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Study: Missing DNA can promote childhood obesity
NEW YORK (AP) — Some children get severely obese because they lack particular chunks of DNA, which kicks their hunger into overdrive, researchers report.
The British researchers checked the DNA of 300 children who'd become very fat, on the order of 220 pounds by age 10. They looked for deletions or extra copies of DNA segments.
They found evidence that several rare deletions may promote obesity, including one kind they studied further and found in less than 1% of about 1,200 severely obese children.
That deletion, on chromosome 16, apparently causes trouble because it removes a gene that the brain needs to respond to the appetite-controlling hormone leptin, said Dr. Sadaf Farooqi of Cambridge University.
In her study, children with a chromosome 16 DNA deletion "have a very strong drive to eat," said Farooqi, who co-led the research. "They're very, very hungry, they always want to eat."
The work, reported online Sunday by the journal Nature, has already produced a real-world payoff. Farooqi said four children with the chromosome 16 deletion had drawn the attention of British child welfare authorities, who blamed the parents for overfeeding them.
"We were able to intervene" and get the parents of two children off the hook, and the other two cases are under discussion, she said.
That's happened before when the scientists uncovered genetic causes for severe childhood obesity, she said.
"It's a slightly unusual outcome of our research, but one we think is very important," she said.
While scientists had previously discovered particular genes that promote obesity when damaged, the new work looked at larger chunks of DNA that can span several genes. The chromosome 16 deletion includes nine genes.
Eric Ravussin, an obesity expert at the Pennington Biomedical Research Center in Baton Rouge, who wasn't involved in the study, said the work provides "a gold mine of information." That's because it identifies specific chromosome areas that scientists can explore to discover obesity-related genes, he said.
NEW YORK (AP) — Some children get severely obese because they lack particular chunks of DNA, which kicks their hunger into overdrive, researchers report.
The British researchers checked the DNA of 300 children who'd become very fat, on the order of 220 pounds by age 10. They looked for deletions or extra copies of DNA segments.
They found evidence that several rare deletions may promote obesity, including one kind they studied further and found in less than 1% of about 1,200 severely obese children.
That deletion, on chromosome 16, apparently causes trouble because it removes a gene that the brain needs to respond to the appetite-controlling hormone leptin, said Dr. Sadaf Farooqi of Cambridge University.
In her study, children with a chromosome 16 DNA deletion "have a very strong drive to eat," said Farooqi, who co-led the research. "They're very, very hungry, they always want to eat."
The work, reported online Sunday by the journal Nature, has already produced a real-world payoff. Farooqi said four children with the chromosome 16 deletion had drawn the attention of British child welfare authorities, who blamed the parents for overfeeding them.
"We were able to intervene" and get the parents of two children off the hook, and the other two cases are under discussion, she said.
That's happened before when the scientists uncovered genetic causes for severe childhood obesity, she said.
"It's a slightly unusual outcome of our research, but one we think is very important," she said.
While scientists had previously discovered particular genes that promote obesity when damaged, the new work looked at larger chunks of DNA that can span several genes. The chromosome 16 deletion includes nine genes.
Eric Ravussin, an obesity expert at the Pennington Biomedical Research Center in Baton Rouge, who wasn't involved in the study, said the work provides "a gold mine of information." That's because it identifies specific chromosome areas that scientists can explore to discover obesity-related genes, he said.