2013 OSU Molecular Life Sciences
Interdisciplinary Graduate Programs Symposium
Poster abstracts
Abstract:
Skeletal muscle constitutes more than 40% of body mass and has been suggested to play an important role in thermogenesis and metabolism. Studies in our laboratory have shown that Sarcolipin (SLN) (31 amino acid trans-membrane peptide) an inhibitor of SR Ca2+ ATP ase (SERCA) is critical for muscle-based thermogenesis. Therefore we investigated the importance of SLN during early mouse neonatal development and in dystrophic muscle. We found that SLN expression is several fold higher at birth in most skeletal muscles studied, which then gradually decreases in adult fast twitch skeletal muscles but preserved in oxidative/slow twitch fibers. Gradual cold acclimatization of these neonatal mice extended the duration of SLN expression in all the muscles. We also observed that in SLN KO neonates the expression of key metabolic regulators involved in fatty acid and glucose oxidation were altered. When compared to skeletal muscle from dystrophic MDX mice, SLN expression was significantly upregulated in the utrophin-dystrophin double knock out (DKO) mice. Interestingly, the DKO mice exhibit a higher level of whole body oxygen consumption but they show decreased mobility. These data together suggest that increased expression of SLN is associated with an increased metabolic rate which is important for maintaining thermogenesis in neonatal stages and an oxidative phenotype in dystrophic muscle.
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Keywords: sarcolipin, metabolism, muscle dystrophy