Brown adipose tissue is different from the white fat around human belly and thighs. Brown fat helps to turn calories into heat and it was once thought that only small animals like mice and newborns had brown fat but some adults retain it.
If some people have it, perhaps others can activate it also, and a study found a previously unknown built-in mechanism that switches it off shortly after being activated. Which means it doesn't help against obesity. A group discovered a protein responsible for this switching-off process called AC3-AT. Mice that genetically didn't have AC3-AT were protected from becoming obese, partly because their bodies were simply better at burning off calories and were able to increase their metabolic rates through activating brown fat.
The work involved two groups of mice that were fed a high-calorie diet for 15 weeks, which rendered them obese. The group that had their AC3-AT protein removed gained less weight than the control group and were metabolically healthier. They accumulated less fat and increased their lean mass when compared to the control mice.
Credit: Morten Mosin/University of Southern Denmark
Humans have brown fat also but it decreases as we age. Adults don't have as much brown fat as newborns but it can still be activated, like during cold exposure, and hen it gets activated, it enhances the rate of metabolism of these individuals, which may help to stabilize weight loss in individuals with poor impulse control, like Ozempic when it is used off-label to replace dieting for rich people.
AC3-AT, a shorter, previously unknown form of the AC3 protein, was not the only reveal. The researchers also identified other unknown protein/gene versions that respond to cold exposure, similar to AC3-AT, but that is a grant for another time.
Citation: Sajjad Khani, Hande Topel, Ronja Kardinal et al; Cold-induced expression of a truncated Adenylyl Cyclase 3 acts as rheostat to brown fat function; Nature Metabolism
DOI: 10.1038/s42255-024-01033-8
Brown Fat’s “Off-Switch” Isn't A New Ozempic Diet Exploit
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