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KMID : 0376219640010020223
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Chonnam Medical Journal
1964 Volume.1 No. 2 p.223 ~ p.233
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Effects of L-Thyroxine on the Oxidation of Glucose and Palmitate in Vivo and in Vitro
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Abstract
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The effects of L-thyroxine on the oxidation of glucose and palmitate in vivo and in vitro were studied by determining the oxidative conversion to CO₂of differentially labeled glucose-C14 and palmitate-1-C14 by tissue homogenates obtained from normal, hyper and hypothyroid rats.
1. In hyperthyroidism, hipatic oxidation of glucose showed more than two-fold increases over those of normal and hypothyroid rats with concomitant increase of G-1/G-6 ratio(C14O₂from glucose-1-C14/C14O₂ from glucose-6-C14)from 7.0 to 8.0. Inother words, hepatic oxidation of glucose through both Embden-Meyerhof pathway and pentose cycle was enhanced in hyperthyroidism, the latter being more marked than the former. In hypothyroidism, G-1/G-6 ratio remained within normal limits with a slight decrease in the glucose oxidation rate.
The brain showed a greater glucose oxidation rate compared to the liver. However, G-1/G-6 ratio was around 1.0 and both of glucose oxidation and G-1/G-6 ratio were not changed according to the thyroid states.
2. The oxidation of palmitate, in contrast to the glucose oxidation, responded quite differently to various thyroid states. Thus, it was depressed most in hyper-thyroidism and enhanced in hypothyroidism. The difference among the thyroid states was more pronounced in the liver than in the brain.
3. In vitro additon of thyroxine (10-4M) did not produce any singificant change int eh glucose oxidation by mormal liver, kidney and heart homogenates even in the presence of NAD or ATP(10-3M)which increased th glucose oxidation equally in thepresence and in the absence of thyroxine. In brain homogenates, the addition of thyroxine caused a decrease in the glucose oxidation, however.
4. By contrast, the oxidation of palmitate was uniformly depressed in every tissue homogenates examined by thyroxine addedin vitro. The depressed palmitate oxidation, however, was recovered almost to normal by the simultaneous additon of ATP(10-3M), but not by NAD (10-3M).
5. The palmitate oxidation by liver mitochondria was also depressed by thyroxine added in vitro. And as with the whloe homogenate, the depression was recovered to noraml by ATP(10-3M) and lidewise by cytochrome c(10-3M), but not by either NAD or succinate.
These results were interpreted as indicating that in hyperthyroidism the depressed oxidation of palimtate occurs chiefly due to a disturbance in the generation of available ATP, and leads to concomitant increase in the gluceose oxidation with a preferential stimulation of the pentose cycle of glycolytic pathways.
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