科学家发现肥胖基因
Scientists have created strains of mice that can eat a high-fat diet without getting chubby using a single gene that might lead to a new obesity treatment for people.
In its normal form, the gene, called HMGIC, apparently helps mice make more cells to store fat when they have been eating a fatty diet, researchers said. But the mice in the experiment had a defective version of the gene.
They apparently failed to create storage cells in response to the high-fat diet, and so avoided putting on weight, the researchers said in the April issue of the journal Nature Genetics.
The finding could lead to a human obesity treatment if scientists can find a drug that interferes with the effect of the normal HMGIC gene, said Kiran Chada, a biochemistry professor at the University of Medicine and Dentistry of New Jersey and senior author of the paper. He is also president of a company formed to develop products related to the gene.
Dr. Bradford Lowell, an obesity expert at Harvard Medical School, said it will take a lot more work to find out how promising Chada‘s approach would be for humans.
Dr. Rudy Leibel, an obesity expert at Columbia University in New York, said if a person‘s supply of fat-storing cells were restricted, fat might build up in the liver instead. That could seriously interfere with liver function, he said.
Chada said he has seen no sign of fatty liver buildup in the mice.
Mice born with the genetic defect develop only about 10 percent of the normal amount of body fat but are otherwise normal, Chada said. Mutant mice that ate a high-fat diet for six months didn‘t put on any more weight than mutants that ate a standard diet.
Normal mice, in contrast, did become obese on the high-fat diet. All three groups of mice ate about the same amount., 百拇医药
In its normal form, the gene, called HMGIC, apparently helps mice make more cells to store fat when they have been eating a fatty diet, researchers said. But the mice in the experiment had a defective version of the gene.
They apparently failed to create storage cells in response to the high-fat diet, and so avoided putting on weight, the researchers said in the April issue of the journal Nature Genetics.
The finding could lead to a human obesity treatment if scientists can find a drug that interferes with the effect of the normal HMGIC gene, said Kiran Chada, a biochemistry professor at the University of Medicine and Dentistry of New Jersey and senior author of the paper. He is also president of a company formed to develop products related to the gene.
Dr. Bradford Lowell, an obesity expert at Harvard Medical School, said it will take a lot more work to find out how promising Chada‘s approach would be for humans.
Dr. Rudy Leibel, an obesity expert at Columbia University in New York, said if a person‘s supply of fat-storing cells were restricted, fat might build up in the liver instead. That could seriously interfere with liver function, he said.
Chada said he has seen no sign of fatty liver buildup in the mice.
Mice born with the genetic defect develop only about 10 percent of the normal amount of body fat but are otherwise normal, Chada said. Mutant mice that ate a high-fat diet for six months didn‘t put on any more weight than mutants that ate a standard diet.
Normal mice, in contrast, did become obese on the high-fat diet. All three groups of mice ate about the same amount., 百拇医药