Postbiotics May Prevent Diabetes in Obesity

You’ve likely heard about probiotics—live bacteria with long, colorful names found in your yogurt that help generate a happy gut. You may have even heard of prebiotics, which are compounds that have a beneficial effect on the bacteria in your body. But you’re probably less familiar with postbiotics—factors derived from bacteria that can also have a positive impact on our health.

Researchers at McMaster University who study diabetes and obesity have discovered a postbiotic factor called MDP that prevents pre-diabetic obese mice from developing diabetes. Their surprising results were recently published in Cell Metabolism.

When bacteria in the gut become chronically out of balance—known as intestinal dysbiosis [PDF]—a person can become insulin resistant, or prediabetic. Dysbiosis is often found in people with obesity. “Key markers on the road to diabetes are insulin sensitivity and insulin resistance—how well that hormone can lower blood glucose,” Jon Schertzer, lead study author and assistant professor of biochemistry at McMaster University tells Mental Floss. Insulin’s job is to bring your blood glucose back up to normal after you eat or drink something. If you’re insulin resistant, or improperly sensitive, insulin can’t do its job properly. “What a postbiotic does is allow the insulin to do a better job,” he says.

Schertzer’s team sought to investigate whether postbiotics could have an impact on obesity before a person becomes overtly diabetic. “The focus of this study is prediabetes—the stage before the overt disease has developed and it’s still reversible. Obesity is the biggest risk factor for prediabetes,” he explains.

The team found that a postbiotic called muramyl dipeptide (MDP), derived from a bacterial cell wall, was able to reduce insulin resistance in mouse models—regardless of weight loss or changes in the intestinal microbiome during obesity.

To test this, Schertzer separated mice into two groups. One group was given MDP at the same time as they were fed a high-fat diet intended to cause obesity. In that experiment, the mice were given MDP four days per week for five weeks. The MDP injections improved insulin and glucose tolerance after five weeks—remarkably, without altering body mass or fatty tissue levels.

In the second group, the team fed the mice into a state of obesity over 10 weeks, putting them into a state of prediabetes. Then they injected MDP into the mice three times over three days and saw a rapid improvement in blood glucose by the third day. “It’s not that the injection itself is lowering blood glucose, but those three short duration injections set the program up to allow insulin to work better,” he says.

When the body senses MDP is present, it increases the amount of a protein in fat tissue, called IR4, which sends out signals that lower blood glucose. “We don’t fully understand how it signals the body to lower blood glucose,” he admits. “We do know it reduces inflammation.”

While that may not sound dramatic, he says they were quite surprised, given that the typical immune response is to increase inflammation. “The postbiotic actually reduced inflammation in fat tissue, which are the tissues that control blood glucose,” he says.

While the results are exciting, he’s quick to point out that “we’re interested in discovery. We’ll leave the clinical aspect to clinicians.” They’d like to achieve a version of MDP that could be taken orally and not injected, but more research will be required. Plus, postbiotics can be a finicky area of research. He describes testing a different postbiotic that's a “a close cousin" to MDP, being "a different type of cell wall that was different by only one peptide.” But that postbiotic made glucose tolerance and inflammation much worse.

However, they also tested what’s called an “orphan drug”—approved only for clinical trials but not likely to make the drug company any money—called mifamurtide, typically used in treating bone cancers. Mifamurtide is synthetic, but chemically identical to the MDP postbiotic. It, too, improved blood glucose and insulin tolerance when administered to mice. The promising part about it is that since the drug is already given to humans in clinical trials, “it could make the transition to humans far more rapid,” he says.

One of their next steps is to expand the models they’re using, starting with age-induced diabetes. “Obesity is only one factor that promotes diabetes,” he says.

The most pressing question now, he says, is “to understand what is actually happening in the gut during obesity.” This compound promises a future in which obesity would pose less of a risk factor for diabetes. And postbiotics hold a lot of potential for future research.

“Postbiotics are a new source of drugs. Bacteria have different physiology from us, and can make all kinds of things that we can’t make,” Schertzer says.

How Did 6 Feet Become the Standard Grave Depth?

iStock
iStock

It all started with the plague: The origins of “six feet under” come from a 1665 outbreak in England. As the disease swept the country, the mayor of London literally laid down the law about how to deal with the bodies to avoid further infections. Among his specifications—made in “Orders Conceived and Published by the Lord Mayor and Aldermen of the City of London, Concerning the Infection of the Plague”—was that “all the graves shall be at least six feet deep.”

The law eventually fell out of favor both in England and its colonies. Modern American burial laws vary from state to state, though many states simply require a minimum of 18 inches of soil on top of the casket or burial vault (or two feet of soil if the body is not enclosed in anything). Given an 18-inch dirt buffer and the height of the average casket (which appears to be approximately 30 inches), a grave as shallow as four feet would be fine.

A typical modern burial involves a body pumped full of chemical preservatives sealed inside a sturdy metal casket, which is itself sealed inside a steel or cement burial vault. It’s less of a hospitable environment for microbes than the grave used to be. For untypical burials, though—where the body isn’t embalmed, a vault isn’t used, or the casket is wood instead of metal or is foregone entirely—even these less strict burial standards provide a measure of safety and comfort. Without any protection, and subjected to a few years of soil erosion, the bones of the dearly departed could inconveniently and unexpectedly surface or get too close to the living, scaring people and acting as disease vectors. The minimum depth helps keep the dead down where they belong.

Have you got a Big Question you'd like us to answer? If so, let us know by emailing us at bigquestions@mentalfloss.com.

This article originally appeared in 2012.

One Good Reason Not to Hold in a Fart: It Could Leak Out of Your Mouth

iStock/grinvalds
iStock/grinvalds

The next time you hold in a fart for fear of being heard by polite company, just remember this: It could leak out of your mouth instead of your butt. Writing on The Conversation, University of Newcastle nutrition and dietetics professor Clare Collins explains that pent-up gas can pass through your gut wall and get reabsorbed into your circulation. It's then released when you exhale, whether you like it or not.

“Holding on too long means the build up of intestinal gas will eventually escape via an uncontrollable fart,” Collins writes. In this case, the fart comes out of the wrong end. Talk about potty mouth.

A few brave scientists have investigated the phenomenon of flatulence. In one study, 10 healthy volunteers were fed half a can of baked beans in addition to their regular diets and given a rectal catheter to measure their farts over a 24-hour period. Although it was a small sample, the results were still telling. Men and women let loose the same amount of gas, and the average number of “flatus episodes” (a single fart, or series of farts) during that period was eight. Another study of 10 people found that high-fiber diets led to fewer but bigger farts, and a third study found that gases containing sulphur are the culprit of the world’s stinkiest farts. Two judges were tapped to rate the odor intensity of each toot, and we can only hope that they made it out alive.

Scientific literature also seems to support Collins’s advice to “let it go.” A 2010 paper on “Methane and the gastrointestinal tract” says methane, hydrogen sulfide, and other gases that are produced in the intestinal tract are mostly eliminated from the body via the anus or “expelled from the lungs.” Holding it in can lead to belching, flatulence, bloating, and pain. And in some severe cases, pouches can form along the wall of the colon and get infected, causing diverticulitis.

So go ahead and let it rip, just like nature intended—but maybe try to find an empty room first.

[h/t CBS Philadelphia]

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