For most, Thanksgiving is a time of overindulgence: from Grandma’s specially roasted turkey and homemade gravy to Aunt Betty’s prize-winning pumpkin pie, it’s hard to say no to seconds. But researchers looking for a treatment for obesity have found a molecule that might well tell your brain that your stomach is full. So maybe if we listen more closely tomorrow, we won’t suffer a postmeal food coma after all.

Researchers at the Yale School of Medicine and the University of Cincinnati conducted experiments with rats and mice and found that their small intestines release large quantities of a molecule called N-acylphospatidylethanolamine (NAPE) shortly after a fatty meal. This chemical apparently travels straight to the brain and puts a halt to further hunger signals. The researchers then synthesized NAPE and injected it into rats. After just five days of treatment, they showed a reduced appetite and significant weight loss. The findings are published today in the journal Cell.

Lead researcher Greg Shulman and his team are now monitoring NAPE levels in humans to see if they rise the same way after a big meal. Ultimately, their studies could help researchers design better appetite suppressants or obesity-fighting drugs.

From the press release:

The team used Shulman’s lipid analysis system to investigate what happens to fat that enters the blood after ingesting a high-fat meal. The scientists reasoned that the fat derivatives that enter the bloodstream might themselves serve as messengers to signal the brain that the body has been fed. They used this approach to compare the lipids present in blood plasma from rats that had fasted or eaten, and they zeroed in on NAPE.

They found only low levels of NAPE in the blood of rats that had fasted for 12 hours. The level of NAPE shot up 40 to 50 percent in animals that had dined on high-fat chow. Furthermore, NAPE didn’t increase in rodents that ate only protein or carbohydrate, suggesting that NAPE levels reflect the amount of fat eaten in a meal.

The researchers found that when they injected synthetic NAPE into the abdominal cavity or blood, the rodents’ appetites diminished substantially. The more NAPE they received, the less food they ate. “It’s really quite effective,” Shulman says. “At the highest doses, it keeps the animals from eating for up to 12 hours.” At a low dose–comparable to the spike in NAPE that occurs naturally after a meal–the rodents still ate 25 percent less than controls. They even acted full, going into “siesta mode” as if they had just eaten, Shulman says, noting that additional tests confirmed that the animals were only lethargic, not ill or incapacitated.

When the researchers delivered tiny amounts of NAPE directly into the brain, it had the same effect as a larger dose delivered to the blood. This suggests that the compound communicates directly with the brain, Shulman says.