Re: Bacteria may make people obesity-prone

[Guest guest]

--- aequalsz <aequalsz@...> wrote:

> Bacteria may make people obesity-prone

>

> http://www.telegraph.co.uk/news/main.jhtml?

> xml=/news/2006/12/21/uobesity121.xml

>

> http://tinyurl.com/yh6264

Hi All,

The better links to the story may be:

http://www.telegraph.co.uk/news/main.jhtml;jsessionid=STV25LCHUKU11QFIQMFSFFOAVC\

BQ0IV0?xml=/news/2006/12/21/uobesity121.xml

http://tinyurl.com/yefeea

PPS: Have your bacteria fed you today?

" The intestinal bacteria in obese humans and mice

differ from those in lean individuals " .

Physiology: Obesity and gut flora

Matej Bajzer and Randy J. Seeley

Nature 444, 1009-1010

The intestinal bacteria in obese humans and mice

differ from those in lean

individuals. Are these bacteria involved in how we

regulate body weight, and

are they a factor in the obesity epidemic?

See our streaming video for more on this research.

Much has been said and written about the sequencing of

the human genome, and

the research avenues that it has opened up. But our

own genome is not the

only one with which we need to be concerned. In

particular, trillions of

bacteria - collectively referred to as the microbiota

- reside in our

gastrointestinal tracts (Fig. 1), and each brings its

own genome to this

genetic party.

Reports by Gordon and colleagues1, 2 on pages 1022 and

1027 of this issue

explore the potential relationship between the types

of microbiota found in

the gut and the regulation of body weight. Although

there is no doubt that

human genetics plays a large part in determining body

weight3, it is equally

undisputed that the increase in prevalence of obesity

over the past 25 years

cannot be attributed to changes in the human genome4.

The inference is that

other factors are responsible, such as the

availability of inexpensive,

calorically dense foods, or the reduction in physical

activity in our daily

lives. The work described by Gordon and colleagues1, 2

raises the

possibility that our gut bacteria are another factor

that contributes to

differences in body weight among individuals.

Diverse evidence points to the importance of

biological control systems that

result in a close match between caloric intake and

caloric expenditure. For

the vast majority of humans (including obese

individuals), caloric intake

exceeds caloric expenditure by less than 1%, but even

these small

differences can accumulate over years to lead to

detrimental increases in

body weight4. The body's ability to match caloric

intake to caloric

expenditure is the result of the brain's ability to

monitor the amount of

fat in the body through changes in the levels of

circulating hormones. One

such hormone is leptin, the levels of which increase

with increasing body

fat5. Leptin deficiency in mice and humans results in

unrestrained caloric

intake and low caloric expenditure, with a consequent

rapid increase in body

weight6. Similarly, falling leptin levels are a

primary reason for the

difficulty in maintaining weight loss.

The two reports1, 2 compare the genetic material

collected from the

microbiota in the gut of lean and obese mice and

humans to assess the

relative abundance of various types of bacterium. The

two predominant

populations of microbiota in both the mouse and the

human gut are members of

the bacterial groups known as the Firmicutes and the

Bacteroidetes (Box 1).

The authors1 studied a small number of obese humans,

and found that the

proportion of the genetic material from Firmicutes was

higher than the

proportion in lean individuals. Moreover, when obese

individuals lost weight

over a year, the proportion from Firmicutes became

more like that of lean

individuals.

In the second report2, the authors describe how

differences in the

microbiota of lean and obese mice confirmed this

result, with obese mice

having a higher proportion of intestinal Firmicutes.

Importantly, the

microbiota of obese mice was rich in genes encoding

enzymes that break down

otherwise indigestible dietary polysaccharides. These

differences seem to

have functional consequences, as obese mice had more

fermentation

end-products and fewer calories remaining in their

faeces than lean mice.

Thus, the bacteria in obese mice seemed to assist

their host in extracting

extra calories from ingested food that could then be

used as energy.

These two results collectively suggest that obesity

alters the nature of the

intestinal microbiota, but they do not prove that

different relative

proportions of bacteria can lead to different body

weights. To test this

possibility, the authors performed a clever experiment

in which the

microbiota of obese, leptin-deficient mice was

transferred to lean,

microbe-free recipient mice2. Over a two-week period,

mice given the

microbiota from obese mice extracted more calories

from their food and had a

modest fat gain that was statistically greater than

that of mice receiving

microbiota from lean mice. Taken together, these data

suggest that

differences in the efficiency of caloric extraction

from food may be

determined by the composition of the microbiota,

which, in turn, may

contribute to differential body weights.

