Iron deficiency impairs thermoregulation, partially through altering t
he conversion of thyroxine,(T-4) to triiodothyronine (T-3). We studied
the distribution and excretion of I-125- 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 de
ficiency. Male weanling Sprague-Dawley rats were placed on either iron
-sufficient (CN, 35 ppm Fe, n=7) or iron-deficient (ID, approximate to
5 ppm Fe, n=7) diets. A third group was pair-fed (PF, n=6) the CN die
t 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 mu Ci bolus of I-125
-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 ra
te throughout the 2 h period. Tracer distribution was unaffected by ir
on deficiency. The percent of I-125-T-4, dose in heart, kidney and bro
wn adipose tissue after 2h was similar in ID and CN rats (p>0.05 by AN
OVA). The rate of hormone excretion into bile was slightly elevated in
ID rats. In a second study, thyroid hormone binding by nuclear recept
ors tended to be lower in ID rats when compared to CN controls. These
results suggest that the metabolism of T, is altered in iron deficienc
y and that ID rats are functionally hypothyroid. Future studies are re
quired to further clarify the effects of iron deficiency on thyroid ho
rmone metabolism.