Insulin and leptin are two hormones that regulate glucose metabolism, satiety and starvation. Researchers at Monash University have found that these hormones activate "satisfying" neurons in the hypothalamus of mice, causing white fat to turn into brown fat.

Recently, scientists have found that insulin and leptin act on specific neurons in the hypothalamus of mice, promoting the browning of white fat.

White energy that stores energy can be converted to metabolically active beige fat through browning, and people have been trying to understand the specific mechanisms behind this process. Insulin and leptin are two hormones that regulate glucose metabolism, satiety and starvation. Researchers at Monash University have found that these hormones activate "satisfying" neurons in the hypothalamus of mice, causing white fat to turn into brown fat. The study was published in the January 15 issue of Cell.

Appetite-promoting POMC (proopiomelanocortin) neurons in the hypothalamus control the energy balance in the body based on satiety signals in the blood. "The new finding in this study is that stimulating browning of white fat is a way for POMC neurons to promote calorie burning," commented Dr. Yang Xiaoyong of Yale University (he did not participate in the study).

At present, the difference between beige fat and brown fat is not clear, but beige fat is usually referred to as metabolically active fat in white adipose tissue. Both beige and brown fats burn calories, so understanding the browning mechanism of white fat is critical. Studies have shown that insulin and leptin can promote browning of white fat through the brain, said Tony Tiganis of Monash University.

When the blood sugar rises, the pancreas produces insulin, which is produced by white fat. These two hormones can send signals to the brain to regulate satiety and weight. To analyze the association of this control system with adipose tissue, Garron Dodd et al. of Tiganis Laboratories knocked out specific phosphatases in mouse POMC neurons. These two phosphatases act in the hypothalamus, affecting glucose metabolism and body weight by regulating leptin or insulin signaling, respectively. The researchers found that mice that knocked out both phosphatases had less white adipose tissue and higher levels of insulin and leptin signaling.

"These phosphatases in POMC neurons control the sensitivity of leptin and insulin receptors," Dodd said. Simultaneous knockdown of both enzymes increases the beige and brown fat of the mice, which do not gain weight when eating a high-fat diet. This suggests that leptin and insulin signaling are important for controlling body weight and fat metabolism.

The researchers injected leptin and insulin directly into the hypothalamus of wild-type mice, successfully promoting browning of white fat. However, if the nerve connection between the brain and white fat is cut off when the hormone is injected, browning will not occur, and only the fat that is in contact with the brain can be browned. "It can be seen that the direct innervation of the brain is a necessary condition for browning, and the two hormones work together to regulate energy consumption," Tiganis said.

There is another neuron in the hypothalamus, "starved" neurons or AgRP neurons. These neurons are activated by a starvation signal that promotes energy storage. Dr. Yang Xiaoyong had previously discovered that fasting activates AgRP neurons and inhibits browning of white fat. "These two studies are complementary and together reveal a complete system: hunger and satiety neurons control the browning of fat based on the energy state of the body," Dr. Yang Xiaoyong said.

Whether these results are applicable to humans remains to be further studied. It is currently known that the levels of two phosphatases in the hypothalamus of obese patients are higher.

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