The effect of maternal hypothyroidism on maternal and fetal tissue glucose-1-14C incorporation in rats.
These experiments were conducted to help elucidate the mechanism for the impaired fetal development occurring during maternal hypothyroidism. The disposition of glucose was measured using glucose-1-14C. Maternal hypothyroidism depressed glucose utilization in thematernal-fetal system. Maternal net glycogen synthesis from the labeled glucose was impaired. However, while the fetal glycogen storage system may be capable of at least relatively normal glycogen synthesis, abnormally low levels of glycogen were measured. If, as the data suggest, enzymatic deficiencies do not exist, the low liver glycogen might be a result of the inability of the maternal-placental system to provide adequate substrate to the fetus.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D005260:Female; D005333:Fetus / Q000502:physiology; D005947:Glucose / Q000378:metabolism*; D006003:Glycogen / Q000378:metabolism; D007037:Hypothyroidism / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D008112:Liver Glycogen / Q000378:metabolism; D008431:Maternal-Fetal Exchange; D009132:Muscles / Q000378:metabolism; D009928:Organ Specificity; D010920:Placenta / Q000378:metabolism; D011247:Pregnancy; D011248:Pregnancy Complications / Q000378:metabolism; D051381:Rats; D013965:Thyroidectomy
D001786:Blood Glucose; D008112:Liver Glycogen; D006003:Glycogen; D005947:Glucose