The reason is because your other organs and your brain start communicating - and many of them get a break from constantly processing food.
Studies have found that mice who accumulated the most glycogen in the liver did not gain weight in spite of having access to an appetizing diet. In addition to observing that those animals ate less, researchers have found that the brains of the animals showed scarce appetite-stimulating molecules but rather many appetite-suppressing ones.
Hepatic glycogen content (pink) of control mice, not subjected to any mutation. Image: I López-Soldado, IRB Barcelona
Why so? The liver stores excess glucose - sugar - in the form of glycogen, which are chains of glucose later 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 - their blood sugar levels are too high. A new study headed by Joan J. Guinovart at the Institute for Research in Biomedicine (IRB Barcelona) found that high hepatic glucose stores in mice prevented weigh gain. The researchers observed that in spite of having free access to an appetizing diet, the animals’ appetite was reduced.
The first time that a link has been observed between the liver and appetite, so the researchers argue that the stimulation of hepatic glycogen production would provide an efficient treatment to improve diabetes and obesity.
“It is interesting to observe that what happens in the liver has direct effects on appetite. Here we reveal what occurs at the molecular level,” explains Guinovart.
The key to the liver-brain link is ATP, the 'energy currency created by mitochondria and used by all living organisms, which is commonly altered in diabetes and obesity. “We have seen that high levels of hepatic glycogen, stable levels of ATP, and high levels of appetite-suppressing molecules in the mouse brain are perfectly correlated,” explains post-doctoral researcher Dr. Iliana López-Soldado.
Citation: Liver glycogen reduces food intake and attenuates obesity in a high-fat diet fed mouse model, Iliana López-Soldado, Delia Zafra, Jordi Duran, Anna Adrover, Joaquim Calbó, Joan J. Guinovart, Diabetes, 2014 Oct 2. doi:10.2337/db14-0728