Obesity and Bacteria

The ememy within!!

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Obesity and bacteria

Greedy guts?
Jan 4th 2007
From The Economist print edition

Every week seems to bring a new theory about why people are
getting fatter. The latest is that intestinal microbes are
partly to blame

David Simonds
ALTHOUGH most people prefer not to think about it, human guts
are full of bacteria. And a good thing, too. These intestinal
bugs help digestion, and also stop their disease-causing
counterparts from invading. In return, their human hosts provide
them with a warm place to live and a share of their meals. It is
a symbiotic relationship that has worked well for millions of
years.

Gary James...

Perhaps McDonalds should start giving a free tapeworm to everybody who
orders a Big Mac and fries. One healthy worm could take up the slack
of a colony of incompetent gut bacteria.

Now it is working rather too well. A group of researchers led by
Jeffrey Gordon, of the Washington University School of Medicine,
in St Louis, has found that some types of microbes are a lot
better than others at providing usable food to their hosts. In
the past, when food was scarce, those who harboured such
microbes would have been blessed. These days, paradoxically,
they are cursed, for the extra food seems to contribute to
obesity. Worse still, these once-benign microbes have even
subtler effects, regulating the functioning of human genes and
inducing the bodies of their hosts to lay down more fat than
would otherwise be the case.

Alvin E. Toda...

Encouraging research. I wish it were as simple as
microbes.

Dr Gordon's research is outlined in a paper published in this
week's Proceedings of the National Academy of Sciences (PNAS)
and two others published last month in Nature. In the Nature
papers, he and his team reported that obese people have a
different mix of gut microbes from that found in lean people—a
mix that is more efficient at unlocking energy from the food
they consume. Although individuals can harbour up to a thousand
different types of microbes, more than 90% of these belong to
one or other of two groups, called Bacteroidetes and Firmicutes.
The researchers sequenced bacterial DNA from faecal samples
taken from volunteers and discovered that those who were obese
had a higher proportion of Firmicutes than lean people did.

Bugs in the system
This also turned out to be true in mice, and working with these
rodents, the researchers discovered that the types of Firmicute
found in obese animals are more efficient at converting complex
polysaccharides (a form of carbohydrate that mammals have a hard
time digesting by themselves) into simple, usable sugars such as
glucose. In effect, the Firmicutes made more energy available
from the same amount of food. The researchers were even able to
make mice that had been raised in a germ-free environment fatter
or thinner by colonising their guts with microbes from either
obese or lean mice.

It sounds simple enough. Unfortunately, further probing showed
that the story is a little more complicated, for Dr Gordon did
not merely count the gut bacteria of fat and thin people—he then
put some of the fat ones on a diet. As these once-obese humans
lost weight over the course of a year, their mix of gut microbes
changed to reflect their new, svelte status. Why this happened
is not clear. It does not seem to have been a result of the
composition of the diet, since the effect was the same whether
people lost weight with a low-fat diet or a low-carbohydrate
diet. Nevertheless, this part of the experiment suggests it is
weight that determines gut biodiversity, not the other way
round.

The paper published in PNAS, though, supports the idea that the
bacterial mixture is cause not effect, by adding yet another
element to the story. In this study, Dr Gordon took normal mice
and germ-free mice, and fed both groups a “Western” diet that
was high in fat and sugar. The normal mice gained weight; the
germ-free mice stayed lean.

Part of the reason was that the normal mice had microbes that
made more useful sugar available. But the researchers looked
more closely and found that there was even more going on. By
comparing the two kinds of mice, they discovered that the gut
microbes in the regular mice were tinkering with their hosts'
metabolisms, regulating them in at least two different ways.

First, they suppressed production by the mice's bodies of a
substance called fasting-induced adipose factor. This encouraged
the mice to store fat. Second, they caused lower levels of
another substance, called adenosine monophosphate-activated
protein kinase, which made it harder for them to burn fat that
they had already accumulated. The upshot is that gut microbes
not only release energy from food, they also encourage bodies to
store that energy as fat and to keep the fat on.

The practical upshot of this is hard to see at the moment. But
if these two suppression mechanisms could, themselves, be
suppressed, that might stop people putting on weight. The
findings do, however, emphasise how profound the relationship is
between people and their gut bacteria. These bacteria can be
thought of as an additional digestive organ. Alternatively,
humans might view themselves as a sort of collective organism—a
human casing surrounding a vast colony of microbes. It is just a
pity that this colony is working so hard on behalf of its casing
that, in an era when food comes from the supermarket rather than
the savannah, the result is rather too good.