Show simple item record

dc.contributor.authorChanoine, Jean-Pierre
dc.contributor.authorVeronikis, Irini E.
dc.contributor.authorAlex, Sharon
dc.contributor.authorStone, Scott
dc.contributor.authorFang, Shih-Lieh
dc.contributor.authorLeonard, Jack L.
dc.contributor.authorBraverman, Lewis E.
dc.date2022-08-11T08:10:02.000
dc.date.accessioned2022-08-23T16:52:57Z
dc.date.available2022-08-23T16:52:57Z
dc.date.issued1993-12-01
dc.date.submitted2008-07-09
dc.identifier.citation<p>Endocrinology. 1993 Dec;133(6):2604-9.</p>
dc.identifier.issn0013-7227 (Print)
dc.identifier.pmid8243283
dc.identifier.urihttp://hdl.handle.net/20.500.14038/42165
dc.description.abstractIn the rat, selenium deficiency causes a near-complete loss of the selenoenzyme type I 5'-deiodinase (5'D-I), resulting in a marked decrease in hepatic T4 to T3 conversion. In adult rats, serum T4 concentrations are consistently increased, whereas serum T3 and rT3 concentrations are unaffected or slightly decreased and increased, respectively. In rat fetuses near term, serum T4 and rT3 concentrations are not affected by selenium deficiency. We have now studied the effect of selenium deficiency on thyroid function in the neonatal rat. Weanling female rats were fed either a selenium-supplemented or a selenium-deficient diet for 4 weeks before mating and then throughout gestation and lactation. Neonatal rats were killed at 7, 14, 21, and 28 days. Selenium deficiency was confirmed by a more than 89% decrease in liver 5'D-I activity in mothers and pups. Selenium deficiency resulted in significant increases in serum T4 concentrations in 3- and 4-week-old pups. In contrast, selenium deficiency led to a striking increase in serum rT3 concentrations. The normal postnatal serum T3 surge was not affected by selenium deficiency at any age. In 2- and 4-week-old selenium-deficient pups obtained from a second litter from the same mothers, liver 5'D-I activity was markedly decreased, but thyroid 5'D-I activity was not affected. The increased serum rT3 and, less so, T4 concentrations observed in selenium-deficient pups were associated with a significant decrease in brain 5'D-II activity in 14- and 28-day-old pups and in brown adipose tissue 5'D-II activity in 14-day-old pups. In conclusion, the present study demonstrates that the increase in serum T4 concentrations consistently observed in selenium-deficient adult rats occurs only after the second week of life. The normal physiological postnatal 12-fold increase in serum T3 concentrations observed in selenium-deficient pups despite the marked decreases in liver 5'D-I and brain and brown adipose tissue 5'D-II activities suggests that T4 to T3 conversion by peripheral tissues may not be a major source of T3 in the neonate. In contrast, the thyroid gland, whose 5'D-I activity is not affected by selenium deficiency, is probably the principal source of circulating T3 in the neonate. Finally, the early and marked increase in serum rT3 concentrations observed in selenium-deficient pups suggests that liver 5'D-I is important in rT3 deiodination.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=8243283&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1210/en.133.6.2604
dc.subjectAdipose Tissue, Brown
dc.subjectAnimals
dc.subjectAnimals, Newborn
dc.subjectBrain
dc.subjectFemale
dc.subjectIodide Peroxidase
dc.subjectLiver
dc.subjectOsmolar Concentration
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectThyroid Gland
dc.subjectThyrotropin
dc.subjectThyroxine
dc.subjectTriiodothyronine
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleThe postnatal serum 3,5,3'-triiodothyronine (T3) surge in the rat is largely independent of extrathyroidal 5'-deiodination of thyroxine to T3
dc.typeJournal Article
dc.source.journaltitleEndocrinology
dc.source.volume133
dc.source.issue6
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/537
dc.identifier.contextkey545019
html.description.abstract<p>In the rat, selenium deficiency causes a near-complete loss of the selenoenzyme type I 5'-deiodinase (5'D-I), resulting in a marked decrease in hepatic T4 to T3 conversion. In adult rats, serum T4 concentrations are consistently increased, whereas serum T3 and rT3 concentrations are unaffected or slightly decreased and increased, respectively. In rat fetuses near term, serum T4 and rT3 concentrations are not affected by selenium deficiency. We have now studied the effect of selenium deficiency on thyroid function in the neonatal rat. Weanling female rats were fed either a selenium-supplemented or a selenium-deficient diet for 4 weeks before mating and then throughout gestation and lactation. Neonatal rats were killed at 7, 14, 21, and 28 days. Selenium deficiency was confirmed by a more than 89% decrease in liver 5'D-I activity in mothers and pups. Selenium deficiency resulted in significant increases in serum T4 concentrations in 3- and 4-week-old pups. In contrast, selenium deficiency led to a striking increase in serum rT3 concentrations. The normal postnatal serum T3 surge was not affected by selenium deficiency at any age. In 2- and 4-week-old selenium-deficient pups obtained from a second litter from the same mothers, liver 5'D-I activity was markedly decreased, but thyroid 5'D-I activity was not affected. The increased serum rT3 and, less so, T4 concentrations observed in selenium-deficient pups were associated with a significant decrease in brain 5'D-II activity in 14- and 28-day-old pups and in brown adipose tissue 5'D-II activity in 14-day-old pups. In conclusion, the present study demonstrates that the increase in serum T4 concentrations consistently observed in selenium-deficient adult rats occurs only after the second week of life. The normal physiological postnatal 12-fold increase in serum T3 concentrations observed in selenium-deficient pups despite the marked decreases in liver 5'D-I and brain and brown adipose tissue 5'D-II activities suggests that T4 to T3 conversion by peripheral tissues may not be a major source of T3 in the neonate. In contrast, the thyroid gland, whose 5'D-I activity is not affected by selenium deficiency, is probably the principal source of circulating T3 in the neonate. Finally, the early and marked increase in serum rT3 concentrations observed in selenium-deficient pups suggests that liver 5'D-I is important in rT3 deiodination.</p>
dc.identifier.submissionpathoapubs/537
dc.contributor.departmentDepartment of Physiology
dc.contributor.departmentDepartment of Medicine, Division of Endocrinology
dc.source.pages2604-9


This item appears in the following Collection(s)

Show simple item record