Targeted Disruption of the Type 2 Selenodeiodinase Gene (DIO2) Results in a Phenotype of Pituitary Resistance to T4

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Abstract
Mice, none was detected in BAT RNA from com- parably-treated D2KO mice. Levels of D1 in the liver, thyroid, and pituitary were the same in WT and D2KO animals, whereas D3 activity in D2KO cerebrum was twice that in WT cerebrum. Serum T3 levels were comparable in adult WT and D2KO mice. However, serum T4 and TSH levels were both elevated significantly (40% and 100%, respectively) in the D2KO mice, suggesting that the pituitary gland of the D2KO mouse is resistant to the feed- back effect of plasma T4. This view was substan- tiated by the finding that serum TSH levels in hypo- thyroid WT mice were suppressed by administration of either T4 or T3, but only T3 was effective in the D2KO mouse. The data also suggest that the clear- ance of T4 from plasma was reduced in the D2KO mouse. In summary, targeted inactivation of the sel- enodeiodinase Dio2 gene results in the complete loss of D2 activity in all tissues examined. The in- creased serum levels of T4 and TSH observed in D2KO animals demonstrate that the D2 is of critical importance in the feedback regulation of TSH secretion. (Molecular Endocrinology 15: 2137-2148, 2001)

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