Researchers have discovered a new hormone called asprosin, that regulates blood-glucose levels. New studies on the hormones showed that asprosin also acts on the brain, stimulating the hunger center in the hypothalamus to control appetite and body weight. This opens an intriguing possibility for developing treatments for overweight people. They discovered asprosin when studying individuals affected by a rare medical condition called neonatal progeroid syndrome.
Patients with neonatal progeroid syndrome have a mutation in the FBN1 gene that causes them to lack a small piece of the fibrillin-1 protein. In individuals without the FBN1mutation, this small piece, which we named asprosin, is cut and released into the circulation from the end of the protein.
One of the cardinal features that defines neonatal progeroid syndrome is extreme thinness or very low body weight. This allowed measurement of how much food they ate relative to the number of calories they burned every day.
Compared with individuals with normal weight, neonatal progeroid syndrome patients have abnormally low appetite.
To investigate how the mutation affected the patients’ appetite, the researchers genetically engineered mice to carry the same genetic mutation the patients have. The result was mice that mimicked the human condition; they had low blood asprosin levels, low appetite and were very thin.
In the mouse model, researchers were able to reverse the low appetite by administering asprosin to the mice.
To understand how asprosin controls appetite. Asprosin interacts with neurons in the appetite center of the hypothalamus. There are two types of neurons involved in appetite control. One type, the AgRP neurons, stimulates appetite while the other type, POMC neurons, suppresses it.
Asprosin works on both types of neurons in an opposite manner; it activates appetite-stimulating AgRP neurons and it deactivates appetite-suppressing POMC neurons. The resulting effect of these two asprosin actions in the brain is an increase in appetite, a phenomenon that is deficient in individuals and mice with neonatal progeroid syndrome. The researchers also studied individuals with obesity and found that they had increased levels of blood asprosin.
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