Increased appetite and insulin resistance can be transferred from one mouse to another via intestinal bacteria, according to research being published online by Science magazine.
The finding strengthens the case that intestinal bacteria can contribute to human obesity and metabolic disease, since previous research has shown that intestinal bacterial populations differ between obese and lean humans.
"It has been assumed that the obesity epidemic in the developed world is driven by an increasingly sedentary lifestyle and the abundance of low-cost high-calorie foods," says senior author Andrew Gewirtz, PhD, associate professor of pathology and laboratory medicine at Emory University School of Medicine. "However, our results suggest that excess caloric consumption is not only a result of undisciplined eating but that intestinal bacteria contribute to changes in appetite and metabolism."
The first author of the paper is Emory faculty member Matam Vijay-Kumar, PhD, who has been studying a mouse strain with an altered immune system. These mice were engineered to lack a gene, Toll-like receptor 5 (TLR5), which helps cells sense the presence of bacteria. TLR5 recognizes flagellin, the main component of the apparatus (flagella) that many bacteria use to propel themselves.
The finding strengthens the case that intestinal bacteria can contribute to human obesity and metabolic disease, since previous research has shown that intestinal bacterial populations differ between obese and lean humans.
"It has been assumed that the obesity epidemic in the developed world is driven by an increasingly sedentary lifestyle and the abundance of low-cost high-calorie foods," says senior author Andrew Gewirtz, PhD, associate professor of pathology and laboratory medicine at Emory University School of Medicine. "However, our results suggest that excess caloric consumption is not only a result of undisciplined eating but that intestinal bacteria contribute to changes in appetite and metabolism."
The first author of the paper is Emory faculty member Matam Vijay-Kumar, PhD, who has been studying a mouse strain with an altered immune system. These mice were engineered to lack a gene, Toll-like receptor 5 (TLR5), which helps cells sense the presence of bacteria. TLR5 recognizes flagellin, the main component of the apparatus (flagella) that many bacteria use to propel themselves.
