In a world where heart disease continues to rank as the top cause of death, scientists are urgently searching for ways to prevent it—especially among people facing obesity. Now, new research points to a powerful discovery in the heart’s metabolism that could one day change how we treat or even prevent heart failure triggered by high-fat diets.
A team led by scientists at the Masonic Medical Research Institute (MMRI) has identified a key enzyme in heart cells that, when removed, protects against heart damage caused by unhealthy eating. Their study, recently published in Science Signaling, focuses on a protein called PTP1B. This molecule is known to interfere with insulin signaling in the brain, muscle, and fat tissue—especially in people who are obese or diabetic. But now, its role in the heart is coming into focus.
A Shift in Heart Metabolism
Under normal conditions, heart cells—known as cardiomyocytes—burn fat to fuel the constant work of pumping blood. This process, called fatty acid oxidation, keeps the heart strong and energy-efficient. However, when exposed to the stress of a high-fat diet, the heart begins to change how it gets its energy. Instead of burning fat, it starts relying more heavily on sugar.
That switch may sound harmless, but it isn’t. This shift in energy sources leads to the buildup of fat inside heart cells, damaging their mitochondria—the energy factories of the cell. Over time, these changes can trigger cardiomyopathy, a condition where the heart thickens, becomes stiff, and struggles to pump blood.
Blocking a Dangerous Enzyme
To test whether blocking PTP1B could stop these dangerous changes, the scientists created a special group of mice. In these animals, PTP1B was removed only from heart cells. These mice, referred to as PTP1Bfl/fl::αMHCCre/+, looked perfectly normal at first. Their hearts worked just like any other mouse’s.
But things changed when the animals were fed a high-fat diet. While regular mice developed signs of heart trouble—thickened heart walls, weakened pumping, fat buildup, and mitochondrial breakdown—the mice lacking PTP1B in their heart cells stayed healthy. Their heart structure remained normal, and their cells continued burning fat efficiently.
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“We found that targeting PTP1B in the heart blocks a harmful shift in metabolism caused by poor diet,” said Dr. Maria I. Kontaridis, senior author of the study and chair of biomedical research at MMRI. “By preserving fatty acid oxidation and preventing excessive lipid accumulation, we can protect against heart disease progression in at-risk populations.”
Finding the Molecular Pathway
The scientists didn’t stop there. They used metabolomics and phosphoproteomics—powerful tools that track chemicals and protein changes in cells—to understand how deleting PTP1B worked. What they found was a clear pattern: heart cells without PTP1B kept using fat as their primary fuel. These cells had stronger signals from two important enzymes—PKM2 and AMPK. These enzymes help boost fatty acid burning while holding back fat creation and sugar use.
“PTP1B acts like a metabolic switch that pushes the heart toward glucose dependence during stress, which may worsen cardiac outcomes,” explained Dr. Yan Sun, a postdoctoral fellow at MMRI and first author of the study. “Disabling this switch allows the heart to remain metabolically flexible and resilient.”
That flexibility could be key to long-term heart health. When the heart can keep using fat, even under stress, it avoids the damaging effects of sugar overload and lipid buildup. The results suggest that people who are obese or who eat high-fat diets might one day benefit from drugs that target PTP1B directly in the heart.
A Growing Public Health Concern
The discovery comes at a critical time. The World Health Organization predicts that by 2030, half of all Americans could be considered obese. Children are especially at risk, with early exposure to poor diets laying the groundwork for serious health problems later in life.
In obesity, the body’s ability to respond to insulin becomes weaker, increasing the risk of diabetes and heart disease. Since PTP1B is already known to block insulin signals in several tissues, its role in the heart suggests it could be a common link in many health problems.
By finding ways to turn off PTP1B specifically in heart cells, researchers hope to interrupt this harmful chain reaction. “This research lays the foundation for potential new therapies that can help prevent heart failure in people dealing with obesity,” said Dr. Kontaridis. “More work is needed, but we’re hopeful this path could lead to real change.”
Looking Ahead
While this study was conducted in mice, the results open a door to future studies in people. If researchers can create safe treatments that block PTP1B in human hearts, doctors might one day prevent heart failure before it begins.
The team is already exploring the next steps, hoping to turn this research into therapies that could improve life for millions. With obesity on the rise and heart disease still leading the charts, the need has never been greater.
Note: The article above provided above by The Brighter Side of News.
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