Obesity is known to cause cardiometabolic diseases like high blood pressure and diabetes.
In a new study from the University of Pennsylvania, researchers found attributing these diseases to merely an overabundance of fat is a simplification.
On a basic level, fat acts as a receptacle to store energy, but upon a closer look, it is an essential actor in vital bodily processes like the immune response, the regulation of insulin sensitivity, and maintenance of body temperature.
Researchers argue that the negative health effects of obesity stem not simply from an excess of fat but from the decline in its ability to respond to changes, or in other words, its plasticity.
The makeup and functioning of this tissue change in response to weight fluctuations and aging. As fat declines in plasticity due to aging and obesity, it loses its ability to respond to bodily cues.
In the current model of this phenomenon, the rapid growth of adipose tissue outpaces its blood supply, depriving the fat cells of oxygen and causing the accumulation of cells that no longer divide.
This leads to insulin resistance, inflammation, and cell death accompanied by the uncontrolled spill of lipids from these cells.
The team says the central role of fat dysfunction in disease and the incredible plasticity of fat tissue supports the promise of modulating fat tissue phenotypes for therapeutic purposes.
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The study is published in Cell and was conducted by Claudio J. Villanueva et al.
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