Dodger
Mon, Oct-10-05, 10:18
http://www.dailymail.co.uk/pages/live/articles/health/thehealthnews.html?in_article_id=364840&in_page_id=1797
A gene that regulates inflammation could underlie a host of disorders including cancers, heart disease, obesity and Alzheimer's, scientists say.
Targeting the gene could open up a wide range of new treatments.
Investigators pinpointed the SEPS1 gene on chromosome 15, one of the bundles of DNA in every cell that contain the genetic code. It produces a protein that helps clear cells of faulty "misfolded" proteins. Inflammation develops when these defective proteins accumulate in stressed cells. People with a genetic variation that impairs SEPS1 tend to suffer higher levels of inflammation than people with a more efficient version of the gene.
Research leader Dr John Blangero, from the Southwest Foundation for Biomedical Research (SFBR) in San Antonio, Texas, USA, said: "Practically every common disease involves an inflammation component. So the discovery of a new player in the inflammation pathway opens up many potential avenues for intervention on a broad range of health issues."
The findings, published in the journal Nature Genetics, emerged from an investigation into the causes of obesity.
Researchers were studying the desert sand rat, an animal that like humans has certain individuals with a greater propensity for obesity and diabetes. It was found that obese and diabetic sand rats had a distinct version of a previously unknown gene, now identified as SEPS1.
This led to a DNA analysis of 522 individuals from a slimmer's organisation in Wisconsin called Tops (take off pounds sensibly), which identified a particular SEPS1 mutation linked to inflammation. The same pattern was seen in a separate group of 500 Mexican Americans from San Antonio. Further experiments revealed how the defective variant of SEPS1 put cells at a disadvantage when dealing with stress.
"Basically, this rarer form of SEPS1 gives you a lazy cellular 'garbage truck' that doesn't properly do its job of clearing out the misfolded proteins that lead to inflammation," said Dr Blangero.
Scientists are now looking at how the gene influences heart disease, diabetes, the high blood pressure pregnancy disorder pre-eclampsia, and a range of infectious conditions.
Professor Ahmed Kissebeh, from the Medical College of Wisconsin, said: "Now that we have identified SEPS1's role in inflammation, which is known to initiate the process of arterial wall hardening and the onset of Type 2 diabetes, we are developing an understanding of why obese persons with a faulty SEPS1 gene may be at higher risk of developing heart disease and diabetes."
A gene that regulates inflammation could underlie a host of disorders including cancers, heart disease, obesity and Alzheimer's, scientists say.
Targeting the gene could open up a wide range of new treatments.
Investigators pinpointed the SEPS1 gene on chromosome 15, one of the bundles of DNA in every cell that contain the genetic code. It produces a protein that helps clear cells of faulty "misfolded" proteins. Inflammation develops when these defective proteins accumulate in stressed cells. People with a genetic variation that impairs SEPS1 tend to suffer higher levels of inflammation than people with a more efficient version of the gene.
Research leader Dr John Blangero, from the Southwest Foundation for Biomedical Research (SFBR) in San Antonio, Texas, USA, said: "Practically every common disease involves an inflammation component. So the discovery of a new player in the inflammation pathway opens up many potential avenues for intervention on a broad range of health issues."
The findings, published in the journal Nature Genetics, emerged from an investigation into the causes of obesity.
Researchers were studying the desert sand rat, an animal that like humans has certain individuals with a greater propensity for obesity and diabetes. It was found that obese and diabetic sand rats had a distinct version of a previously unknown gene, now identified as SEPS1.
This led to a DNA analysis of 522 individuals from a slimmer's organisation in Wisconsin called Tops (take off pounds sensibly), which identified a particular SEPS1 mutation linked to inflammation. The same pattern was seen in a separate group of 500 Mexican Americans from San Antonio. Further experiments revealed how the defective variant of SEPS1 put cells at a disadvantage when dealing with stress.
"Basically, this rarer form of SEPS1 gives you a lazy cellular 'garbage truck' that doesn't properly do its job of clearing out the misfolded proteins that lead to inflammation," said Dr Blangero.
Scientists are now looking at how the gene influences heart disease, diabetes, the high blood pressure pregnancy disorder pre-eclampsia, and a range of infectious conditions.
Professor Ahmed Kissebeh, from the Medical College of Wisconsin, said: "Now that we have identified SEPS1's role in inflammation, which is known to initiate the process of arterial wall hardening and the onset of Type 2 diabetes, we are developing an understanding of why obese persons with a faulty SEPS1 gene may be at higher risk of developing heart disease and diabetes."