Olive oil may help diseased heart muscle process and use fuel

Posted by AFN Staff Writers on 6th October 2014
Olive oil may help diseased heart muscle process and use fuel
Olive oil may help diseased heart muscle process and use fuel

Oleate, a common dietary fat found in olive oil, may restore proper metabolism of fuel in heart cells, according to research from the Chicago College of Medicine at the University of Illinois.

The findings, reported in the journal Circulation in September 2014, showed that oleate restored proper metabolism of fuel in heart cells in animals.

Study method

The researchers looked at how healthy and failing hearts beating in rats reacted to being supplied with either oleate or palmitate, a fat associated with the Western diet and found in dairy products, animal fats and palm oil.

Dr E. Douglas Lewandowski, director of the UIC Center for Cardiovascular Research and senior and corresponding author on the study, said that when the researchers perfused failing rat hearts with oleate, they saw an “immediate improvement in how the hearts contracted and pumped blood”.

Dr Lewandowski and colleagues tracked the location of fat molecules in the cells of the diseased hearts by tagging them with a nonradioactive heavy isotope of carbon, which is detected using magnetic resonance spectroscopy. This technology allows researchers to watch biochemical reactions, like metabolism, as they occur in real-time in functioning organs. Using this technique, Dr Lewandowski noticed that the metabolism of fats within the cardiac cells of these hearts became normalised.

In contrast, when the researchers perfused the diseased hearts with palmitate, fat metabolism was imbalanced, and cells struggled to access fuel. There was also a rise in toxic fatty byproducts — another consequence of dysregulated or impaired fat metabolism.

Oleate also activated genes for metabolising fat

In addition to balancing fat metabolism and reducing toxic fat metabolites in hypertrophic hearts, Dr Lewandowski said, oleate also increased the activation of several genes for enzymes that metabolise fat.

“These genes are often suppressed in hypertrophic hearts,” Dr Lewandowski said. “So the fact that we can restore beneficial gene expression, as well as more balanced fat metabolism, plus reduce toxic fat metabolites, just by supplying hearts with oleate – a common dietary fat — is a very exciting finding,” he said.

“This gives more proof to the idea that consuming healthy fats like oleate can have a significantly positive effect on cardiac health,” Dr Lewandowski said.

Heart health in the US and Australia

Heart failure affects nearly 5 million Americans, and more than half a million new cases are diagnosed each year. Heart failure is not the same as having a heart attack — it is a chronic disease state where the heart becomes enlarged, or hypertrophic, in response to chronic high blood pressure which requires it to work harder to pump blood. As the heart walls grow thick, the volume of blood pumped out diminishes and can no longer supply the body with enough nutrients.

Failing hearts are also unable to properly process or store the fats they use for fuel, which are contained within tiny droplets called lipid bodies in heart muscle cells. The inability to use fats, the heart’s primary fuel source, causes the muscle to become starved for energy. Fats failing hearts manage to metabolise break down into toxic intermediary by-products that further contribute to heart disease.

In Australia, cardiovascular disease (CVD) is the leading cause of death, with 43,946 deaths attributed to CVD in Australia in 2012. Cardiovascular disease kills one Australian every 12 minutes.  According to the National Heart Foundation, cardiovascular disease is one of Australia’s largest health problems. Despite improvements over the last few decades, it remains one of the biggest health burdens on the Australian economy.

Coronary heart disease or heart disease affects around 1.4 million Australians, and claimed the lives of 20,046 Australians (13 per cent of all deaths) in 2012.

UIC College of Medicine Medical Scientist Training Program student Ryan Lahey is the lead author on the University of Illinois paper. Postdoctoral fellow Andrew Carley, and Xuerong Wang, research specialist, were co-authors.

The research was supported by the US National Heart, Lung and Blood Institute grants R37 HL40244 and RO1 HL62702 and American Heart Association Predoctoral Fellowship grant 12PRE1178002.