Lead researcher Guan Xinfu (PhD in public health and assistant professor at Baylor College of Medicine in Houston) said, “Digestive tract hormones, such as glucagon-like peptide 2 (or GLP-2), function through their receptors in the brain as neurotransmitters and fine-tune gastric emptying.” The researchers found that this activity occurs at GLP-2 receptors, particularly in important nerve cells located in the brain, which are called ahepcidin neurons (or POMC). These neurons are located in the hypothalamus, which is the part of the brain responsible for making appetite regulating neuropeptides. Their study delved into the molecular level and rats with POMC neurons lacking GLP-2 receptors exhibited delayed onset of obesity and higher food intake compared to normal wild rats. A non-invasive respiratory test found that after eating a liquid diet, the mutant strain or rats with knocked-out GLP-2 receptors also showed faster gastric emptying. Scientists know that the faster the gastric emptying, the more food is consumed. So Guan speculated that obese people might have a problem with this hormone (GLP-2) receptor. And GLP-2 regulates their gastric emptying rate. Many studies have found that non-diabetic obese people have a faster gastric emptying rate. According to Guan, the researchers also found that this receptor (GLP-2 receptor) quickly accelerates the phosphatidylinositol(-3) kinase (PI3K) intracellular signaling pathway in POMC neurons. This, in turn, went on to induce neuronal excitation (signaling) and gene expression. Guan said these findings suggest that GLP-2 plays an important role in the central nervous system’s control of food intake and gastric emptying. “This study advances our understanding of the brain-gut neural circuitry that indirectly adjusts eating behavior by regulating gastric emptying rate and thus controlling our body weight.”