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Rapid Publication Free access | 10.1172/JCI109751

Dietary Modification of Thyroxine Deiodination in Rat Liver is Not Mediated by Hepatic Sulfhydryls

Laurence A. Gavin, Francis A. McMahon, and M. Moeller

Division of Endocrinology-Metabolism, Veterans Administration Medical Center, University of California, San Francisco, California 94121

Department of Medicine, University of California, San Francisco, California 94121

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Division of Endocrinology-Metabolism, Veterans Administration Medical Center, University of California, San Francisco, California 94121

Department of Medicine, University of California, San Francisco, California 94121

Find articles by McMahon, F. in: PubMed | Google Scholar

Division of Endocrinology-Metabolism, Veterans Administration Medical Center, University of California, San Francisco, California 94121

Department of Medicine, University of California, San Francisco, California 94121

Find articles by Moeller, M. in: PubMed | Google Scholar

Published April 1, 1980 - More info

Published in Volume 65, Issue 4 on April 1, 1980
J Clin Invest. 1980;65(4):943–946. https://doi.org/10.1172/JCI109751.
© 1980 The American Society for Clinical Investigation
Published April 1, 1980 - Version history
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Abstract

The enzymatic deiodination of thyroxine (T4) is thiol dependent. Fasting (72 h) depresses hepatic T4 deiodination and lowers the hepatic content of nonprotein sulfhydryls (NP-SH) and reduced glutathione (GSH). It has been proposed that the fasting effect may be mediated through these alterations in hepatic sulfhydryls. To test the importance of tissue (hepatic) thiol content in the modification of T4 deiodination consequent to dietary manipulation, we examined the sequential deiodination of T4 to 3,5,3′-triiodothyronine (T3) (5′-deiodination) and 3,3′,5-triiodothyronine (reverse T3, rT3) (5-deiodination) in liver homogenates without added thiol from groups of rats fed Purina lab chow (P) (a protein-rich diet), glucose alone (G), or glucose plus cysteine (Gc) for 72 h or fasted (F) for the same period. The initial rate of each reaction was compared to the tissue concentrations of NP-SH and GSH.

Dietary manipulation induced significant changes in hepatic deiodination of T4 to T3 and rT3 and sulfhydryl content. There was a marked dissociation between the rate of each reaction and hepatic NP-SH and GSH levels. T4 deiodination by the alternative pathways was significantly higher (P < 0.01) in G > P > F. In contrast both hepatic NP-SH and GSH concentrations were greater (P < 0.05) in P > F > G. The lack of a relationship between these parameters was further emphasized on analysis of tissue from rats fed Gc. Despite the clearcut (P < 0.01) increase in hepatic NP-SH and GSH consequent to Gc feeding, there was no alteration in iodothyronine deiodination compared to the group fed glucose alone.

These data indicate that the effects of diet on T4 monodeiodination in liver are not mediated by changes in the tissue level of sulfhydryl compounds but rather involve alterations in the concentrations of the deiodinases.

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