The soft and squishy fat rolls on a baby serve a significant purpose. They are an important depot for brown adipocytes—fat cells that burn energy to release heat—that help keep the baby warm. As babies grow up, they lose a majority of these brown fat stores. Adults have a higher proportion of white adipose tissue (WAT), which stores fat as energy reserves for the body. However, some cells embedded within WAT can burn fat; these cells that show brown adipocyte-like properties are called beige adipocytes.
Now, researchers have found that suppressing a protein in subcutaneous WAT confers the fat-burning properties of beige adipocytes. The results, published in the Journal of Clinical Investigation, reveal that mature adipocytes exhibit plasticity, and identify a pathway that could inform the development of therapies for obesity and metabolic diseases.
Inducing fat burning by converting other cell types into those that expend energy is not a new concept; researchers have previously coaxed stem cells to become energy-burning beige adipocytes for therapeutic purposes. “But what’s sort of been a stumbling block in the field is that [adult] stem cells are rare,” said Brian Feldman an academic pediatric endocrinologist at the University of California, San Francisco and coauthor of the study. In contrast, white adipocytes are easier to come by.
Feldman and his team previously found that the transcription factor Krüppel-like factor 15(KLF15) affects adipogenesis, the process by which stem cells create fat cells. To test whether KLF15 is involved in maintaining adipocytes, Feldman’s team measured its expression in fat isolated from various parts of the bodies of mice. They observed that WAT expressed higher levels of Klf15 compared to brown adipose tissue (BAT). Deleting Klf15 from white adipocytes isolated from mice induced the expression of genes associated with brown fat identity and function. These findings led the researchers to hypothesize that decreased Klf15 levels may be required for BAT to produce heat.
Cold exposure activates BAT, which results in heat production via a beta-adrenergic signaling pathway. When the researchers deleted Klf15 in white adipocytes from mice, they observed increased expression of the gene encoding beta-1 adrenergic receptor. Treating Klf15-deleted adipocytes with a beta-adrenergic stimulant enhanced the expression of brown fat-associated genes.
By Sneha Khedkar
Article can be accessed on: The Scientist