The researchers disrupted communication between the bacteria and the hosts in two ways: raising normal mice under germ-free conditions so they lacked the bacteria, and genetically engineering other mice to lack Gpr41 so they were unable to respond to the bacteria.
In both cases, the mice weighed less and had a leaner build than their normal counterparts even though they all ate the same amount.
The researchers also found that in mice without Gpr41, the intestines passed food more quickly. They hypothesized that one action of Gpr41 is to slow down the motion that propels food forward, so that more nutrients can be absorbed. Thus, if the receptor cannot be activated, food is expelled more quickly, and the animal gets less energy from it.
Because mice totally lacking Gpr41 were still healthy and had intestinal function, the receptor may be a likely target for drugs that can slow, but not stop, energy intake, Dr. Yanagisawa said.
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| Contact: Aline McKenzie aline.mckenzie@utsouthwestern.edu 214-648-3404 UT Southwestern Medical Center Source:Eurekalert |