Which came first: obese chicken or its obese microflora?

Which came first: The obese chicken or its obese microbiota? « Nothing in Biology Makes Sense!

Good summary of a recently published paper on how our gut microflora influences metabolism of the entire organism. Most people tend to think of the gut simply as a container to periodically fill and empty. Only until recent years has science demonstrated that our gut is an organ actively involved in our entire physiology, including communication with the brain and immune system. In fact, just as our body fat is an endocrine organ, the gut is also involved in our endocrine system, including inflammation.

While we consciously or subconsciously interact with thousands of environment components on a daily basis, our gut contains another environment, the microflora, which interacts in ways we are unaware of. Part of that is comprised of what we swallow, sometimes microbes that hitch a ride on food we eat or drink. But that is why we have such a complex environment inside our gut. Hordes of 'good' bacteria often battle with 'bad' bacteria, and sometimes the latter may win. We usually become aware of those battle victories. Others are minor skirmishes that go unnoticed.

It is the chronic battles that alert the big army of our defenses, the immune system. And when the balance is continually upset, the rest of the body responds and other systems may malfunction.

Although epidemiological studies have suggested that some enteric bacteria are associated with obesity and chronic inflammation, the authors of this study demonstrated that a specific bacteria strain causes obesity. (Remember that association is not proof of causation.) However, a limitation of this study is the model: gnotobiotic (aka germ-free) mice. Regardless, it is a logical progression from in vitro models to study interactions of the gut microflora and metabolism. But we have more work to do on this.

My comments submitted on the website's post:

Gnotobiotic studies have their limitations despite that they are a logical progression from in vitro studies and isolate otherwise complex immune and intestinal interactions. Gnotobiotic animals typically have immune systems and intestinal walls that are under-developed. Also, all the food must be antigen free, which is difficult to achieve. Often, secondary infections can rapidly kill off an entire gnotobiotic colony or mask effects of controlled dietary variables. In our experience with gnotobiotic pigs (which are more relevant to human nutrition and gut microflora), administered probiotics had no effect on morbidity when challenged by a single-strain pathogen, whereas pigs in conventional state (non-gnotobiotic conditions) fared significantly better. Animals in a germ-free environment do not fully represent their counterparts in a conventional environment, and variables in studies with gnotobiotic animals must be strictly controlled (and are very expensive).

I found it interesting that in neither the paper or the supplementary information was provided the specific ingredients of the ‘WTP’ diet except for the major nutrient composition. ‘Chinese medicinal medicine’? ‘Prebiotics’? As a reviewer, I would have requested this information be more specific.