This is a potentially revolutionary idea that could

change our views of what

causes obesity and how we depend on the bacteria that

inhabit our gut. But a

great deal remains poorly understood. Most notably, it

is not clear whether

such small changes in caloric extraction can actually

contribute to

meaningful differences in body weight. There are few

data that substantiate

the predicted increased caloric extraction in obese

humans. Small but

persistent increases in efficiency might potentially

cause the accumulation

of excess body weight over long periods, but these

small differences are not

the cause of obesity in leptin-deficient mice. These

mice have a single gene

mutation that prevents the production of biologically

active leptin7. The

resulting increased caloric intake and reduced caloric

expenditure is many

times larger than the small difference in extraction

that could be produced

by differences in the microbiota. In fact, the

differences in body fat

between mice given the 'obese microbiota' and those

given the 'lean

microbiota' are so small that they could be accounted

for entirely by the

tiny differences in food intake, rather than by

differences in caloric

extraction.

Another unknown is why and how the make-up of the

microbiota is shifted by

differences in body weight. Given that acquiring food

from the environment

can be both calorically expensive and potentially

dangerous, it would seem

to be most adaptive to extract as many calories from

every bite of food as

possible. Moreover, if caloric extraction does become

more efficient, the

regulatory system would dictate that the organism

responds by reducing its

caloric intake. If a host organism had the ability to

change its microbiota

so as to increase caloric extraction, it would seem

most adaptive to do so

when facing famine conditions and losing weight.

However, the data indicate

just the opposite - the microbiota seems to be more

efficient in obese

humans who already have the most stored energy, and

shifts to being less

efficient as the subjects lose weight1.

There is also the issue of how conditions in the host

organism could change

the make-up of the microbiota. Low levels of leptin

are a signal of

starvation that triggers several changes in the

neuroendocrine system that

work to conserve calories6. Consequently, it would

make sense that low

leptin might also impart a signal to the microbiota to

become more efficient

at extracting calories from food. This hypothesis

would fit the microbiota

of the obese, leptin-deficient mice. However, in

humans where obesity is

associated with increased leptin, the same trends in

microbiota composition

are found, making it unlikely that the microbiota is

responding to leptin

directly. Moreover, it seems that when the bacteria

are transferred to a

lean mouse in which leptin is normal, the bacteria

retain their 'obese'

character over a two-week period. Thus, it is not

clear how gut bacteria

'know' whether the host is obese or lean.

Gordon and colleagues' results1, 2 tempt consideration

of how we might

manipulate the microbiotic environment to treat or

prevent obesity. But

questions about how and why the composition of gut

microbiota is regulated

will have to be answered first. As we have discussed,

those questions are

many and various. The two papers nonetheless open up

an intriguing line of

scientific enquiry that will ally microbiologists with

nutritionists,

physiologists and neuroscientists in the fight against

obesity.

References

Ley, R. E., Turnbaugh, P. J., Klein, S. & Gordon,

J. I. Nature 444,

1022-1023 (2006).

Turnbaugh, P. J. et al. Nature 444, 1027-1031 (2006).

-- Al Pater, PhD; email: Alpater@...

__________________________________________________

[Guest guest]

I wonder if this implies that you can " catch " obesity, particularly

from your spouse?

- Diane

>

> Hi,

>

> Bacteria may make people obesity-prone

>

> http://www.telegraph.co.uk/news/main.jhtml?

> xml=/news/2006/12/21/uobesity121.xml

>

> http://tinyurl.com/yh6264

>

> So how does this article relate to CRON? Well I believe it simply

> points out that weight gain or loss is not simply due to X calories

> ingested but more likely efficiency of X calories utilized. Also

> CRONies perhaps should insure that they are actually utilizing the

> calories they do consume. (Unfortunately can't say how. May have to

> resurrect the Kefir - the old ones didn't like organic milk powder

> mixed with fluorinated tap water.)

>

> a=z

>

> PS Have you adequately fed your 10 - 100 trillion digestive system

> bacteria today? :-)

>

[Guest guest]

IMO, this bacteria/obesity issue is like the proverbial chicken and

egg problem. We all know that the foods that we eat influence

substantially the kinds of bacteria that colonize our digestive tract.

Fiber, for example, is a good substrate for the bacteria which

convert long-chain polysaccharides into short-chain fatty acids. I

would expect that a high-protein low-carb diet would support different

types of bacteria than a high-carb diet. It is possible that the

bacteria that make people fat thrive on carbs and that by reducing the

percentage of carbs in the diet (e.g., Zone diet) the bacteria that

cause obesity can be reduced.

In any case, this bacterial issue is another handy excuse for being

overweight, similar to being " big boned " .

Tony

> >

> > Hi,

> >

> > Bacteria may make people obesity-prone

> >

> > http://www.telegraph.co.uk/news/main.jhtml?

> > xml=/news/2006/12/21/uobesity121.xml

> >

> > http://tinyurl.com/yh6264

> >

> > So how does this article relate to CRON? Well I believe it simply

> > points out that weight gain or loss is not simply due to X calories

> > ingested but more likely efficiency of X calories utilized. Also

> > CRONies perhaps should insure that they are actually utilizing the

> > calories they do consume. (Unfortunately can't say how. May have to

> > resurrect the Kefir - the old ones didn't like organic milk powder

> > mixed with fluorinated tap water.)

> >

> > a=z

> >

> > PS Have you adequately fed your 10 - 100 trillion digestive system

> > bacteria today? :-)

> >

>