Researchers say the disappearance of a beneficial form of body fat activates a genetic pathway that stiffens arteries and raises blood pressure, offering a new explanation for obesity-related cardiovascular disease.
By yourNEWS Media Newsroom
Scientists have identified a critical biological mechanism explaining why obesity so often leads to high blood pressure, tracing the problem not to excess fat in general but to the loss of a specific, protective type known as beige fat. The research, conducted at The Rockefeller University and published in the journal Science, shows that the disappearance of beige fat activates a genetic program that stiffens blood vessels and drives hypertension.
Doctors have long observed a strong link between obesity and high blood pressure, a major risk factor for heart attacks and strokes, but the underlying biology remained unclear. “We’ve known for a really long time that obesity raises the risk of hypertension and cardiovascular disease, but the underlying biology has never been fully understood,” said Dr. Paul Cohen, who led the research team. The new findings suggest that maintaining beige fat may be central to protecting vascular health.
Unlike white fat, which primarily stores energy, beige fat is metabolically active and burns calories to generate heat, a process known as thermogenesis. Humans are born with brown fat, a closely related tissue that helps regulate body temperature in infancy, while beige fat can develop later in life through factors such as cold exposure and physical activity. Previous studies suggested people with more thermogenic fat tend to have lower blood pressure, but those observations did not establish a direct cause-and-effect relationship.
To test whether beige fat itself plays a protective role, researchers engineered mice that were otherwise healthy but lacked the ability to form beige fat. “We wanted the only difference to be whether the fat cells in the mouse were white or beige,” said study co-author Mascha Koenen. “In that way, the engineered mice represent a healthy individual who just happens to not have brown fat.” The results were striking: the mice developed high blood pressure and early signs of heart damage.
Further investigation showed that the fat surrounding the animals’ blood vessels began behaving like white fat, producing a precursor to a hormone known to raise blood pressure. At the same time, the arteries themselves became abnormally sensitive to pressure. Researchers found that the loss of beige fat activated genes involved in fibrosis, a process in which stiff, fibrous tissue accumulates around blood vessels, reducing their flexibility and forcing the heart to work harder.
At the center of this process was an enzyme called QSOX1. In healthy conditions, beige fat suppresses the activity of QSOX1. When beige fat was absent, levels of the enzyme rose sharply. To confirm its role, the team created mice lacking both beige fat and QSOX1. Those animals did not develop arterial stiffness or hypertension, identifying the enzyme as a key driver of the damage.
Evidence suggests the findings may extend to humans. The researchers noted that people with mutations in the PRDM16 gene, which in mice leads to activation of QSOX1 when beige fat is lost, tend to have higher blood pressure in existing clinical data. That genetic overlap strengthens the relevance of the mouse findings to human cardiovascular disease.
The study reframes body fat as a complex organ with distinct functions rather than a uniform health risk. Cohen said the work could pave the way for more precise treatments. “The more we know about these molecular links, the more we can move towards conceiving of a world where we can recommend targeted therapies based on an individual’s medical and molecular characteristics,” he said.
Researchers say the findings point to the possibility of therapies aimed at preserving or activating beige fat, rather than simply reducing body weight overall. Such approaches could eventually allow doctors to tailor hypertension treatment based on the biological characteristics of a patient’s fat tissue, offering a more targeted strategy in the fight against cardiovascular disease.
Source: Natural News
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