A genetic variant at the fatty acid-binding protein aP2 locus reduces the risk for hypertriglyceride

Proceedings of the National Academy of Science (U.S.A.) – May, 2006:

Mice with aP2 deficiency are partially resistant to obesity-induced insulin resistance and type 2 diabetes, have lower circulating triglycerides, and exhibit marked protection against atherosclerosis. Here, we demonstrate a functionally significant genetic variation at the aP2 locus in humans that results in decreased adipose tissue aP2 expression due to alteration of the CAAT box/enhancer-binding protein binding and reduced transcriptional activity of the aP2 promoter.

Boo yah. Shoot me up with a retroviral baby.

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1 Comment »

  1. Nudecybot said

    Hey you’re blogging again! Very cool.

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