Disruptions in signalling mechanisms within fat cells may boost cell death in the enlarged hearts of these oversized rodents, researchers say. They speculate that similar effects may be at play in obese humans suffering from heart failure.

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Route for potential therapies
The finding "suggests a biological route for potential therapies that could block or reverse obesity's harmful effects on the heart," lead investigator Dr Lili Barouch, cardiologist and an assistant professor at Johns Hopkins University School of Medicine and its Heart Institute, said in a prepared statement.

She and her colleagues studied heart muscle enlargement in more than 20 mice. Some of the mice were normal and some were bred for obesity linked to changes in the amount and function of the hormone leptin, which is made by fat cells and regulates appetite and energy balance.

Normally, when an animal is full, fat cells release greater quantities of leptin to signal that the animal should stop eating. However, this signal becomes blocked in obese animals.

Tissue samples compared
The Hopkins team compared heart tissue samples from the normal mice and the obese mice. The samples revealed that when leptin signalling was disrupted in the mice, their hearts became enlarged and cardiac levels of programmed cell death - a natural process technically known as apoptosis - was boosted by more than 10 times above normal levels.

When leptin levels and function were restored, however, apoptosis levels returned to near normal, the researchers report.

The study was presented Tuesday at the American College of Cardiology scientific sessions in Orlando, Florida. – (HealthDayNews)
 

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