О роли кишечных бактерий в физиологической регуляции аппетита и энергетического обмена

The current “homeostatic theory” of appetite regulation assumes that alternation of hunger and satiety depends on energy balance in the host tissues encoded and transmitted to the brain by neuronal and hormonal signals. However, relatively low metabolic activity of fat tissue cannot explain short-term regulation of appetite. In this paper, I am presenting the evidence supporting bacterial contribution to the appetite regulation by showing that energy metabolism of gut bacteria can be linked to the host appetite cycles. Indeed, the daily metabolic activity of gut bacteria (~2 kcal/g) is about 100 times higher than that of the human body. Importantly, the reproduction cycle of gut bacteria, which is independently regulated from the host, is temporally identical to the short-term changes of appetite; 20 min of the bacterial exponential growth duration corresponds to 20 min necessary for physiological satiation. In further support of the “microbial theory”, molecular pathways linking gut bacteria with the host regulation of appetite have been identified. For instance, bacterial caseinolytic protease B (ClpB), whose production increases during the bacterial stationary growth phase, i. e., when the host is satiated, acts as a conformational mimetic of anorexigenic α-melanocyte-stimulating hormone and activates the intestinal satiety pathway. The practical utility to stimulate this pathway and to control body weight gain in obesity was recently validated using ClpB-expressing probiotics. Thus, an important functional contribution of gut bacteria to the host energy metabolism should be considered as a new integral part of the “homeostatic theory” of appetite regulation.