The makeup and functioning of this tissue changes 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 central role of adipose tissue dysfunction in disease and the incredible plasticity of fat tissue supports the promise of modulating fat tissue phenotypes for therapeutic purposes,” write the authors, led by Claudio J. Villanueva from the College of Life Sciences/David Geffen School of Medicine and Patrick Seale from Perelman School of Medicine at the University of Pennsylvania. “Many questions and opportunities for future discovery remain, which will yield new insights into adipose tissue biology and hopefully lead to improved therapies for human disease.”
Research reported in this publication was supported by NIDDK at the National Institutes of Health, the UCLA Life Sciences Fund, and the UCLA Graduate Council Diversity Fellowship. The authors declare no competing interests.
Image Caption: The hallmarks of adipose tissue dysfunction
Image Credit: Sakers et al./Cell Licence BY-SA
