Astaxanthin ameliorates dexamethasone-induced skeletal muscle atrophy and disorders of glucolipid metabolism.

Long-term use of glucocorticoids, such as dexamethasone, can lead to skeletal muscle atrophy and disturbances in glucolipid metabolism. Astaxanthin, a ketocarotenoid, has a variety of physiological activities. In this study, we investigated the effects of astaxanthin on dexamethasone-induced skeletal muscle atrophy and disorders of glycolipid metabolism. Male C57Bl/6J mice were administered dexamethasone alone or supplemented with different doses of astaxanthin (30 mg/kg/d, 60 mg/kg/d, 120 mg/kg/d) for 4 weeks. The results showed that astaxanthin improved locomotor performance and attenuated dexamethasone-induced reductions in skeletal muscle mass and cross-sectional area in mice. Further exploration of the mechanism revealed that astaxanthin was able to balance the catabolism and synthesis of skeletal muscle proteins and protect mitochondria by reducing the expression of the mitochondrial autophagy-associated proteins Lc3B and BNIP3. In addition, astaxanthin reduced the accumulation of fatty acid metabolites and visceral fat and improved the ability of skeletal muscle to utilize sugars, suggesting that astaxanthin may alleviate dexamethasone-induced disturbances in glycolipid metabolism. This study illustrates that astaxanthin can alleviate skeletal muscle atrophy and metabolic disturbances induced by long-term dexamethasone treatment. This suggests that astaxanthin may be a functional dietary supplement to reduce the side effects of glucocorticoid therapy.