Key points • skeletal muscle mass depends on the balance between protein synthesis and degradation rates; • muscle wasting in pathological states is mainly associated with activation of protein breakdown above control levels; • myostatin is a negative regulator of skeletal muscle mass, acting on both myogenesis and protein turnover; • increased myostatin expression is a frequent finding in diseases characterized by the occurrence of muscle atrophy; • glutamine levels are generally decreased in acute and chronic illnesses, and glutamine supplementation to critically ill patients results in improved clinical conditions; • myotube atrophy induced by glucocorticoid or proinflammatory cytokine exposure can be reverted by glutamine treatment. Such an effect is associated with normalization of myostatin hyperexpression and signaling; • glutamine effectiveness in restoring normal myostatin pathway could depend on the inhibition of proinflammatory cascades as well as on the regulation of microRNA expression.
Glutamine and myostatin expression in muscle
PENNA, FABIO;BACCINO, Francesco Maria;COSTELLI, Paola
2015-01-01
Abstract
Key points • skeletal muscle mass depends on the balance between protein synthesis and degradation rates; • muscle wasting in pathological states is mainly associated with activation of protein breakdown above control levels; • myostatin is a negative regulator of skeletal muscle mass, acting on both myogenesis and protein turnover; • increased myostatin expression is a frequent finding in diseases characterized by the occurrence of muscle atrophy; • glutamine levels are generally decreased in acute and chronic illnesses, and glutamine supplementation to critically ill patients results in improved clinical conditions; • myotube atrophy induced by glucocorticoid or proinflammatory cytokine exposure can be reverted by glutamine treatment. Such an effect is associated with normalization of myostatin hyperexpression and signaling; • glutamine effectiveness in restoring normal myostatin pathway could depend on the inhibition of proinflammatory cascades as well as on the regulation of microRNA expression.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.