The researchers are asking: Are there parallels to humans?
We recently posted here a summary and brief explanation of the research that enabled the discovery of the cause of long suspected but not proven link between obesity and diabetes that was announced in July of this year, 2009.
Now we are in November of 2009 and a new discovery, announced by scientists in Germany at the University of Bonn, has identified a previously unknown gene that, in fruit flies, controls fat metabolism, and a defective version of that gene that prevents the building of body fat.
In other words: the defective gene prevents the manufacture of body fat necessary for the survival of the organism.
[Metabolism is the formal name for all the essential chemical and physical changes occurring in living cells that permit their continued growth and maintenance of life’s processes.]
If this gene process occurs the same way in human beings, it seems in some ways to have a somewhat “compensating” end result to the discovery in July. In that case, the growth of fat cells in the human body impaired insulin activity, leading to diabetes and continued fat build up as obesity worsens. Whereas the new research shows the impairment in the production of fat, resulting in their organism being deprived of an essential nutrient and therefore remaining thin, but an equally unhealthy condition that may lead to death.
The research results were published October 15, 2009 in the Advance Online version of the EMBO Journal. EMBO is an influential molecular biology journal that specializes in the rapid publication of original molecular biological research and related topics.
Hope for new medicines in the future for the treatment of obesity
The gene research is with fruit flies, but taking the positive view, animals also have a very similar gene that scientists had not previously associated with controlling fat metabolism but now think that it is probable they do perform the same function as in the fruit flies. And according to Professor Hoch, a member of the University of Bonn research team, if that proves to be correct, it will provide a promising approach in developing new medications for the treatment of obesity.
The researchers named the gene that controls the fat building process in the fruit fly “schlank”, meaning slim in the German language. In animals, the similar gene is called the Lass gene of which there are six known varieties in human beings, we are part of the animal kingdom of course. And it is known that mutations in Lass genes lead to serious metabolic problems in animals.
This appears to be another example that living organisms, whatever their differences, share similar genetic codes, supporting the belief that such genes have been inherited in the distant past from a common ancestor.
A non-scientific thought occurs to me: Could this be a reason that some people stay thin, even though they eat close to the same diet as obese people? Could they have some defective fat building genes?
Mouse gene saves fly larvae
Additional work involving the Lass genes of mice seems to bear out the scientists’ conclusions. When fruit fly larvae having the defective gene that would have caused their death immediately after hatching, were given the non-defective mouse Lass gene, the larvae survived and they were able to continue building the essential body fat.
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