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Adrenaline: Decreases T3, Increases Reverse T3

Adrenaline decreases the conversion to T4 to T3, and increases the formation of the antagonistic reverse T3 (Nauman, et al., 1980, 1984). -Ray Peat, PhD

Eur J Clin Invest. 1980 Jun;10(3):189-92.
In vivo and in vitro effects of adrenaline on conversion of thyroxine to triiodothyronine and to reverse-triiodothyronine in dog liver and heart.
Nauman A, Kamiński T, Herbaczyńska-Cedro K.
Infusion of adrenaline in healthy dogs in a dose simulating spontaneous release of the catecholamine during experimental myocardial infarction produced a significant decrease in the conversion of thyroxine (T4) to triiodothyronine (T3) and a moderate increase in the conversion of T4 to reverse-triiodothyronine (rT3). Similar changes in deiodination of T4 to T3 and to rT3 were also observed when adrenaline was added in vitro to liver and heart homogenates. These results are consistent with a direct effect of adrenaline on T4 deiodination as degradation of exogenous T4, T3 and rT3 was only slightly increased under the experimental condition employed. The present study suggests that increased tissue exposure to adrenaline might contribute to the hormonal changes seen in at least some case of the ‘low T3 syndrome’.

Horm Metab Res. 1984 Sep;16(9):471-4.
The effect of adrenaline pretreatment on the in vitro generation of 3,5,3′-triiodothyronine and 3,3′,5′-triiodothyronine (reverse T3) in rat liver preparation.
Nauman A, Porta S, Bardowska U, Fiedorowicz K, Sadjak A, Korsatko W, Nauman J.
The effects of adrenaline (A) on liver T3 and rT3 neogenesis from T4 were studied in Wistar rats. The animals were implanted subcutaneously either with A or placebo (P) especially coated tablets which linearly released the hormone. The serum A values 6 hrs after implantation of 7.5, 15.0 and 45.0 mg tablets were 6.5 +/- 1.31, 6.8 +/- 1.8 and 16.4 +/- 1.9 ng/ml, respectively vs 4.4 +/- 2.5 ng/ml seen in P pretreated group. The output rates of A were 0.11 (7.5 mg), 0.18 (15 mg) and 0.52 microgram/ml (45 mg). The pretreatment with A led to hyperglycemia and the “low T3 syndrome”. Neogenesis of T3 from T4 in medium containing liver microsomes of P pretreated rats was 5.49 +/- 0.25 pmol of T3/mg protein/min and decreased in A pretreated rats to 3.82 +/- 0.17, 3.12 +/- 0.27 and 3.06 +/- 0.11 pmol of T3/mg of protein/min. Neogenesis of rT3 from T4 in microsomes from P group was 1.52 +/- 0.09 pmol rT3/mg protein/min and increased after A to 2.71 +/- 0.11, 2.60 +/- 0.21 and 2.21 +/- 0.34 pmol of rT3/mg protein/min thus showing no dose dependency. Enrichment of microsomes medium with cytosol either from P or A pretreated rats had no effect on T3 generation thus excluding effect of A on cytosolic cofactor. Although cytosol further increased rT3 neogenesis this was seen regardless of whether cytosol was obtained from A or P implanted rats. It is concluded that A decreases the activity of T4-5′-deiodinase in liver, and possibly increases the activity of T4-5-deiodinase.

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