In mice, fat cells show increased activity of YAP/TAZ proteins when they are fed again after fasting or when fed a high-fat diet, and this activity is linked to changes in leptin levels, a hormone...

In mice with a specific genetic change that causes fat loss, the absence of the hormone leptin leads to high blood sugar, high insulin levels, and fat accumulation in the liver, even when energy use remains normal.

In mice, turning on the YAP/TAZ proteins in fat cells causes those cells to lose their fat content and revert to a less mature state, while also raising leptin levels in the blood without changing the amount of fat tissue, which helps avoid metabolic problems typically seen in fat tissue deficiency.

Two proteins, YAP and TAZ, attach to a specific DNA region far upstream of the leptin gene in both mice and humans, and this attachment is required for the gene to produce more leptin, even when fat tissue levels change.

In mice, activating two specific proteins (YAP/TAZ) only in fat cells leads to higher energy use and increased breakdown of fats in the liver, which stops fat from building up in the wrong places and prevents impaired glucose processing, even when most body fat is lost.

Obese mice eat less after fasting than lean mice—even when given their favorite food—and this isn’t just because they’re heavier; it’s linked to higher levels of the fat hormone leptin.