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We reported that chow-fed, adult-onset, hepatocyte-specific, GH receptor knockdown aHepGHRkd mice rapidly within 7 days develop steatosis associated with increased hepatic de novo lipogenesis DNL , independent of changes in systemic metabolic function.
In this study, we report that 6 months after induction of aHepGHRkd early signs of NASH develop, which include hepatocyte ballooning, inflammation, signs of mild fibrosis, and elevated plasma alanine aminotransferase.
These changes occur in the presence of enhanced systemic lipid utilization, without evidence of white adipose tissue lipolysis, indicating that the liver injury that develops after aHepGHRkd is due to hepatocyte-specific loss of GH signaling and not due to secondary defects in systemic metabolic function.
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