Thyroid function disturbance and type 3 iodothyronine deiodinase induction after myocardial infarction in rats a time course study.
In humans, there is a significant decrease in serum T(3) and increase in rT(3) at different time points after myocardial infarction, whereas serum TSH and T(4) remain unaltered. We report here a time course study of pituitary-thyroid function and thyroid hormone metabolism in rats subjected to myocardial infarction by left coronary ligation (INF). INF- and sham-operated animals were followed by serial deiodination assays and thyroid function tests, just before, and 1, 4, 8, and 12 wk after surgery. At 4 and 12 wk after INF, liver type 1 deiodinase activity was significantly lower, confirming tissue hypothyroidism. Type 3 deiodinase (D3) activity was robustly induced 1 wk after INF only in the infarcted myocardium. Reminiscent of the consumptive hypothyroidism observed in patients with large D3-expressing tumors, this induction of cardiac D3 activity was associated with a decrease in both serum T(4) ( approximately 50% decrease) and T(3) (37% decrease), despite compensatory stimulation of the thyroid. Thyroid stimulation was documented by both hyperthyrotropinemia and radioiodine uptake. Serum TSH increased by 4.3-fold in the first and 3.1-fold in the fourth weeks (P < 0.01), returning to the basal levels thereafter. Thyroid sodium/iodide-symporter function increased 1 wk after INF, accompanying the increased serum TSH. We conclude that the acute decrease in serum T(4) and T(3) after INF is due to increased thyroid hormone catabolism from ectopic D3 expression in the heart.
Olivares
Emerson L
EL
Departamento de Ciências Fisiológicas, Instituto de Biologia, Universidade Federal Rural do Rio de Janeiro BR 465, Km 7, 23851-000 Seropédica, Rio de Janeiro, Brazil. elopes@ufrrj.br
Marassi
Michelle P
MP
Fortunato
Rodrigo S
RS
da Silva
Alba C M
AC
Costa-e-Sousa
Ricardo H
RH
Araújo
Iracema G
IG
Mattos
Elisabete C
EC
Masuda
Masako O
MO
Mulcahey
Michelle A
MA
Huang
Stephen A
SA
Bianco
Antonio C
AC
Carvalho
Denise P
DP
D000818:Animals; D006321:Heart / Q000503:physiopathology; D007453:Iodide Peroxidase / Q000096:biosynthesis* / Q000378:metabolism; D007457:Iodine Radioisotopes / Q000493:pharmacokinetics; D008297:Male; D009203:Myocardial Infarction / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D011863:Radioimmunoassay; D051381:Rats; D017208:Rats, Wistar; D027981:Symporters / Q000378:metabolism; D013961:Thyroid Gland / Q000378:metabolism / Q000503:physiopathology*; D013972:Thyrotropin / Q000097:blood; D013973:Thyrotropin-Releasing Hormone / Q000494:pharmacology; D013974:Thyroxine / Q000097:blood; D013997:Time Factors; D014284:Triiodothyronine / Q000097:blood; D000099209:Sodium-Iodide Symporters
D007453:Iodide Peroxidase; D007457:Iodine Radioisotopes; D027981:Symporters; D013972:Thyrotropin; D013973:Thyrotropin-Releasing Hormone; D013974:Thyroxine; D014284:Triiodothyronine; D000099209:Sodium-Iodide Symporters; C109812:iodothyronine deiodinase type I; C117274:iodothyronine deiodinase type III