Bacteria have been around for a long time, much longer than the eukaryotes and MUCH longer than us Johnny-come-lately multicellular organisms. They know where it's at as regards survival. Anyone who thinks of bacteria as "simple" clearly has no concept of the effect of a few billion years of selection pressure on the sophistication of survival strategies.
There is a lot of information in this paper and the current review below:
The gut microbiota as an environmental factor that regulates fat storage.
Mechanisms underlying the resistance to diet-induced obesity in germ-free mice.
From what I can extract there are a number of things that our gut bacteria do that are very interesting. Obviously gut bacteria are both careless and careful. That is, they don't care about you or me. Their priority is to maintain an environment which is convivial to their own chances of repeated division. Keeping us alive helps.
They do this rather well. The main aspect of Bäckhed et al's research I want to talk about is Fiaf and fat storage.
Fiaf stands for Fasting induced adipose factor. Fiaf (amongst its many other actions) blocks the action of lipoprotein lipase, that enzyme which packs on the pounds of fat in humans. Fiaf is normally made by our liver, muscles and in particularly by our gut wall in times of starvation. It appears to be a signal to the body to stop storing fat, crank up blood triglycerides and start running metabolic processes on fat, but fat derived from our adipocytes (obviously, it's a starvation hormone, there is no dietary fat).
But Fiaf from the gut wall is under the control of the gut bacteria. Active bacteria stop Fiaf production, inactive (hungry) bacteria allow Fiaf to be produced. It's pretty obvious that starvation gives quiescent gut bacteria, to the point where starvation actually mimics not having any gut bacteria at all.
Germ free mice really do have no gut bacteria at all, so they produce lots of Fiaf, all of the time. This suppresses their LPL and so they are slim, whatever they eat! Bacteria added to their gut immediately suppress Fiaf production from the intestine wall and so allow recently colonised (ex germ free) mice to store fat as soon as ever they have access to food. Lots of fat.
Also the mice rapidly become insulin resistant as well as obese. That's interesting.
But under more standard laboratory conditions Fiaf is ONLY produced from the gut of normal animals in times of starvation. My presumption here is that it is the hunger of the GUT BACTERIA that allow Fiaf levels to rise, which allows the stored fat of the host to be burned, in order to keep their microbial bioreactor (our colon) alive. A dead host is of no use to a bacterium.
Why have the bacteria organised things this way?
A bacterium cannot store energy. It's got no where to put it, no storage organ. But after surviving for millenia they are hardly likley to put their furture survival down to chance. So they take any energy source that they can get, particularly those sugar moieties that mammalian digestion cannot hope to extract, those from fiber. They extract sugars, upregulate sugar transport across the intestinal wall, modify the host's liver metaboism to convert them to triglycerides and then make sure lipoprotein lipase is fully active to store the triglycerides in adipocytes. Other bacteria ferment these sugars to short chain fatty acids, then shunt these to the liver for triglyceride production too. All the same in the end. It's bacterial derived energy stored as mammalian fat.
Fiaf also controls a host of fat burning genes. So the gut microbes only allow Fiaf to rise when they, and by inference their hosts, are hungry and need stored fat to live on. By doing this they allow us to burn "our" fat to get about to find more food. But who's fat is it? Which organsims organised its storage? Which organisms are controlling access?
It's not our fat.
Hunger, of the intestinal bacteria, is needed to before it can be accessed.
There is a point to all this, beyond it being absolutely fascinating.
That'll be the next post.