What is it about?
We have removed PPARgamma expression from hepatocytes to test the role of hepatocyte-specific in diet-induced steatosis. PPARgamma is required to increase expression of genes involved in the uptake and esterification of FA, but it is not required to maintain DNL gene expression.
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Why is it important?
To the best of our knowledge, this is the first study to report a efficient knockdown of hepatocyte-specific PPARgamma in adult mice. PPARgamma may be regulating the expression of steatogenic genes: Cd36 and Mogat1.
Perspectives
Despite pharmacological activation of PPARgamma by thiazolidinediones (TZD) has been shown to reduce hepatic fat accumulation, loss of hepatocyte PPARgamma expression in adult mice shows that hepatocyte PPARgamma works as a steatogenic factor (promote accumulation of fat in the liver). Therefore, hepatocyte PPARgamma may promote steatosis and counterbalance the positive/therapeutic activation of PPARgamma by TZD in adipose tissue and muscle.
Jose Cordoba Chacon
University of Illinois at Chicago
Read the Original
This page is a summary of: Hepatocyte-specific, PPARγ-regulated mechanisms to promote steatosis in adult mice, Journal of Endocrinology, October 2016, Bioscientifica,
DOI: 10.1530/joe-16-0447.
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