The purpose of this study was to clarify the role which disordered iron metabolism and alterations in the homeostatic regulation of red cell production play in hypothyroid anemia. Following the measurement of the oxygen consumption, rats were thyroidectomized and given an ablative dose of sodium 131iodine. The oxygen consumption was again measured and the experiments initiated 8 weeks thereafter. The 18-hr red cell radioiron incorporation was used as an index of erythropoiesis. The gastrointestinal absorption of radioiron and the 24-hr urinary erythropoietin levels were assessed. Hypothyroid rats demonstrated a decreased red cell radioiron incorporation and a diminished GI iron absorption. The diminution in erythropoiesis was reverted toward normal by the administration of erythropoietin, D-triiodo-thyronine, L-triiodothyronine or exposure to hypobarbaric hypoxia. Erythropoietin, which completely corrected the erythropoietic depression in the hypothyroid rats, did not correct the decreased GI radioiron absorption whereas L-triiodothyronine restored both to normal. Urinary erythropoietin was decreased in the hypothyroid rat and reverted to normal following L-triiodothyronine administration. These data suggest that the mechanism producing the erythropoietic decompensation in hypothyroid states is complex and involves the lack of erythropoietic stimulation by erythropoietin. Acute erythropoietic compensation appears possible by the administration of nonspecific erythropoietic stimulants; however, the defect in gastrointestinal iron absorption can only be repaired by the administration of thyroid hormones.
|Original language||English (US)|
|Number of pages||5|
|Journal||Proceedings of the Society for Experimental Biology and Medicine|
|State||Published - Oct 1973|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)