MedicalResearch.com Interview with: Sean Davies PhD Department of Pharmacology Vanderbilt University Medical Research: What are the main findings of the study? Dr. Davies: N-acyl phosphatidylethanolamine (NAPE) is a fat-like molecule normally produced by small intestine of mammals in response to eating high fat foods that helps signal a feeling of fullness to the brain.  This sensation of fullness is what normally helps us decide to stop eating, but in obese people it appears that not enough NAPE is produced so that not enough of that signal gets sent to the brain.  So we wanted to find a way to increase the amount of NAPE made in the intestinal tract, with the hope that this would help protect against obesity. Our approach was to engineer a probiotic bacteria that normally colonizes the gut of humans and other mammals so that it would make NAPE.  Our hope was that when this gut bacteria made the NAPE, it would be absorbed by the intestine and help supplement the NAPE already being made by the intestine so that a more complete sensation of fullness would be send to the brain. What we found was that our engineered bacteria made a significant amount of NAPE and that when fed to mice, the bacteria would colonize the gut like normal and that the intestinal cells could absorb this NAPE.  Most importantly, we found that mice that received this bacteria ate less of the high fat diet than mice that were not treated or that received bacteria that did not make NAPE. Because the mice ate less of the high fat diet, and also because they burned the fat they had more effectively, the mice receiving the bacteria producing NAPE had only 50% of  the body fat of the control mice.  While the control mice showed the early signs of developing diabetes, the mice that received the NAPE producing bacteria showed almost no signs of developing diabetes. So the presence of these NAPE producing bacteria protected the mice from the harmful effects of the high fat diet. Another key findings was that because the bacteria live in the GI tract and keep producing the NAPE for many weeks, we didn’t have to keep administering the bacteria to the mice to keep up the protective effect.  Even a month after we stopped giving the bacteria producing NAPE, the mice were still protected from the effects of the high fat diet.  Eventually after about six weeks, the bacteria died out and the mice started eating the same amount of food as the control mice, but even for at least another six weeks after this, they still weighed less than the control mice.