# Scientists Found a Way to Make Fat Cells "Ignite"

Scientists from Weill Cornell Medical College have established that the AAC enzyme promotes the destruction of white fat cells with heat release - essentially triggering a process of their "self-ignition." The results of the preclinical study have been published in the journal Nature Metabolism (NatMet).

The focus is on white adipocytes - cells that accumulate fat and significantly increase in number during obesity. Unlike brown fat, which is inherently adapted for heat production, white adipose tissue was primarily considered an energy "warehouse."

Researchers discovered that when the natural process of lipolysis - fat breakdown - is activated, uncoupling of oxidative phosphorylation can occur in the mitochondria (energy stations) of white adipocytes. Normally, mitochondria convert fats and sugars into ATP molecules - the universal "energy currency" of the cell, with some energy being released as heat. However, during uncoupling, energy is almost entirely dissipated as heat rather than being stored.

A key role in this mechanism is played by the interaction of released fatty acids with the AAC enzyme (acyl carrier protein) - a "relative" of proteins responsible for thermogenesis in brown fat. Previously, it was believed that such a mechanism in white adipocytes had no significant effect.

Experiments on obese mice showed that activation of thermolipolysis led to increased body temperature and higher energy expenditure even when brown fat activity and muscle shivering were suppressed. Over time, this effect should contribute to weight loss.

The authors emphasize that this new approach could complement existing weight loss medications, which primarily suppress appetite and often cause side effects. In the future, targeted stimulation of thermogenesis in white fat cells could become a safer way to combat obesity.