Indices of in vivo and in vitro thyroid hormone metabolism in iron-deficient rats

Abstract

Iron deficiency impairs thermoregulation, partially through altering the conversion of thyroxine (T 4) to triiodothyronine (T 3). We studied the distribution and excretion of 125I-T 4 and the hepatic thyroid hormone receptor concentrations to determine the in vivo relationships between hepatic deiodinase activity and disposition of T 4 in iron deficiency. Male weanling Sprague-Dawley rats were placed on either iron-sufficient (CN, 35 ppm Fe, n=7) or iron-deficient (ID, } 5 ppm Fe, n=7) diets. A third group was pair-fed (PF, n=6) the CN diet in amounts equal to that of matched ID rats. Following 6–7 weeks of dietary treatment, animals were anesthetized and cannulas were placed in the right jugular vein and the bile duct. A 20 μCi bolus of 125I-T 4 was infused into the jugular vein. Bile samples were obtained at timed intervals. Animals were killed after 2h and organs were removed for determination of labeled hormone content. There was no effect of iron status on bile flow rate, and there was no change in bile flow rate throughout the 2h period. Tracer distribution was unaffected by iron deficiency. The percent of 125I-T 4 dose in heart, kidney and brown adipose tissue after 2h was similar in ID and CN rats (p>0.05 by ANOVA). The rate of hormone excretion into bile was slightly elevated in ID rats. In a second study, thyroid hormone binding by nuclear receptors tended to be lower in ID rats when compared to CN controls. These results suggest that the metabolism of T 4 is altered in iron deficiency and that ID rats are functionally hypothyroid. Future studies are required to further clarify the effects of iron deficiency on thyroid hormone metabolism.