New Obesity Drug Tested
New Obesity Drug Tested
Feb. 6, 2001 -- If the striking results of animal experiments hold up in humans, a recently discovered protein may become a powerful antiobesity treatment. In a series of experiments, overweight mice injected with the protein exhibited dramatic and sustained weight loss, without any changes in their eating habits.
"We've discovered a protein called Acrp30 that is made only by fat cells. Its biological activity is to increase the amount of fat burned by muscle," researcher Harvey F. Lodish, PhD, tells WebMD. Injecting mice with a fragment of the protein markedly changes the way high-fat meals are broken down by the body, he says. And giving it to obese mice, without making any changes to their diet, causes quick, dramatic weight loss.
The findings are "one more piece of evidence that fat cells play an active role in determining our metabolism, that they don't just sit there collecting whatever fat is around," says Susan K. Fried, PhD, professor of nutritional sciences at Rutgers University in New Brunswick, N.J. She reviewed the research for WebMD. "It looks like this protein has pretty potent effects on metabolism and body weight."
Earlier work had indicated that fat cells in both obese mice and obese people make less Acrp30 protein, says Lodish, who is professor of biology at Massachusetts Institute of Technology and research director of the Whitehead Institute in Cambridge, Mass.
In a preliminary assessment, "we looked at 70 obese young adults and saw a 30-40% reduction in Acrp30 levels compared with lean [people]," says Bernard E. Bihain, MD, vice president of functional genomics at Genset Corporation in La Jolla, Calif. The French-owned firm is developing the protein fragment under the trade name Famoxin.
Lodish explains that normally, dietary fat is broken down into fatty acids and transported throughout the body in the bloodstream. "Some is taken up and burned by muscle, and much is stored as body fat," he tells WebMD. So after eating a fatty meal, there will be a rapid rise in free-floating fatty acid, which declines slowly.
In their collaborative work published in the Feb. 13 issue of the Proceedings of the National Academy of Sciences, the researchers tested Famoxin's effect on normal and obese mice. First, they showed that injecting the protein fragment prior to a high-fat meal caused significant decreases in the amount of free-floating fatty acid and a much faster-than-normal decline to normal levels. Lodish attributes these effects to "increased uptake and oxidation by muscle." That is, the muscles were burning much more fat than normal.
Drug Shown to Control Obesity in Mice, MIT Researcher Says
"We've discovered a protein called Acrp30 that is made only by fat cells. Its biological activity is to increase the amount of fat burned by muscle," researcher Harvey F. Lodish, PhD, tells WebMD. Injecting mice with a fragment of the protein markedly changes the way high-fat meals are broken down by the body, he says. And giving it to obese mice, without making any changes to their diet, causes quick, dramatic weight loss.
The findings are "one more piece of evidence that fat cells play an active role in determining our metabolism, that they don't just sit there collecting whatever fat is around," says Susan K. Fried, PhD, professor of nutritional sciences at Rutgers University in New Brunswick, N.J. She reviewed the research for WebMD. "It looks like this protein has pretty potent effects on metabolism and body weight."
Earlier work had indicated that fat cells in both obese mice and obese people make less Acrp30 protein, says Lodish, who is professor of biology at Massachusetts Institute of Technology and research director of the Whitehead Institute in Cambridge, Mass.
In a preliminary assessment, "we looked at 70 obese young adults and saw a 30-40% reduction in Acrp30 levels compared with lean [people]," says Bernard E. Bihain, MD, vice president of functional genomics at Genset Corporation in La Jolla, Calif. The French-owned firm is developing the protein fragment under the trade name Famoxin.
Lodish explains that normally, dietary fat is broken down into fatty acids and transported throughout the body in the bloodstream. "Some is taken up and burned by muscle, and much is stored as body fat," he tells WebMD. So after eating a fatty meal, there will be a rapid rise in free-floating fatty acid, which declines slowly.
In their collaborative work published in the Feb. 13 issue of the Proceedings of the National Academy of Sciences, the researchers tested Famoxin's effect on normal and obese mice. First, they showed that injecting the protein fragment prior to a high-fat meal caused significant decreases in the amount of free-floating fatty acid and a much faster-than-normal decline to normal levels. Lodish attributes these effects to "increased uptake and oxidation by muscle." That is, the muscles were burning much more fat than normal.
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