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/ Health News / 2008 / October 2008 / October 18, 2008 Waste from gut bug helps maintain weight |
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In a mouse study, researchers have found that waste from gut bacteria activates a single molecule, and that in turn helps the host animals to control their weight.
Washington, Oct 18 : In a mouse study, researchers have found that waste from gut bacteria activates a single molecule, and that in turn helps the host animals to control their weight.
The team of researchers including scientists from UT Southwestern Medical Center, have found that the waste products from gut bacteria, plays a large role in controlling whether the host animals are lean or fatty.The receptor molecule in the gut wall, called Gpr41, when activated, slows the movement of food through the intestine, allowing the animal to absorb more nutrients and thus gain weight. But, in the absence of this signal, the animals weigh less.
The study underlines that the host can use bacterial byproducts not only as a source of nutrients, but also as chemical signals to regulate body functions. It also points towards a potential method of controlling weight.
"It's quite possible that blocking this receptor molecule in the intestine might fight a certain kind of obesity by blocking absorption of energy from the gut," said Dr. Masashi Yanagisawa, professor of molecular genetics at UT Southwestern and a senior co-author of the study.
It is known that humans, like other animals, have a large number of beneficial bacteria in the intestines, which break up large molecules and helps the host in digesting and absorbing many of the resulting small molecules for energy and nutrients.
"The number of bacteria in our gut far exceeds the total number of cells in our bodies. It's truly a mutually beneficial relationship. We provide the bacteria with food, and in return they supply energy and nutrients," said Dr. Yanagisawa.
In their study on mice, the scientists took into account two species of bacteria that break up dietary fibers from food into small molecules called short-chain fatty acids.
It was earlier found that short-chain fatty acids bind to and activate Gpr41, but little was known about the physiological outcome of Gpr41 activation.
In the current study, communication between the bacteria and the hosts was disrupted 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.
It was found that 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 speculated 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.
Yanagisawa said that as mice without any trace of 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.
The study is appearing online in Proceedings of the National Academy of Sciences.
ANI
