Impaired Release of Hepatic Triiodothyronine (T3) in the Diabetic Low T3 Syndrome
Previous studies have shown that experimental diabetes causes a significant decrease in serum thyroxine (T4) and 3,5,3′-triiodothyronine (T3) concentrations and reduces hepatic generation of T3 from T4 (1–4). Since hypothyroidism per se induces a reduction in 5′-deiodinase activity (5,6), some studies have suggested that the abnormalities seen in diabetes could be a consequence of this low serum T4 level (7,8). In fact, administration of T4 prevents the decrease in serum T4 concentration and corrects the abnormal T3 production in diabetic animals, but fails to normalize the serum T3 levels (9). Thus, the low T3 syndrome in this situation cannot be fully explained by decreased peripheral conversion of T4 to T3 consequent to a reduction in 5′-deiodinase activity. The present study explores the hypothesis that an alteration of T3 release from intracellular to extracellular space may be an additional factor contributing to the low T3 syndrome observed in diabetes.
KeywordsDiabetic Animal Perfusion Medium Serum Thyroxine Deiodinase Activity Impaired Release
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