|
NTI is characterized by a low serum T3 level and occurs in the sick euthyroid
syndrome and after fasting. Boelen et al., Amsterdam, The Netherlands,
studied the possible role of interleukin-6 (IL-6) in the development of
NTI in so-called knock-out mice (IL-6-/-) and compared the results with
those in normal (wild) type mice (IL-6+/+). Mice were made sick by administration
of bacterial endotoxin, infection with Listeria monocytogenes, and by injection
of turpentine. Serum IL-6 increased to all stimuli in IL-6+/+ mice, but
not in IL-6-/- mice. The decrease observed in serum T3 as seen in all three
types of induced illnesses was greater in the IL-6+/+ mice than in the
knock-out mice. These findings suggest that IL-6 to some extent is involved
in the generation of the low T3 syndrome during illness, but that other
factors may be involved as well.
Rolleman et al., Rotterdam, The Netherlands, studied renal handling of T3 and T4 in 4 healthy subjects prior to and on the third day of fasting. During fasting daily T3 as well T4 urinary excretion decreased by 46 and 37% respectively. Also serum T3 decreased, but not serum T4. To exclude effects of changes of serum thyroid hormone concentrations on urinary T3 and T4 excretion, renal clearances of the free hormone fractions (F) were determined. Both FT3 and FT4 renal clearances decreased significantly (38% and 46% respectively) during fasting. Before fasting FT4 clearance was lower, but FT3 clearance was higher than creatinin clearance. It is concluded that in the fed state there is net excretion of T3 into the urine and net T4 absorption. The decreased renal clearances during fasting are possibly caused by decreased basolate-ral uptake of T4 and T3 induced by the reduced energy state in the proximal tubule cell effected by fasting. |
