Scientists at the Institute for Research in Biomedicine (IRB Barcelona) have explained how our liver and brain communicate to regulate appetite.
Joan J. Guinovart, who led the study, demonstrated that high hepatic glucose stores in mice prevented weight gain. The researchers observed that in spite of having free access to an appetizing diet, the animals' appetite was reduced. This was the first time that a link had been observed between the liver and appetite.
The liver stores excess glucose, sugar, in the form of glycogen-chains of glucose-, which later gets released to cover body energy requirements. Diabetic patients do not accumulate glucose well in the liver and this is one of the reasons why they suffer from hyperglycemia, that is to say, their blood sugar levels are too high.
On the basis of the results, the researchers argued that the stimulation of hepatic glycogen production would provide an efficient treatment to improve diabetes and obesity.
The researchers questioned why mice that accumulated most glycogen in the liver did not gain weight in spite of having access to an appetising diet. In addition to observing that these animals ate less, the scientists found that the brains of these animals showed scarce appetite-stimulating molecules but rather many appetite-suppressing ones.
Iliana Lopez-Soldado, a postdoctoral researcher who has been working on these experiments for three years explained that they finally found the clue-with the signal that could explain the liver-brain connection.
The key to the liver-brain link is ATP, the molecule used by all living organisms to provide cells with energy and which is commonly altered in diabetes and obesity. Lopez-Soldado said that they had seen that high levels of hepatic glycogen, stable levels of ATP, and high levels of appetite-suppressing molecules in the mouse brain were perfectly correlated.
The study was published in published in Diabetes.