It has long been known that weight gain can lead to high blood pressure. However, the biological mechanism behind this link has remained unclear until now.
In this regard, a team from Rockefeller University in New York studied the effect of a specific type of fat tissue, called beige fat, on blood pressure regulation. This fat, similar to brown fat in humans, helps the body burn energy and convert food into heat, and it is activated when exposed to cold, thus contributing to body warmth. It is typically found in the neck, upper back, and around the kidneys and spinal cord.
The study showed that the loss of beige fat in genetically modified mice made their blood vessels more sensitive to pressure signals, leading to high blood pressure. Researchers found that the fat surrounding the blood vessels began to convert to white fat, which secretes hormones such as angiotensinogen, known to raise blood pressure.
Early signs of heart damage also appeared, including the accumulation of hardened connective tissue around blood vessels, which reduces their elasticity and impairs their normal expansion and contraction. Single-cell analysis revealed that the absence of beige lipids triggers a genetic program that promotes fibrous tissue formation, forcing the heart to pump blood with greater force.
The researchers confirmed that fat cells lacking beige fat produce an enzyme called QSOX1, which triggers a cascade of reactions leading to high blood pressure, while beige fat normally inhibits the production of this enzyme. The team also noted that patients with mutations in the PDM16 gene—responsible for activating QSOX1 in mice—also tend to have high blood pressure, suggesting that the findings may apply to humans.
Dr. Paul Cohen, the study's lead author, said: "The more we understand these molecular links, the closer we get to developing treatments tailored to each individual's medical and molecular characteristics."
