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Thursday, September 10, 2009

Discovery Of Gene That Protects High-Fat-Diet Mice From Obesity



Good for the mice. (See the preceding and following posts. Note size comparison with 747)
"University of Michigan researchers have identified a gene that acts as a master switch to control obesity in mice. When the switch is turned off, even high-fat-diet mice remain thin.

Deleting the gene, called IKKE, also appears to protect mice against conditions that, in humans, lead to Type 2 diabetes, which is associated with obesity and is on the rise among Americans, including children and adolescents."
For this crap to make a difference, let me offer a suggestion.

Since we are experts at fixing fat mice, instead of trying to work it out for humans, where there are apparently at least 6000 genes relating to overweight/obesity, let's research how to turn fatsos into mice.
"Scientists think that the mouse genome will be even important than the human genome to medicine and human welfare. That seems bizarre: why is that? The reason is that, because of the relatively 'recent' divergence of the mouse and human lineages from our common ancestor (about 75 million years ago), an astonishing 99% of mouse genes turn out to have analogues in humans. Not only that, but great tracts of code are syntenic - that means the genes appear in the same order in the two genomes...

The astonishingly close homology that has been revealed in the code between mouse and human genome extends to functionality. Many homologous genes have identical functions in the two species, anatomy, physiology and metabolism are similar and genetic disease pathology can be very similar. So the fact that we can study the mouse empirically, means that we can identify the functions of genes in people and both understand human disease pathology and create ways to treat it." (source)
Clearly, this is a simpler matter.

Grant writers: Start Your Engines!

The rest of you, visit www.turnfatpeopleintomice.com

Fat mouse (lower) vs. skinny mouse:


Ain't science great?

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