Studies on rats and mice have led to the identification of a new satiety factor, a chemical messenger that tells the brain that the stomach is full, thus raising the hope of new treatments for obesity
Scientists from Yale University School of Medicine and the University of Cincinatti found that a chemical called N-acylphosphatidylethanolamine, or NAPE, was made in the small intestine of mice and rats after they had eaten a fatty meal. Furthermore, a study on rats given intravenous NAPE for five days revealed that those treated with NAPE ate less and lost weight in a dose-dependent manner.
Using radiolabeled NAPE the scientists found that NAPE is able to pass through the blood brain barrier, and is particularly concentrated in the hypothalamus, the part of the brain that controls appetite. This finding, together with the fact that the injection of small amounts of NAPE directly into the brain reduced food intake, suggests that NAPE interacts directly with the brain. “Most appetite regulation is hypothalamic, so we were excited that [NAPE] was working centrally,” said study leader Gerald Shulman in a news release. “That suggests [NAPE] is involved in the gut-brain axis. It’s a way the gut communicates to the brain that there’s energy coming in and you need to shut down food intake.”
The team is now monitoring NAPE levels in humans and is planning to test the molecule on non-human primates. If these studies are successful it is likely that the next step will be clinical trials of NAPE or NAPE-like compounds.
Gillum MP, Zhang D, Zhang XM, et al. N-acylphosphatidylethanolamine, a Gut- Derived Circulating Factor Induced by Fat Ingestion, Inhibits Food Intake. Cell 2008;135:813-824. doi:10.1016/j.cell.2008.10.043
News release: Molecule shuts down food intake and turns on ‘siesta mode’. Howard Hughes Medical Institute. November 26th 2008.
