@Nathan needless to say, fat -> obesity -> metabolism syndrom/diabetes
(problem).
you mentioned studying obesity to fight hunger? that's an interesting
and probably more noble approach worth exploring but the aim here is
to 'destroy' fat.
by 'destroy' fat I mean accelerating beta-oxidation of fatty acids;
this is my hypothesis however the other possible outcomes could be:
(1) nothing or (2) fat-to-carbs conversion (may or may not be
favorable as you've mentioned).
in the case of human liver cells, expressing these two enzymes
resulted in a metabolic shift towards fatty acid degradation (and
releasing CO2). however, i am not sure what the outcome will be when
expressing the enzymes in human gut bacteria, which are under the
anaerobic conditions of the gut (we can clone the enzymes from
pathogenic bacteria such as salmonella, which are stable and
functional in the harsh gastric juices). liver cell vs. gut microbe;
completely different systems but who knows what the phenotype will be.
we'll find out.
rahim
On Feb 28, 2:35 pm, Nathan McCorkle <nmz...@gmail.com> wrote:
> On Tue, Feb 28, 2012 at 12:11 PM, naiverahim <rahim.ba...@gmail.com> wrote:
> > Recently I've been really interested in the idea of designing 'good
> > bacteria' to do even more good for the gut. I've conceived of a way to
> > design Bifidobacteria (with 2 genes --> 2 enzymes) to destroy fat
> > before it's absorbed into the body or excreted in feces. This would be
>
> By destroy do you mean 'turn to CO2 and heat', or turn into
> non-fat/simpler carbon compounds.... non-fat may be more easily
> absorbed by the body, which can
> then just jump into fatty acid synthesis (consuming simple carbon
> compounds are more likely to make you 'fat', than consuming fats)
>
> --
> Nathan McCorkle
> Rochester Institute of Technology
> College of Science, Biotechnology/Bioinformatics
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