Scientists find a drug (currently used) to turn white fat to brown
It seems like we’ve been on a weight loss campaign here at the labs, but there just has been so much new and interesting research on the subject to report on; this is no exception. Researchers have uncovered the mechanism by which white fat cells from humans (an important distinction) gets reprogrammed to become browner.
White adipose tissue stores excess calories as fat that can be released for use in other organs during fasting. Mammals also have small amounts of brown adipose tissue, which primarily acts as an effective fat burner for the production of heat.
Browning of white adipose tissue increases the energy consumption of the body and therefore constitutes a potential strategy for future treatment of obesity. The challenge is to reprogram the energy storing white fat cells into so-called “brite” (brown-in-white) fat cells in the body’s white adipose tissue and thus make adipose tissue burn off excess energy as heat instead of storing it.
“We have investigated how the genome of white adipocytes is reprogrammed during browning using advanced genome sequencing technologies. We stimulated browning in human white adipocytes by a drug used to treat type II diabetes and compared white and “brite” fat cells.”
“This showed that “brite” fat cells have distinct gene programs which, when active, make these cells particularly energy-consuming,” says Susanne Mandrup, lead researcher.
“By identifying the areas of the genome that are directly involved in the reprogramming, we have also identified an important factor in the process – the gene regulatory protein KLF11 (Kruppel Like Factor-11), which is found in all fat cells, and we have shown that it is required for the reprogramming to take place.”
The authors mention that the work has been long, but the results are very promising.
“It has been a long process, and it has taken us four years to get where we are now, so it’s obviously very satisfying when the results are so interesting and useful, as is the case here,” says Anne Loft and points to the future prospects of the research on “brite” fat cells.
“The discovery of the “brite” fat cell mechanisms and the specific regulatory areas brings us closer to understanding how reprogramming of white fat cells takes place.”
“This knowledge potentially means, that in the future we can target drugs to activate the genomic regions and browning factors like KLF11 in the treatment of obesity,” says Anne Loft, first author of the paper.
One thing to mention however, despite brown fat burning more calories than white fat, this does not mean we could eat nonstop. Even if we only had brown fat, we would still have to contend with a limit. Since the drugs they used were already used to treat people currently, if further (see: large) research is just as promising we could start seeing this obesity treatment being used clinically very soon (relatively speaking mind you).
Anne Loft, Isabel Forss, Majken Storm Siersbæk, Søren Fisker Schmidt, Ann-Sofie Bøgh Larsen, Jesper Grud Skat Madsen, Didier F. Pisani, Ronni Nielsen, Mads Malik Aagaard, Angela Mathison, Matt J. Neville, Raul Urrutia, Fredrik Karpe, Ez-Zoubir Amri, & Susanne Mandrup (2014). Browning of human adipocytes requires KLF11 and reprogramming of PPARγ superenhancers Genes & Development : 10.1101/gad.250829.114