must depend upon these stores for survival during periods of intrauterine hypoxia. In the newborn period, hypothermia and hypoxia may rapidly deplete energy reserves. With this information, the clinician may more knowledgeably manage dietary demands in the antepartum patient, fetal distress during labor, and the immediate newborn period.
D050260:Carbohydrate Metabolism; D004967:Estrogens / Q000502:physiology; D005260:Female; D005315:Fetal Diseases / Q000209:etiology; D005333:Fetus / Q000378:metabolism*; D005934:Glucagon / Q000502:physiology; D005947:Glucose / Q000378:metabolism; D006801:Humans; D006854:Hydrocortisone / Q000502:physiology; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007339:Insulysin / Q000502:physiology; D008431:Maternal-Fetal Exchange; D010179:Pancreas / Q000502:physiology; D010920:Placenta / Q000201:enzymology / Q000378:metabolism; D010928:Placental Lactogen / Q000502:physiology; D011247:Pregnancy; D011374:Progesterone / Q000502:physiology
D004967:Estrogens; D007328:Insulin; D011374:Progesterone; D005934:Glucagon; D010928:Placental Lactogen; D007339:Insulysin; D005947:Glucose; D006854:Hydrocortisone