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U.S. study suggests excess fat in heart increases cardiac failure risks in diabetics

Xinhua,January 08, 2018 Adjust font size:

SAN FRANCISCO, Jan. 7 (Xinhua) -- People suffering diabetes run two- to five-fold risks of heart failure if they have excess fat in the heart, which harms the cells' essential ability to produce energy, a new study revealed.

Diabetes and obesity are often characterized with excess fat in the heart, which is the most energy-hungry organ in human body.

According to the study, conducted by researchers at the University of Iowa (UI) and published in the latest edition of journal Circulation Research, lipid overload in the heart causes numerous small, misshapen mitochondria that don't produce energy as efficiently as normal mitochondria.

Healthy heart cells, like a combustion engine, consume fuel molecules to create necessary energy to keep the heart pumping.

But diabetes reduces the heart muscle's metabolic adaptability and causes heart cells to overuse fat as a metabolic fuel, which ultimately leads to mitochondrial and cardiac damage.

"Diabetes, which affects almost 30 million Americans, significantly increases the risk of heart failure," said study leader E. Dale Abel, professor of internal medicine at the UI Carver College of Medicine.

Researchers have detected that increased amount of fat in the heart triggers dramatic changes in the structure and function of the mitochondria in the heart.

The findings said that prolonged lipid overload increases the levels of damaging substances called reactive oxygen species (ROS).

Excess ROS alters the activity of several important proteins that work to control the size and shape of mitochondria, thus disrupting the mitochondrial network, the study said.

It found that if ROS in normal heart cells is removed, mitochondria becomes four times as large as normal, indicating that ROS levels are inversely proportional to mitochondria size.

In conclusion, cardiac lipid overload, which disrupts normal mitochondrial structure, will damage energy production and heart function. Enditem