An article titled “Adult-onset hepatocyte GH resistance promotes NASH in male mice, without severe systemic metabolic dysfunction” has been recently co-published by one of our doctors.
The manuscript is co-authored by: Jose Cordoba-Chacon, Andre Sarmento-Cabral, Mercedes del Rio-Moreno, Alberto Diaz-Ruiz, Papasani V Subbaiah, Rhonda D Kineman;
Dr. Kineman serves as the corresponding author of the study.
Brief synopsis: NAFLD and NASH are associated with reduced growth hormone (GH) input/signaling in humans. We have found that mice with adult-onset hepatocyte-specific GH receptor knockdown (aHepGHRkd) developed signs of NASH with enhanced systemic lipid utilization and without major metabolic dysfunction of peripheral tissues. NASH observed in aHepGHRkd mice may be due to hepatocyte-specific loss of GH signaling that enhanced hepatic de novo lipogenesis and lipid uptake without evidence of white adipose tissue lipolysis. These studies suggest that hepatocyte GH signaling could represent an effective therapeutic target to reduce DNL and treat NASH.