Abstract
3,5,3’-triiodothyroacetic acid (TRIAC) has been used to suppress pituitary TSH secretion with reported attenuation of extrapituitary effects. We investigated whether equivalent doses of T3 and TRIAC preventing the induction of goiter by methimazole (MMI) had a different or similar impact on peripheral tissues, such as liver and bone. In particular, we compared the effects of both compounds on the activity of the hepatic thyroid hormone-responsive enzymes, malic enzyme and L-glicerol-3-P dehydrogenase; bone mineral density and biochemical parameters of bone turnover, such as bone alkaline phosphatase (b-ALP) and the carboxy-terminal telopeptide region of type I collagen (β-CTX); and the activity of thyroid ornithine decarboxylase (ODC). We also compared the effects of T3 and TRIAC on the involution of MMI-induced goiter. Our results showed that TRIAC was more effective than T3 to reduce MMI-induced goiter in a short-term goiter involution assay. TRIAC increased hepatic enzymes activity and β-CTX levels, a parameter of bone resorption, more than T3 . However, bone mineral density was not altered by either treatment. Both compounds even reduced ODC activity at doses that were not effective at the pituitary level. These results demonstrate increased TRIAC hepatic and antigoitrogenic activity compared to T3 . TRIAC induces an imbalance in bone remodeling without affecting bone mineral density. Further studies are required to clarify this point.
Key words
Thyroid growth - Malic enzyme - L glycerol 3-P-dehydrogenase - Bone formation - Bone resorption - Methimazole-induced goiter
References
3 ) and its analogs to the in vitro translational products of c-erbA protooncogenes: differences in the affinity of the alpha- and beta-forms for the acetic acid analog and failure of the human testis and kidney alpha-2 products to bind T3 .
Mol Endocrinol.
1990;
4
227-234
dkleiman@fmed.uba.ar
