Is the Mitochondria the answer?

I have read Nick Lane's Power, Sex, Suicide. I have read the FIRKO mouse paper where they gave FIRKO mice the gold thioglucose treatment that is supposed to cause obesity. And now we come to the next paper by these same researchers, studying the mitochondrial gene expression of their FIRKO mice.

In the first paper the authors found that despite an increased food intake, the FIRKO mice never displayed the obesity symptoms that all the other control mice would after the GTG treatment. Now, many people obviously asked the question, "with increased food intake how do they not gain any additional weight?" Well they manage to answer the question in the paper by studying the gene expression of the same fat cells they rendered completely insulin resistant. The answer was an increase in UCP1 protein in the brown adipose tissue of the mice. UCP1 is a protein that causes the uncoupling (hence the name) of the respiratory chain from the making of ATP. When this happens the chain can either form free radicals (We all hope not!), or turn to thermogenesis or heat production.

Now for the new study, the researchers found that the entire body had an increased metabolic rate in the FIRKO mice. They also found increased levels of most of the the mitochondrial metabolism genes, and mitochondrial DNA in white adipose tissue, hinting at increased function and/or number of mitochondria. Could this increased function of the mitochondria be the reason for the protection against obesity in the GTG treated mice from the first paper? It seems to me like that is probably a likely explanation.

Another interesting effect of the FIRKO mouse was increased lifespan. This one will require a little more research, but hopefully we can find some answers to why that happened, and if they will lead to human therapies to increase lifespan as well.