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Coordinating the circadian clock: Molecular pair controls time-keeping and fat metabolism
Date:4/6/2012

me, many of which are near genes involved in the production of fat. Another team member, histone deacetylase 3 (HDAC3), does construction work on the protein scaffold (the epigenome) surrounding the genome to dampen the activity of the fat-related genes.

During the night, the day shift molecules depart the liver genome, and fat production increases due to other regulatory molecules. The fat production is kept in check when the Rev-erb construction team returns to the genome the next day. However, if HDAC3 is absent, the cycles do not occur, and the liver fills with fat.

The absence of both Rev-erbs prevents HDAC3 from doing its job, since Rev-erbs serve as the shuttle delivering HDAC3 to target genes. Sure enough, fat accumulates in the liver to a much great extent when both Rev-erbs are missing compared to when one is still available.

"This work shows that if we want to manipulate the human clock we would likely need to affect both Rev-erb alpha and Rev-erb beta," explains Lazar. "Circadian rhythm of metabolism is important because disruption of this rhythm leads to a fatty liver. This may explain, in part, why altered circadian rhythms in people who do shift work is associated with metabolic disorders."


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Contact: Karen Kreeger
karen.kreeger@uphs.upenn.edu
215-349-5658
University of Pennsylvania School of Medicine
Source:Eurekalert

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