What Role Does PTP1B Play in Heart Damage From Obesity?

Scientists have discovered that PTP1B, a single enzyme in heart cells, plays a central role in how obesity and high-fat diets can damage the heart. This new understanding could offer new hope in preventing heart failure.

Normally, the heart relies on burning fat for energy, a process called fatty acid oxidation. This keeps the heart strong and efficient, even under daily stress.

PTP1B: The Metabolic Switch in Heart Cells

PTP1B (protein tyrosine phosphatase 1B) acts like a metabolic switch. In obesity or high-fat diet conditions, this enzyme nudges the heart away from burning fat and toward burning sugar (glucose) instead. Though sugar is a quick energy source, the heart isn't designed to depend on it for long.

Over time, this shift pushes fat to build up inside heart cells. Excess fat disrupts the cell's mitochondria, the power plants of the heart, leading to weakened pumping action and setting the stage for cardiomyopathy.

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Blocking PTP1B in heart cells allowed mice to maintain healthy fatty acid metabolism even on a high-fat diet, avoiding typical signs of heart failure seen in regular mice.

Consequences: From Fatty Build-Up to Heart Failure

When the heart leans on sugar as its main fuel, it invites trouble. The research showed that mice with normal PTP1B developed thick heart walls, stiff pumping, and fat accumulation in their heart tissue after indulging in a high-fat diet. Their cellular engines started to fail.

The presence of PTP1B makes the heart less flexible. It cuts off healthy fat-burning pathways and causes damaging metabolic changes that worsen with obesity and poor diet.

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Blocking PTP1B Protects the Heart

To test the idea, scientists removed PTP1B only from heart cells in a special group of mice. These animals remained healthy even when fed fatty diets. Their hearts kept efficiently burning fat, showing no signs of thickening or weakness.

Investigators mapped the molecular changes and found that without PTP1B, two key enzymes (PKM2 and AMPK) stayed active, supporting ongoing fat metabolism and muscular health. This preserved the heart’s ability to adapt to stress and protect itself from fat-induced injury.

Potential for New Therapy

Targeting PTP1B in the heart could offer a way to stop or slow down heart failure in people with obesity or those at high risk. While this discovery comes from animal studies, researchers are optimistic. Developing medications that safely block PTP1B in human hearts may provide a breakthrough in keeping hearts healthy in a world where high-fat diets and obesity are common.