Can mucus-loving bacteria cure obesity and diabetes?

Exciting news about an unusual bacteria that might reverse obesity and type 2 diabetes was announced this week from a group of researchers in Belgium, Finland and Holland. What they found may shake the foundations of dietary and diabetic science to the core.

Here’s some background: over the years, we have found that obesity and diabetes have much in common. In fact, there is a term that reflects the connection: diabesity. If that sounds like something you don’t want, you’re right. In diabesity, your gut, which is full of bacteria (pounds of the stuff!) goes through some detrimental changes. Probably in response to the bacteria itself, the gut lining thins out and becomes more permeable. That only leads to more problems, causing the immune system to kick in to high gear, causing inflammation. Diabesity may have as much to do with inflammation as to overeating. So, how can a lowly bacteria turn this situation around?

Your very own brand of bacteria

We tend to think of bacteria as merely some kind of sludge, but that sludge has a lot of “personality.” You have hundreds of different types of bacteria in your gut, and they are likely to be quite different from my bacteria. The composition of your personal sludge is typically set from birth or soon after. How? Well, here it gets a little disgusting (oh, hell, this whole thing is disgusting): when you are born you pick up bacteria from your mother’s birth canal, and possibly from her feces, which is often present due to all that pushing. If you were born by caesarian section, you missed all that, which sounds a lot more sanitary, but could cause problems down the road.

dirty girl collects bacteria

Kids aren’t sanitary

Then, when you are breast-fed, you pick up more bacteria that are actually included in mother’s milk. That’s right, that pure white stuff contains lactobacillus, which helps with the digestion of the milk. How thoughtful of Mother Nature to include the means of digestion along with the meal. And of course as a toddler you consume lots of bacteria because everything must go in your mouth. Children, it turns out, are not sanitary.

All this goes to define your own personal bacterial populations that then establish residence throughout your gut. Once they set up house, the community is pretty resilient. The different species, having fought to a draw, hold tight to their special niches.

Many of them work together symbiotically, helping you to pack on the pounds. Oh joy! One of their tricks is to squeeze calories out of “indigestible” fiber including cellulose and other complex sugars like fructo-oligo-saccharides that we will mercifully refer to as FOS. Although your unassisted gut can’t break these long molecules down, your bacteria can. Some of them are very good at this job, which undoubtedly served our hungry ancestors well. But here and now in the land of plenty, they are really just icing the cake, and some of us don’t need any extra icing. And that is why my distressingly svelte wife can eat as much as I do and yet stay half my weight. My bacteria are clearly superior to hers when it comes to squeezing the most out of our food.

Nothing lasts forever

As you age, however, things may change. Your tissues may dry up a bit. Your diet may not be colon-friendly. Slowly, your gut bacteria may start to turn on you. These changes turn out to be correlated with obesity, type 2 diabetes and inflammation.

So the good news from our friends in Northern Europe is that a freshly discovered bacterium is associated with weight loss. The more of this marvelous microbe you have, the lighter your footsteps. If true, this might help us to lose weight and tame diabetes all at the same time. The microbe’s name is Akkermansis muciniphila, and although it has probably been camping in human guts for millennia, it is new to science, having been discovered by Willem de Vos at Waginingen University in 2004. The first part of the name honors Anton Akkermans, a Dutch scientist who studied microbial ecology (also at Waginingen) until his death in 2006. We mean no disrespect, but most writers shorten the title of his namesake bug to A. muciniphila.

It gets more disgusting?

For the second part of the name, I need to trouble you again with more disgusting information: you have rivers of mucus running through your body in all directions: from your mouth to your anus, from your lungs to your throat, from your eyes to your nose and more. Wads of it are constantly being secreted by the cells lining all your internal plumbing — about a quart a day. Yes, a quart of mucus every day. Hold up a quart bottle and think about it. Better yet, don’t.

There’s an excellent reason for all that snot: it protects your delicate tissues. It snags dust and bacteria in your lungs and then ferries it all out, mosh-pit style, on top of millions of waving cilia. In your gut, it protects the stomach from acid, and in the rest of the intestines it acts as a lubricant to keep your food moving. Most importantly, it protects you from attack by poisons, bacteria, fungi and viruses. We are constantly under siege, and mucus is the brilliant multipurpose solution that arose from millions of years of evolutionary tinkering. It is nature’s duct-tape and WD-40 all wrapped in one, a formidable barrier against microbial invasion. It is, of course, the last place you would expect to find bacteria.

A place for everything

However, as Aristotle pointed out, nature abhors a vacuum and it is truly difficult to find anywhere in the world that doesn’t look like home to some germ or another. Mucus, in all its hot, wet and sticky glory, looks very inviting to some pretty nasty bacteria, like the ones that cause sinusitis.

eating snot like a bacterium

Kids still aren’t sanitary

Fortunately, A. muciniphila is good bacteria and is also fond of mucin (the main component of mucus) — thus the second part of its name. It thrives in the mucus that lines your colon. It’s kind of disgusting (as is most of this article), but these bugs are totally at home in your gut lube. They snuggle up in your gooey insides where they proceed to eat their bedding. That’s right, like kindergartners, these guys eat snot.

But at the same time, they send some kind of signal to the cells lining the gut, encouraging them to squirt out more mucus. Even as they chow down on it, the net effect is to thicken the mucus barrier.

