Regional physiological adaptation of the central nervous system deiodinases to iodine deficiency

Citation
R. Peeters et al., Regional physiological adaptation of the central nervous system deiodinases to iodine deficiency, AM J P-ENDO, 281(1), 2001, pp. E54-E61
Citations number
41
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
ISSN journal
01931849 → ACNP
Volume
281
Issue
1
Year of publication
2001
Pages
E54 - E61
Database
ISI
SICI code
0193-1849(200107)281:1<E54:RPAOTC>2.0.ZU;2-Q
Abstract
The goal of the present investigation was to analyze the types 2 (D2) and 3 (D3) iodothyronine deiodinases in various structures within the central ne rvous system (CNS) in response to iodine deficiency. After 5-6 wk of low-io dine diet (LID) or LID + 2 mug potassium iodide/ml (LID+KI; control), rats' brains were processed for in situ hybridization histochemistry for D2 and D3 mRNA or dissected, frozen in liquid nitrogen, and processed for D2 and D 3 activities. LID did not affect weight gain or serum triiodothyronine, but plasma thyroxine (T-4) was undetectable. In the LID+KI animals, D3 activit ies were highest in the cerebral cortex (CO) and hippocampus (HI), followed by the olfactory bulb and was lowest in cerebellum (CE). Iodine deficiency decreased D3 mRNA expression in all CNS regions, and these changes were ac companied by three- to eightfold decreases in D3 activity. In control anima ls, D2 activity in the medial basal hypothalamus (MBH) was similar to that in pituitary gland. Of the CNS D2-expressing regions analyzed, the two most responsive to iodine deficiency were the CO and HI, in which an similar to 20-fold increase in D2 activity occurred. Other regions, i.e., CE, lateral hypothalamus, MBH, and pituitary gland, showed smaller increases. The dist ribution of and changes in D2 mRNA were similar to those of D2 activity. Ou r results indicate that decreases in the expression of D3 and increases in D2 are an integral peripheral component of the physiological response of th e CNS to iodine deficiency.