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A study indicates that “brown adipose tissue” in the body might aid in regulating blood pressure by counteracting the actions of a certain enzyme.(Image credit: San Francisco Chronicle / Hearst Newspapers / Contributor via Getty Images)ShareShare by:
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Not all fat is the same — a study in mice suggests that while one form of fat in the body elevates blood pressure, another assists in maintaining it.
In humans, an overabundance of body fat has for a long time been correlated with elevated blood pressure, also known as hypertension, and several other heart-related complications. However, the body contains two varieties of fat: “brown” fat, which expends energy and aids in body temperature regulation, and “white” fat, which stores extra calories.
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“We were aiming to better understand how brown fat could possibly accomplish this,” Cohen shared with Live Science.
Currently, in a recent study featured on Jan. 15 in the journal Science, Cohen and his team revealed that eliminating the gene responsible for producing “beige” fat — the murine equivalent of adult human brown fat — transformed every instance of beige fat surrounding blood vessels into white fat. This, in turn, led to the development of hypertension in the mice.
The team correlated the effect to an enzyme secreted by fat cells. Normally regulated by beige fat cells, the enzyme’s levels spiked once beige fat was converted to white fat, as demonstrated by the study. This instigated excessive contraction of blood vessels and consequently higher blood pressure.
Lawrence Kazak, an associate professor at McGill University who researches the energy consumption of brown fat and was not involved in the study, noted that this is a significant study that, for the first time, determines how beige fat directly impacts cardiovascular well-being.
Kazak informed Live Science that it’s extensively documented that obesity influences blood pressure and cardiometabolic health at the system level. However, this research highlights a “specialized function” for beige fat and the mechanism underpinning its “localized effects” on blood vessels, he stated.
How fat controls blood pressure
Cohen’s team initiated their study by removing the Prdm16 gene from the fat cells in lab mice, thereby transforming the beige fat surrounding their blood vessels into white fat. This gene is recognized for its high activity in beige fat, serving as a master control that enables them to uphold an energy-burning function as opposed to becoming white fat.
First study author Mascha Koenen, a postdoctoral fellow at Cohen’s lab, stated that this alteration was visually discernible in the tissue. Tissue rich with beige fat, which typically appears dusky and dotted with tiny droplets, became pale, resembling common white fat.
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The researchers observed that the animals lacking beige fat also exhibited greater blood pressure, and their blood vessels became less pliable and contained more fibrous tissue, making it more challenging for them to relax as blood circulated.
The team subsequently treated the mice’s blood vessels with a hormone known as angiotensin II, which is recognized for increasing blood pressure by constricting arteries, akin to restricting water flow by squeezing a hose. Blood vessels originating from mice lacking beige fat showed a more intense constriction in reaction to the hormone, in comparison to vessels from normal mice.
To ascertain the mechanism responsible for this, the team examined molecular signals emitted by fat cells in proximity to the blood vessels and discovered an enzyme referred to as QSOX1. This enzyme stiffens the connective tissue surrounding blood vessels, complicating their relaxation.
Ordinarily, the protein encoded by the Prdm16 gene maintains the control of this enzyme’s production. However, in the absence of beige fat, the levels of QSOX1 surge, resulting in rigid blood vessels and elevated blood pressure, the team concluded.
Notably, the researchers discovered that eliminating both beige fat and QSOX1 from mice averted this chain reaction, and these mice did not develop high blood pressure, implying that QSOX1 is essential for initiating this mechanism, they inferred.
Beige fat in mice, as well as brown fat in humans, are recognized for their heat generation capabilities; they possess a high concentration of mitochondria, which are the cells’ energy-producing units and give the tissue its distinctive brown hue. However, Koenen indicated that this heat production function is not linked to the QSOX1 mechanism they characterized. Instead, their study underscores an additional function of beige fat as “secretory” cells, which discharge key proteins into the bloodstream.
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Koenen shared with Live Science that even if the beige fat cells are minute, “they can exert this substantial impact on whole-body physiology.” Furthermore, the study might pave the way for novel approaches to address high blood pressure.
Kazak proposed that “You might imagine that molecules capable of inhibiting QSOX1 could potentially offer therapeutic benefits.”
Cohen also holds the belief that targeting QSOX1 could enable scientists to devise precision therapies for hypertension in the times ahead. To achieve this, they would initially need to gain a more profound understanding of this mechanism to counteract it, he pointed out. Be that as it may, the research identifies a “pathway forward” for examining the consequences of QSOX1 inhibitors in humans.
Article Sources
Koenen, M., Becher, T., Pagano, G., Del Gaudio, I., Barrero, J. A., Montezano, A. C., Ruiz Ortiz, J., Lin, Z., Gómez-Banoy, N., Amblard, R., Schriever, D., Kars, M. E., Rubinelli, L., Halix, S. J., Huang Cao, Z. F., Zeng, X., Butler, S. D., Itan, Y., Touyz, R. M., … Cohen, P. (2026). Ablation of Prdm16 and beige fat identity causes vascular remodeling and elevated blood pressure. Science, 391(6782), 306–313. https://doi.org/10.1126/science.ady8644
Zunnash KhanLive Science Contributor
Zunnash Khan is a mechatronics engineer and a science journalist from Pakistan. She has written for Science, The Scientist and Brainfacts.org, among other outlets.
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