They also tamp down the immune system, as if to say: “Take a break, we’ll deal with the bacterial hordes for you.” How that agreement is made is still a mystery, but as a consequence when A. muciniphila is around, inflammation in your gut is strongly muted.

Feeding time at the zoo

Not surprisingly for a gut microbe, what you eat affects its viability. A high-fat diet seems to kill them off, knocking levels to one percent of normal. This is a terrible outcome, and I really hate the implications. There goes the rib-eye! To be fair, these mice were given very high fat diets, where 60% of their calories came from fat. That puts your typical paleo diet, with more like 20% of calories from fat, to shame.

However, when the researchers fed the fat mice a nice big dose of A. muciniphila, the population recovered, even while they were still eating a high-fat diet. They saw similar results by just feeding FOS, which also led to blooms of A. muciniphila. The first treatment is a probiotic, and the second is a prebiotic, but both led to a major resurgence of this friendly microbe.

And then they pulled a rabbit out of a hat

And that’s when the magic happened: the fat mice quickly trimmed down and reduced their insulin resistance. They had lower sugar levels in their blood. Somehow, a big population of A. muciniphila re-tuned their bodies and fixed their diabetic tendencies. This is a remarkable result, and suggests that probiotics and prebiotics may be a part of tomorrow’s treatment for obesity and type 2 diabetes.

But before we pop the champagne, keep in mind that this research shows dramatic improvements – in mice. Although there is evidence that the same processes occur in humans, it would be good to see these results verified. And, as mentioned earlier, your personal gut-bug collection is hard to dismantle, so it may require continuous prodding and feeding. Oh, and the mice were gavaged, which you really don’t want. A better means of consumption will have to be devised.

In the study, they were able to get similar results by feeding with FOS. That is strange because A. muciniphila eats mucus, not FOS. But symbiotic relationships are common in the bacterial world, and there is still much to be learned about this microbial ecosystem. The dose they gave the mice was high, about 1% of body weight. If the same ratio is used for humans, then we’ll need to eat a pound or more of FOS daily. I can barely gag down a teaspoon of the stuff.

Nevertheless, I can’t wait to get my hands on some of those hard-working bacteria so I can eat my rib-eye with equanimity. Okay, my proofreader, who is also my distressingly svelte wife, informs me that I’ll be splitting that steak with her and eating some broccoli as well. I suspect she is already full of A. muciniphila, but I’ll take her up on that meal.

This intriguing research implies that the problems we have with our weight may have a lot to do with the bacterial company we keep. And we might be able to fix that with a little snot-seeking microbe. Hooray! I will keep you posted on this breakthrough in future articles.


References

Schmidt, Maria Inês, and Bruce Bartholow Duncan. “Diabesity: An Inflammatory Metabolic Condition.” Clinical Chemistry and Laboratory Medicine: CCLM / FESCC 41, no. 9 (September 2003): 1120–1130. doi:10.1515/CCLM.2003.174.

Huh, Susanna Y., Sheryl L. Rifas-Shiman, Chloe A. Zera, Janet W. Rich Edwards, Emily Oken, Scott T. Weiss, and Matthew W. Gillman. “Delivery by Caesarean Section and Risk of Obesity in Preschool Age Children: a Prospective Cohort Study.” Archives of Disease in Childhood 97, no. 7 (July 1, 2012): 610–616. doi:10.1136/archdischild-2011-301141.

Martín, Rocío, Susana Langa, Carlota Reviriego, Esther Jimínez, María L Marín, Jordi Xaus, Leonides Fernández, and Juan M Rodríguez. “Human Milk Is a Source of Lactic Acid Bacteria for the Infant Gut.” The Journal of Pediatrics 143, no. 6 (December 2003): 754–758. doi:10.1016/j.jpeds.2003.09.028.

Flint, Harry J., Edward A. Bayer, Marco T. Rincon, Raphael Lamed, and Bryan A. White. “Polysaccharide Utilization by Gut Bacteria: Potential for New Insights from Genomic Analysis.” Nature Reviews Microbiology 6, no. 2 (February 2008): 121–131. doi:10.1038/nrmicro1817.

Li, Min, Baohong Wang, Menghui Zhang, Mattias Rantalainen, Shengyue Wang, Haokui Zhou, Yan Zhang, et al. “Symbiotic Gut Microbes Modulate Human Metabolic Phenotypes.” Proceedings of the National Academy of Sciences 105, no. 6 (February 12, 2008): 2117–2122. doi:10.1073/pnas.0712038105.

Everard, Amandine, Clara Belzer, Lucie Geurts, Janneke P. Ouwerkerk, Céline Druart, Laure B. Bindels, Yves Guiot, et al. “Cross-talk Between Akkermansia Muciniphila and Intestinal Epithelium Controls Diet-induced Obesity.” Proceedings of the National Academy of Sciences (May 13, 2013). doi:10.1073/pnas.1219451110.

Derrien, Muriel, Elaine E. Vaughan, Caroline M. Plugge, and Willem M. de Vos. “Akkermansia Muciniphila Gen. Nov., Sp. Nov., a Human Intestinal Mucin-degrading Bacterium.” International Journal of Systematic and Evolutionary Microbiology 54, no. 5 (September 1, 2004): 1469–1476. doi:10.1099/ijs.0.02873-0.

“Host Interactions and Immune Modulation of Akkermansia Muciniphila.” Wageningen UR. Accessed May 16, 2013. http://www.wageningenur.nl/en/show/Host-interactions-and-immune-modulation-of-Akkermansia-muciniphila.htm.


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