Microbiome 'disruption' in early life linked to obesity in adulthood

25-Aug-2014 - Last updated on 26-Aug-2014 at 14:52 GMT

Researchers have identified a key window for gut bacteria development, suggesting that the disruption of key bacteria types can lead to an increased risk of obesity.

Related tags Bacteria

Certain gut bacteria could help to shape our metabolism in early life, while disrupting these bacteria appears to increase the risk of obesity in later adulthood, say researchers.

Published in Cell, the mouse study suggests that certain microbes shape their hosts' metabolism very early in life and that disrupting, for example through exposure to antibiotics, during infancy can cause metabolic changes that appear to increase the risk of obesity in adulthood.

Led by Martin Blaser from the NYU Langone Medical Center, the research team said that their findings provide further steps in identifying which gut bacteria are crucial to metabolic health - adding that such information could be used to help restore levels of those helpful microbes and promote healthy metabolism in adulthood after an infant encountered microbiome disruption due to illness or from medical treatments such as antibiotics.

"We identified infancy as a critical window where host metabolism is especially vulnerable to microbiota disruption with antibiotics," said Blaser. "This highlights a need for judicious use of antibiotics in clinical practice in early life."

The team also noted that the research characterises important variables in early-life microbe-host metabolic interaction and identifies several taxa consistently linked with metabolic alterations.

Study details

Blaser and his colleagues noted that it has been previously suggested that the microbes which begin to colonise the gut at birth can be easily disrupted during infancy - and that this can have a long-term effect on weight. Indeed, farmers in the USA have been taking advantage of this phenomenon for decades by exposing livestock to low doses of antibiotics to promote growth.

Building on this, the research wanted to examine whether the exact timing and duration of early exposure to antibiotics could make a difference, as well as identify specific bacteria that may protect against the potentially harmful health effects. To address these questions, they gave long-term, low-dose penicillin treatment to two groups of mice: 4-week-old mice after weaning and mouse mothers beginning shortly before their pups' birth.

They found that earlier penicillin exposure led to more substantial obesity in adulthood and worse metabolic health, especially in males. Early exposure to antibiotics also reduced levels of several types of potentially protective bacteria and exacerbated the effects of a high-fat diet on obesity, said the team.

Indeed, in a separate experiment, the researchers found that only 4 weeks of antibiotic exposure beginning shortly before birth was sufficient to produce obesity, which lasted well after penicillin treatment ended.

"These temporal changes indicate that low-dose penicillin suppresses multiple taxa that typically peak early in life. Although high-dose (therapeutic) antibiotic exposures reduce microbiota diversity in animals and humans, low-dose penicillin increased phylogenetic diversity at 4 weeks, which is consistent with decreases in particular prominent taxa and detection of taxa with lower representation," wrote the researchers. "By sampling across time, we identified microbes that were altered prior to the development of adiposity, suggesting roles in host metabolic development."

Furthermore, Blaser and his colleagues noted that it is the alteration of our gut microbiota, rather than use of antibiotics per se caused these metabolic changes:

"Our findings imply that restoring good bacteria could prevent the long-term metabolic effects of early antibiotic exposure," explained Laura Cox, first author of the study.

"We identified four candidate bacteria that may be metabolically protective, and we're working on follow-up studies to determine if we can prevent weight gain by giving these bacteria back following antibiotic therapy."

Source: Cell
Volume 158, Issue 4, 14 August 2014, Pages 705–721, doi: 10.1016/j.cell.2014.05.052
"Altering the Intestinal Microbiota during a Critical Developmental Window Has Lasting Metabolic Consequences"
Authors: Laura M. Cox, Shingo Yamanishi, et al

1 comment

What sort of food is given during and after PC-dosaging ?

Posted by Klaus J.Seelig,MD, 28 August 2014 - 01:11 GMT

The sort of fuel given to any engine is decisive for performance and durability.

When reading this report I wondered, whether the "normal bulk-feed for the mice" was documented as specially analyzed and known for its content of C3-type, C4-type & GMO-transgene C3-->C4-type Carbohydrates and Proteins by IR-MS for the minute differences of all organic matter.
Not every motor designed for light-petrol may be fuelled with "energy-dense" Diesel.

We know that all Mammalia are relatives, at least with their Metabolism. Like-wise weaning baby-mice suckling their mother’s-mice-milk who were fed on "normal" C3-rice might present different results of Microbiomata if the PRRI's new C4-rice is fed, both to the (milk-producing) mother-mouse as well as the later growing pup. [The same applies to other sorts of C3 vs C4-typer fodder-products.]

Some Energy-problems are only to be understood, if minor details like Isotopes are taken seriously.
There are stereo-isotopomerics with some energetic variation at each single Co-enzyme-A- related metabolic step which by slower turn-over disturb the "normally" rapid enzyme activities. So already by alteration of "normal" occurrence those slightly but significantly heavier molecules lagging behind will only show up to be of significance, if this point has been in Focus of Research. [As MRN show us clear variations in all mammals investigated, the question of what is behind that mythos is justified. WATSON’s recent interpretation of Diabetes as a Free-Radical-Disease appears to point to the same direction.]

It is known that organic molecules are selected by numerous Iso-Enzymes for their various isotopes and even variant stereo-isomeric positions (f.i. for processing various isotopomeres of Lactic acid).
And the Hatch-Slack-Pathway (used f.i. for processing ²D-tagged and/or ¹³C-bearing ‘bricks’) produces more ADP than "normal" Glycolysis is used to produce to keep the energetic Homoiostasis balanced.
So if the cells call for 'more energy needed’ this signal means “asking for increased Insulin-release” and may be caused by a normally balanced path-way for "certain metabolic bricks" of rather seldom occurrance to be clogged by food-borne "bricks" well-known as "energy-dense" which are just the ones to require using a different metabolic pathway to compensate for isotopes’ minute difference.

So what may be well tolerated as a minor additive (of C4-type products) to ample light (C3-type-) bulk-feedlots may be of widespread significance. If addition of 10% are well tolerated, 30% may be OK at week-ends, but 100% on long-term-basis may be intolerable for any of the YOPI-Consumers.
(I.e.:Young pups, Old Senescents, Pregnants of all Mammalia, and Immune-incompetent- or -PC-disturbed or 'moderated' Consumers sharing their Protein on basis of altered CAFO-Production).

If the Factum of "Zero-Point-Energy"(as known since UREY-1931 and HEVESY-1942) is deliberately overseen due to energy-promoting (GRAS-Assumptive) Dogmata and (Commodity-) Production and Convenience as Official (assuming Common) Interest then there may be ample Research lurking and soon be well established to keeping a lucrative "Mythos" well covered.

And if Fodder- and Food-Production is supported by Growth-Hormone and prophylactic low-dose Antibiosis with evidence of "excellent weight-gain" and that sort is valued higher than Consumer-Health- then there is Real Danger for Pandemic Collateral Effects.
Because there will be difficulties for all Researchers to get the essentially needed financial basis for the only proper sort of proof about "Truth in the Pudding".