AAV-mediated administration of myostatin pro-peptide mutant in adult Ldlr null mice reduces diet-induced hepatosteatosis and arteriosclerosis.

ABSTRACT:

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Genetic disruption of myostatin or its related signaling is known to cause strong protection against diet-induced metabolic disorders. The translational value of these prior findings, however, is dependent on whether such metabolically favorable phenotype can be reproduced when myostatin blockade begins at an adult age. Here, we reported that AAV-mediated delivery of a myostatin pro-peptide D76A mutant in adult mice attenuates the development of hepatic steatosis and arteriosclerosis, two common diet-induced metabolic diseases. A single dose of AAV-D76A in adult Ldlr null mice resulted in sustained expression of myostatin pro-peptide in the liver. Compared to vehicle-treated mice, D76A-treated mice gained similar amount of lean and fat mass when fed a high fat diet. Howe

SUBMITTER: Guo W 

PROVIDER: S-EPMC3731267 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature