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High-fat diet and lack of enzyme can lead to heart disease in mice
Date:9/12/2011

f Texas Southwestern Medical Center showed that if HDAC3 were deleted in heart tissue in the middle of embryonic development, the animals developed severe thickening of the heart walls (hypertrophic cardiomyopathy) that reduces the organ's pumping efficiency. These animals usually died within months of birth.

Lazar and his team wanted to know what would happen if the gene was inactivated in heart tissue after birth. To their surprise, they found that these animals were essentially normal.

On a diet of regular chow, the engineered mice lived as long as their normal littermates, although they did tend to accumulate fat in their heart tissue. On a high-fat diet, however, these animals deteriorated rapidly, dying within a few months of hypertrophic cardiomyopathy and heart failure.

To understand why, Lazar's team compared the gene expression patterns of young mutant mice to their normal siblings. They found that the mutant mice tended to underexpress genes important in fat metabolism and energy production. Essentially, on a high-fat diet, these animals' hearts cannot generate enough energy and thus cannot pump blood efficiently.

According to Lazar, this study identifies an "interesting and dramatic example" of the link between diet and epigenetics. Now his team is working to identify the molecular nature of that link. They are also investigating whether the same pathway and interaction occurs in humans since it may contribute to the increased heart disease associated with Western diets.

Whatever the outcome of those studies, says Lazar, there is one sure-fire intervention people can always use to stave off the ravages of over-nutrition: Changing your diet. "We don't want to forget that that's still a noble thing to strive for," he says.


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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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