Abstract

Triiodothyronine (T3) can influence lipid metabolism via multiple mechanisms, which generally result in an increase of fatty acids (FAs) oxidation. Consequently, we hypothesize that hyperthyroidism may influence intramuscular lipids accumulation. This increased intramuscular lipid turn-over is possibly accompanied by an increase in fatty acid transporters expression (FAT/CD36, FABPpm, FATP-1,4). In the present study we examined the lipid content and fatty acid saturation status of free fatty acids (FFA), triacylglycerols (TAG), diacylglycerols (DAG) and phospholipids (PL) in skeletal muscle of hyperthyroid rats (n=8). We measured also fatty acid transporters as well as AMP-activated protein kinase (pAMPK/AMPK), peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), acetyl-CoA carboxylase (pACC/ACC), carnitine palmitoyltransferase I (CPT I) and citrate synthase (CS) protein expression in these muscles. In vivo T3 administration, decreased the content of FFA, particularly in the red gastrocnemius and the TAG fraction, in both the red and white portions of the gastrocnemius muscle. Concomitantly, saturated/unsaturated fatty acids (SFA/UFA) ratio was also decreased, but only in the FFA fraction, irrespectively of muscle’s fiber composition. In contrast, T3 treatment had no effect on the lipid content and saturation status in PL fraction. Triiodothyronine induced also modest activation of AMPK/ACC axis with subsequent increased expression of mitochondrial proteins: CPT I and CS. This was accompanied by increased content of FAT/CD36, but only in the red part of gastrocnemius muscle. These findings support the conclusion that hyperthyroidism increases lipid metabolism, especially in skeletal muscles with high capacity for fatty acid oxidation.