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Monday, 3 February, 2003, 01:50 GMT
Gene clue to wasting disease
Eating
Sufferers lose weight regardless of diet
The discovery of genes that control the development of muscles in the fruit fly could help unravel the secrets of a devasting human disease.

Cachexia is a severe wasting disorder normally linked to advanced cancer, Aids and a variety of chronic infections.

It causes not just the loss of fat, but also of bone and muscle, and happens regardless of the amount the patient manages to eat.

The patient's metabolism speeds up, burning more calories.

The condition further robs patients of the ability to fight the disease which triggered the cachexia.

It is believed that chemicals called cytokines released by the body in response to the underlying illness are responsible for the wasting illness.

The latest research, conducted at the University of Texas Southwestern Medical Center in Dallas, has found a gene which, if absent in mice, appears to increase the levels of cytokines circulating around the body.

The gene, known as "twist", regulates muscle development in fruit flies.

Tests on mice

The scientists wanted to know if it had a similar role in mice.

What they found was that the mice engineered to lack the gene were all underweight and frail, developing their own version of cachexia.

Dr Eric Olsen, the lead author of the study, said: "We assumed it would play a role similar to the fruit fly gene in controlling muscle development, but what we discovered was a completely unanticipated function for this ancient gene.

The researchers believe that the twist gene is important when the body wants to switch off the production of cytokines - in its absence their levels rise unchecked and eventually cause the wasting disease.

It is still not clear whether it is a problem with this particular gene in humans which causes this problem, or whether there is another source.

However, the gene offers hope that at some point in the future, there might be a way to control the level of cytokines in the body.

The study was published in the journal Cell.

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30 Jul 98 | Health
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