Background: Skeletal muscle is known to be a target of THs, regulating oxygen consumption, fiber composition, calcium mobilization and glucose uptake. However, a possible role for THs in muscle homeostasis and cellular metabolism under pathological has never been investigated. Food deprivation induces skeletal muscle atrophy, causing metabolic changes, and forcing the tissue to utilize fatty acid as the main oxidation substrate. Aim of this project was to understand whether T3 influence skeletal muscle metabolism during fasting.
Methods: Adult male BALB/C mice were food deprived for 48h (STV), and daily treated with intraperitoneal injections of T3 (100 μg/Kg BW) (STVT3) or vehicle as controls. At the end of the experiments, Tibilias anteriors were collected and firstly laminin stained sections were analyzed for myofiber sizes by IF microscopy. Secondly, the number of glycolytic, intermediate or oxidative fibers per cross section area on NADH stained histological sections was analyzed. Mitochondria content, indicative of a more oxidative metabolism, was then analyzed by qRT Syber Green PCR for PGC-1a mRNA.
Results: As expected, laminin staining evidenced a reduction in Cross Sectional Area of the myofibers induced by fasting (STV), as a sign of atrophy. The cited reduction was significantly hampered by the presence of T3 in the STVT3 group. Secondly, T3 was able to significantly reduce the shift in the metabolism towards a more oxidative state (P<0.05) and a less glycolytic one (P<0.01) induced by fasting. Coherently, T3 reduced the increase in PGC-1a mRNA level induced by fasting in the STV group (P<0.05).
Conclusions: The decrease of the amount in oxidative muscle fibers during T3 treatment in STV agrees with a less expression of PGC-1a, a molecular marker of mitochondriogenesis and fatty acid oxidation. Therefore, T3 treatment during fasting seems to exert a protective role on the metabolism of muscle fibers.
20 May 2017 - 23 May 2017