Identification of brain function that causes irresistible food temptation

The best way to lose weight is to eat less rice. But it’s really hard to resist the temptation to eat. Can you stop the craving for eating in your brain?

The working process of nerve cells in the brain that causes overeating has been identified. It is expected that it will become a clue to the development of new drugs to prevent overeating or obesity.

Researchers at the University of Cologne, Germany, found that ‘AgRP (agouti-related peptide neurons)’ in the brain hypothalamus regulates the secretion of lysophospholipid (LPA), and LPA once more regulates the neurons of the cerebral cortex, They found that it stimulates the person to eat food by making them feel hungry.

In this process, an enzyme called autotaxin that makes LPA was found to play a key role in regulating the signaling pathway. AgRP controls the amount of a substance called lysophosphatidylcholine (LPC) in the blood, and LPC delivered to the brain is converted into LPA by autotaxin and activated at the synapse.

The research team confirmed this process in model mice, in which an increase in LPC in the blood leads to LPA stimulation in the brain, leading to food cravings. Autotaxin-inhibited model mice did not increase food intake following fasting. Obese rats who continued to receive autotaxin inhibition lost weight. They also found that people with abnormal LPA signaling function were more likely to develop obesity and heterozygous diabetes.

Brain neurons in a model mouse (Source: Johannes Vogt)

By modulating the stimulation of the brain’s neural networks that control appetite and food intake, the researchers expect to find ways to solve problems with eating disorders and obesity. The development of new drugs targeting autotaxin is also expected.

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Johannes Vogt, a professor at the University of Cologne, said, “When autotaxin was inhibited through genetic manipulation or pharmacological methods, overeating behavior was significantly reduced.

This study was recently published in the journal Nature Metabolism.

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