AJP - Endocrinology and Metabolism, Vol 240, Issue 2 146-E154, Copyright © 1981 by American Physiological Society
Nuclear binding of T3 and effects of QO2, Na-K-ATPase, and alpha-GPDH in liver and kidney
D. Somjen, F. Ismail-Beigi and I. S. Edelman
Thyroid status was altered by use of a low-iodine-perchlorate (PC) regimen
and either reversal with NaI or injections of L-3,5,3'-triiodothyronine
(T3). The PC regimen decreased renal and hepatic oxygen consumption (QO2),
alpha-glycerophosphate dehydrogenase (alpha-GPDH), and Na+-K+-dependent
adenosine triphosphatase (Na-K-ATPase) to comparable extents (25 vs. 23%,
26 vs. 39%, and 41 vs. 51%, respectively). Administration of T3 to
hypothyroid rats elicited dose-dependent increases in hepatic and renal
cortical QO2, ouabain-sensitive oxygen consumption (QO2(t)), alpha-GPDH,
and Na-K-ATPase activities. The half-maximal increases in all of the
response parameters in both kidney and liver were obtained at dosages of
6-32 micrograms T3/100 g body wt. The equivalences in the renal cortical
vs. hepatic responses were indicated by correlation coefficients of
approximately 0.97. Kidney and liver nuclei also showed similar
high-affinity binding of 125I-T3-K1/2 = 29 vs. 18 micrograms T3/100 g body
wt, and Nmax = 1.8 vs. 2.1 ng T3/mg DNA. The patterns of the responses
plotted as a function of T3 occupancy of the high-affinity nuclear binding
sites were indistinguishable in kidney and liver. These results imply
similar modes of action of T3, probably initiated at the nuclear level, in
both kidney and liver.
