A biological hypothesis: is it possible that human symbiotic microbiota coding hunger genes for human beings?

The increasing number of literatures focus on the correction between symbiotic microbiota and noncommunicable diseases (NCDs) bring new light for prevention to NCDs. It is well known that the microbiota could be largely influenced by different foods, different foods will conversely influence human health. However, there still is no clue bridging the link between hunger sensation and microbiota. Based on recent research progresses between microbiota and obesity and diabetes, together with our studies, we proposed a biological hypothesis that the human symbiotic microbiota might code hunger genes for human beings. This hypothesis was supported with clinical evidences by using the flexible fasting (FF) technology. When we used the FF technology to feed the gut flora with plant polysaccharides and dietary fibers, the candidates can survive normally by using internal glycogen and fat with low or even no hunger sensation. The theory of “gut flora-centric theory (GFCT)” was then developed to explain this phenomenon. When the gut flora begins to reproduce their own offsprings in human gastrointestinal tract, they will digest and destroy the gastrointestinal mucosa to obtain the carbon sources. This signal will be transferred from gut to human brain as hunger sensation. Further efforts should focus on the mechanism underlying how and why did the symbiotic microbiota trigger and transfer the hunger sensation by activating the hunger genes. Taken together, the conjecture linking between human symbiotic microbiota and hunger sensation will probably improve prevention and control on NCDs.