Fiber from crustaceans, insects, mushrooms promotes digestion

Who can forget the stomach-churning moments when "Survivor" contestants forced down crunchy insects, among other unappetizing edibles, for a chance to win $1 million? In daring culinary challenges, the TV show's contestants exhibited gastronomic bravery as viewers watched in discomfort.

Digesting a crunchy critter starts with the audible grinding of its rigid protective covering -- the exoskeleton. Unpalatable as it may sound, the hard cover might be good for the metabolism, according to a new study, in mice, from Washington University School of Medicine in St. Louis.

The researchers, led by Steven Van Dyken, PhD, an assistant professor of pathology & immunology, found in mice that digesting chitin, an abundant dietary fiber in insect exoskeletons and also mushrooms and crustacean shells, engages the immune system. An active immune response was linked to less weight gain, reduced body fat and a resistance to obesity.

"Obesity is an epidemic," Van Dyken said. "What we put into our bodies has a profound effect on our physiology and on how we metabolize food. We're investigating ways to counteract obesity based on what we learn about how the immune system is engaged by diet."

The study is published Sept. 7 in Science.

The immune system is well known for safeguarding the body against various threats, including bacteria, viruses, allergens and even cancer. The researchers found that a particular arm of the immune system also is involved in chitin digestion. Stomach distention after chitin ingestion activates an innate immune response that triggers stomach cells to ramp up production of enzymes, known as chitinases, that break down chitin. Of note, chitin is insoluble -- incapable of being dissolved in liquid -- and thus requires enzymes and harsh acidic conditions to digest.

Do-Hyun Kim, PhD, a postdoctoral research associate and first author on the study, performed the experiments in germ-free mice lacking intestinal bacteria. His results show that chitin activates immune responses in the absence of bacteria.

"We think chitin digestion mainly relies on the host's own chitinases," Van Dyken said. "The stomach cells change their enzymatic output through a process we refer to as adaptation. But it is surprising that this process is happening without microbial input, because bacteria in the gastrointestinal tract are also sources of chitinases that degrade chitin." Van Dyken noted that in mice with intestinal bacteria, dietary chitin altered the bacterial composition in the lower gastrointestinal tract, suggesting that gut bacteria also adapt to chitin-containing food after it leaves the stomach.

The research team found that the greatest impact on obesity in mice occurred when chitin activated the immune system but was not digested. Mice fed a high-fat diet also were given chitin. Some mice lacked the ability to produce chitinases to break down chitin. The mice that ate chitin but couldn't break it down gained the least amount of weight, had the lowest body fat measurements and resisted obesity, compared with mice that didn't eat chitin and with those that did but could break it down.

If the mice could break down chitin, they still benefited metabolically, but they adapted by overproducing chitinases to extract nutrients from chitin.

Van Dyken and his team next plan to follow up on their findings in people, with a goal of determining whether chitin could be added to human diets to help control obesity.

Read more at Science Daily

Bacteria really eat plastic

The bacterium Rhodococcus ruber eats and actually digests plastic. This has been shown in laboratory experiments by PhD student Maaike Goudriaan at Royal Netherlands Institute for Sea Research (NIOZ). Based on a model study with plastic in artificial seawater in the lab, Goudriaan calculated that bacteria can break down about one percent of the fed plastic per year into CO2 and other harmless substances. "But," Goudriaan emphasizes, "this is certainly not a solution to the problem of the plastic soup in our oceans. It is, however, another part of the answer to the question of where all the 'missing plastic' in the oceans has gone."

Special plastic

Goudriaan had a special plastic manufactured especially for these experiments with a distinct form of carbon (13C) in it. When she fed that plastic to bacteria after pretreatment with "sunlight" -- a UV lamp -- in a bottle of simulated seawater, she saw that special version of carbon appear as CO2 above the water. "The treatment with UV light was necessary because we already know that sunlight partially breaks down plastic into bite-sized chunks for bacteria," the researcher explains.

Proof of principle

"This is the first time we have proven in this way that bacteria actually digest plastic into CO2 and other molecules," Goudriaan states. It was already known that the bacterium Rhodococcus ruber can form a so-called biofilm on plastic in nature. It had also been measured that plastic disappears under that biofilm. "But now we have really demonstrated that the bacteria actually digest the plastic."

Underestimate

When Goudriaan calculates the total breakdown of plastic into CO2, she estimates that the bacteria can break down about one percent of the available plastic per year. "That's probably an underestimate," she adds. "We only measured the amount of carbon-13 in CO2, so not in the other breakdown products of the plastic. There will certainly be 13C in several other molecules, but it's hard to say what part of that was broken down by the UV light and what part was digested by the bacteria."

No solution

Even though marine microbiologist Goudriaan is very excited about the plastic-eating bacteria, she stresses that microbial digestion is not a solution to the huge problem of all the plastic floating on and in our oceans. "These experiments are mainly a proof of principle. I see it as one piece of the jigsaw, in the issue of where all the plastic that disappears into the oceans stays. If you try to trace all our waste, a lot of plastic is lost. Digestion by bacteria could possibly provide part of the explanation."

From lab to mudflats

To discover whether 'wild' bacteria also eat plastic 'in the wild', follow-up research needs to be done. Goudriaan already did some pilot experiments with real sea water and some sediment that she had collected from the Wadden Sea floor. "The first results of these experiments hints at plastic being degraded, even in nature," she says. "A new PhD student will have to continue that work. Ultimately, of course, you hope to calculate how much plastic in the oceans really is degraded by bacteria. But much better than cleaning up, is prevention. And only we humans can do that," Goudriaan says.

