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.

Pandemic vs. Epidemic: What’s the Difference?

If scientists can't develop a vaccine for a new virus quickly enough, an epidemic can turn into a pandemic.
If scientists can't develop a vaccine for a new virus quickly enough, an epidemic can turn into a pandemic.
doble-d/iStock via Getty Images

As the new coronavirus continues to spread around the world, the words epidemic and pandemic are showing up in news reports more often than they usually do. While the terms are closely related, they don’t refer to the same thing.

As the Association for Professionals in Infection Control and Epidemiology (APIC) explains on its website, “an epidemic occurs when an infectious disease spreads rapidly to many people.” Usually, what precedes an epidemic is an outbreak, or “a sudden rise in the number of cases of a disease.” An outbreak can affect a single community or several countries, but it’s on a much smaller scale than an epidemic.

If an epidemic can’t be contained and keeps expanding its reach, public health officials might start calling it a pandemic, which means it’s affected enough people in different areas of the world to be considered a global outbreak. In short, a pandemic is a worldwide epidemic. It infects more people, causes more deaths, and can also have widespread social and economic repercussions. The spread of the Spanish influenza from 1918 to 1919, which killed between 20 and 40 million people around the world, was a pandemic; more recently, the H1N1 influenza created a pandemic in 2009.

Here’s where it gets a little tricky: There’s no cut-and-dried classification system for outbreaks, epidemics, and pandemics. Based on the definitions above, it might seem like the current coronavirus disease, now called COVID-19, falls into the pandemic category already—according to a map from the World Health Organization (WHO), there are more than 80,000 confirmed cases in 34 countries, and nearly 2700 people have died from the disease. It’s also beginning to impact travel, stock markets, and the global economy as a whole. But WHO maintains that although the situation has the potential to become a pandemic, it’s still an epidemic for now.

“It really is borderline semantics, to be honest with you,” Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, told CNN earlier this month. “I think you could have people arguing each end of it. Pandemics mean different things to different people.”

[h/t APIC.org]

Fat Bats Might Be Resistant to Deadly White-Nose Syndrome

Penn State, Flickr // CC BY-NC-ND 2.0
Penn State, Flickr // CC BY-NC-ND 2.0

Good news for flying mammals: chubby little brown bats might be genetically resistant to white-nose syndrome, a fungal disease that’s killed more than 5.5 million bats since it was first documented in 2006 [PDF]. A new study in the journal Scientific Reports describes three genetic adaptations in the bats that could protect them from the pathogen.

Little brown bats (Myotis lucifugus), common in Canada and the eastern United States, are especially susceptible to white-nose syndrome. According to lead author Giorgia G. Auteri, a doctoral candidate at the University of Michigan, white-nose syndrome kills bats by disrupting their hibernation cycles.

“When they’re in hibernation in the winter, they’re not meant to be waking up. They’re supposed to be asleep,” Auteri tells Mental Floss. “But this fungus grows on them, and it causes the bats to keep waking up during hibernation. And because they’re waking up when they shouldn’t be, they’re running out of fat reserves too early.”

But while white-nose syndrome has devastated bat populations in North America, not all infected bats die from the disease—some recover. Auteri wanted to find out what made the survivors so special.

Auteri and her team compared the genetic makeup of nine surviving and 29 non-surviving little brown bats from northern Michigan. They discovered that survivors share three important genetic distinctions. “One is involved with fat metabolism,” she says. “And another is involved with regulating when the bats wake up from hibernation. And the third gene is involved in their echolocation ability, in their sonar for hunting insects.”

The results make sense, Auteri says. Because white-nose syndrome interrupts bats’ hibernation schedules, bats with genes that relate to more optimal fat storage (i.e., they’re fatter) and better hibernation regulation (i.e., they sleep longer) are more likely to survive the disease.

Auteri’s research could help scientists and conservationists find ways to preserve little brown bat populations. Besides being adorable, little brown bats also play an important ecological role as predators of insects like mosquitoes, moths, and other pests that are destructive to crops and forests.

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