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Protein That Transport Fat to Heart Might Help to Protect It from Aging

by VR Sreeraman on November 4, 2007 at 1:25 PM
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Protein That Transport Fat to Heart Might Help to Protect It from Aging

A study has shown that a protein responsible for transporting fat into the heart might protect the organ from aging.

A young healthy heart normally uses a balance of fat and sugar to generate energy to allow the heart to beat and pump blood efficiently. However, as the heart ages, the ability to use fat as an energy source deteriorates, which compromises heart function in the elderly.

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The University of Alberta study, conducted by Jason Dyck and his research team, revealed that at a time when the heart is using less fat for energy, a protein responsible for transporting fat into the contractile cells of the heart actually increases.

Therefore, the researchers proposed that the mismatch between fat uptake and fat use in the heart could lead to an accumulation of fat in the heart resulting in an age-related decrease in heart function.
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In the elderly, an age-related decline in heart function is a risk factor for heart disease. Alterations in the types of fuels the heart uses to produce energy contribute to a progressive age-related decline in heart function.

In the research, various types of fuels used by the heart in young and aged mice were studied.

The researchers used a genetically engineered mouse that was deficient in a protein, which was responsible for transporting fat into the cells of the heart. They studied these mice as they aged.

The genetically altered mice were mainly given sugar as a fuel source because they lacked the protein that allowed them to use fat as a primary fuel source.

In the finding, Dyke showed that old genetically modified mice did not accumulate fat in their hearts, as did ordinary mice.

Additionally, the team showed that the old genetically altered mice out-performed ordinary old mice on a treadmill test, were completely protected from age-related decline in heart function, and in many ways their hearts looked and performed like hearts from a young mouse.

Dyck hopes that the finding, which holds great promise for human beings, might lead to the development of medications that inhibit the uptake of fatty acids into the heart and prevent and/or reverse the effects of aging on the heart muscle.

The study is published in Circulation.

Source: ANI
SRM /B
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