Excess fat in the heart may contribute to the two-to five-fold increased risk of heart failure in people with diabetes, a study has found. The heart is the most energy-hungry organ in the body. Just like a combustion engine burning fuel to power the pistons, healthy heart cells consume fuel molecules to create the necessary energy to keep the heart pumping. This essential energy production takes place inside mitochondria, the self-contained “powerplant” organelles inside cells. Although mitochondria in a healthy heart primarily use fatty acids as fuel, they can easily adapt to use other fuel molecules as needed, including glucose, lactate, and ketone bodies. Diabetes, however, reduces the heart muscle?s metabolic adaptability and causes heart cells to overuse fat as a metabolic fuel.

The study, published in the journal Circulation Research, found this cardiac lipid overload leads to numerous small, misshapen mitochondria that don’t produce energy as efficiently as normal mitochondria. “Diabetes, which affects almost 30 million Americans, significantly increases the risk of heart failure, and one of the cardinal manifestations of the hearts of people with diabetes is the tendency to overuse fat as a metabolic fuel, which ultimately leads to mitochondrial and cardiac damage,” said E Dale Abel, from the University of Iowa in the US. “We have demonstrated and detected how increasing the amount of fat (lipid) that the heart consumes leads to dramatic changes in the structure and function of the mitochondria in the heart,” Abel said. “These studies provide a new window into how these changes to mitochondria could occur in the lipid-overloaded heart,” he said. To investigate the consequences of cardiac lipid overload on mitochondria, the team used genetically modified mice that mimic the increased fatty acid uptake (lipid overload) that characterises diabetes. In the mouse model, lipid uptake to heart is doubled. This modest increase resulted in mitochondria that became thinner and more twisted than mitochondria in healthy heart cells. These structural changes (almost like a noodle snaking through the heart) lead to an appearance of mitochondrial fragmentation when imaged by conventional electron microscopy.

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The study also revealed the molecular cause of the change in mitochondrial structure. Prolonged lipid overload leads to increased levels of damaging substances called reactive oxygen species (ROS). The findings suggest that cardiac lipid overload disrupts normal mitochondrial structure, which may impair energy production and compromise heart function.

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