'Fat switch' makes cells turn to flab, study says

WASHINGTON (Reuters) -- A protein that switches fat cell formation on and off may help explain some of the causes of both obesity and the increasing flabbiness that comes with age, researchers said on Thursday.

The protein stops cells from becoming fat cells when it is on. When it is absent, or produced at low levels, fat cells are born, a team at the University of Michigan reported.

The protein is called Wnt-10b, the researchers reported in the journal Science.

"Wnt signaling functions as a fat switch," Sarah Ross, a graduate student who led the study, said in a statement.

"When it's on, fat-cell formation is repressed. When it's off, fat is initiated."

Ormond MacDougald, an assistant professor of physiology who oversaw the work, stressed that the finding is not an answer for the 55 percent of Americans who are overweight and the 18 percent who are obese, or 30 percent over ideal weight.

"It's not the cure for obesity next week," MacDougald said in a telephone interview.

"Obesity is a complicated problem and it's largely controlled by centers in the brain that control our appetite and also control whole body energy metabolism."

But, he said, the study will help scientists understand just how obesity develops, and also add to the understanding of the signals that tell cells what to do.

All cells start out as stem cells, which are a kind of master cell that have the ability to become any one of a number of kinds of cell. From there they become precursor cells, which have a more limited number of choices.

Understanding the signals that control these processes is a major goal.

Ross and MacDougald's team worked with fat precursor cells, exposing them to Wnt, which is a cell signaling protein.

"During development, Wnt signaling seems to tell the cells, 'You're supposed to be a fat cell, you're supposed to be a muscle cell,' and so forth," Ross told Science.

"This signaling mechanism helps direct the cell's fate. If that toggle is switched the wrong way, then we see more fat formation."

Muscle precursor cells called myoblasts also turned into fat cells when Wnt was suppressed, they said.

That suggests that the "fat cell" setting is a kind of default, at least for these particular cells, MacDougald said.

One next step would be to see if it is possible to make a fat precursor cell turn into a muscle cell.

"We are also interested in what regulates expression of Wnt 10b in adult tissues. Is it aberrantly regulated in obesity? Is it associated with increased fat cell mass found in aging?" MacDougald asked.

"Does it explain the fatty tissue differences between males and females? Is it regulated within a given day depending on the feeding cycle? Those things could all be really cool."

Ross did her initial work in laboratory dishes but has also injected fat cell precursors, some of them lacking Wnt, under the skin of mice. When Wnt was present, little fat pads grew. When it was absent in the injected cells, undifferentiated tissue that was neither fat nor muscle developed.

The team wants to use genetic engineering to try to create a fat-free mouse. "We are in the process," MacDougald said. They would also like to find a "knockout" mouse lacking any Wnt 10b at all to see if it would be especially flabby.

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