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Human evolution wasn't just the sheet music, but how it was played

A team of Duke researchers has identified a group of human DNA sequences driving changes in brain development, digestion and immunity that seem to have evolved rapidly after our family line split from that of the chimpanzees, but before we split with the Neanderthals.

Our brains are bigger, and are guts are shorter than our ape peers.

"A lot of the traits that we think of as uniquely human, and human-specific, probably appear during that time period," in the 7.5 million years since the split with the common ancestor we share with the chimpanzee, said Craig Lowe, Ph.D., an assistant professor of molecular genetics and microbiology in the Duke School of Medicine.

Specifically, the DNA sequences in question, which the researchers have dubbed Human Ancestor Quickly Evolved Regions (HAQERS), pronounced like hackers, regulate genes. They are the switches that tell nearby genes when to turn on and off. The findings appear Nov.23 in the journal Cell.

The rapid evolution of these regions of the genome seems to have served as a fine-tuning of regulatory control, Lowe said. More switches were added to the human operating system as sequences developed into regulatory regions, and they were more finely tuned to adapt to environmental or developmental cues. By and large, those changes were advantageous to our species.

"They seem especially specific in causing genes to turn on, we think just in certain cell types at certain times of development, or even genes that turn on when the environment changes in some way," Lowe said.

A lot of this genomic innovation was found in brain development and the GI tract. "We see lots of regulatory elements that are turning on in these tissues," Lowe said. "These are the tissues where humans are refining which genes are expressed and at what level."

Today, our brains are larger than other apes, and our guts are shorter. "People have hypothesized that those two are even linked, because they are two really expensive metabolic tissues to have around," Lowe said. "I think what we're seeing is that there wasn't really one mutation that gave you a large brain and one mutation that really struck the gut, it was probably many of these small changes over time."

To produce the new findings, Lowe's lab collaborated with Duke colleagues Tim Reddy, an associate professor of biostatistics and bioinformatics, and Debra Silver, an associate professor of molecular genetics and microbiology to tap their expertise. Reddy's lab is capable of looking at millions of genetic switches at once and Silver is watching switches in action in developing mouse brains.

"Our contribution was, if we could bring both of those technologies together, then we could look at hundreds of switches in this sort of complex developing tissue, which you can't really get from a cell line," Lowe said.

"We wanted to identify switches that were totally new in humans," Lowe said. Computationally, they were able to infer what the human-chimp ancestor's DNA would have been like, as well as the extinct Neanderthal and Denisovan lineages. The researchers were able to compare the genome sequences of these other post-chimpanzee relatives thanks to databases created from the pioneering work of 2022 Nobel laureate Svante Pääbo.

"So, we know the Neanderthal sequence, but let's test that Neanderthal sequence and see if it can really turn on genes or not," which they did dozens of times.

"And we showed that, whoa, this really is a switch that turns on and off genes," Lowe said. "It was really fun to see that new gene regulation came from totally new switches, rather than just sort of rewiring switches that already existed."

Along with the positive traits that HAQERs gave humans, they can also be implicated in some diseases.

Most of us have remarkably similar HAQER sequences, but there are some variances, "and we were able to show that those variants tend to correlate with certain diseases," Lowe said, namely hypertension, neuroblastoma, unipolar depression, bipolar depression and schizophrenia. The mechanisms of action aren't known yet, and more research will have to be done in these areas, Lowe said.

"Maybe human-specific diseases or human-specific susceptibilities to these diseases are going to be preferentially mapped back to these new genetic switches that only exist in humans," Lowe said.

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Why breast-fed premature infants have a healthier gut than formula-fed ones

Human breastmilk has long been considered "liquid gold" among clinicians treating premature infants in a newborn intensive care unit (NICU). Breastmilk-fed "preemies" are healthier, on average, than those fed formula. Why is that true, however, has remained a mystery.

New research from the University of Maryland School of Medicine's (UMSOM) Institute for Genome Sciences (IGS), published online in the journal mBio in June found it is not just the content of breastmilk that makes the difference. It is also the way the babies digest it.

The research, led by Bing Ma, PhD, Assistant Professor of Microbiology and Immunology at UMSOM and a researcher at IGS, discovered a strain of the Bifidobacterium breve bacteria or B. breve in the gut of breastfed babies who received higher volumes of breastmilk than their counterparts. Those preemies had better nutrient absorption because they developed an intact intestinal wall, one week after birth. B. breve was much less prevalent in both formula-fed babies and breastfed babies with "leaky gut." Babies with leaky gut do not develop a barrier to protect against bacteria and digested food from getting into the bloodstream. For the first time, the team also found that the way B. breve metabolizes breastmilk keeps breastfed babies healthier and allows them to gain weight by strengthening their underdeveloped intestinal barrier.

An immature or "leaky" gut can lead to necrotizing enterocolitis (NEC), which is the third leading cause of newborn death in United States and worldwide. In fact, NEC impacts up to 10 percent of premature babies with a devasting mortality rate as high as 50 percent.

"Our discovery could lead to promising and practical clinical interventions to strengthen the babies' gut and, therefore, increase survival rates of the most vulnerable preemies," said Dr. Ma.

Bifidobacterium in the gut or microbiome has long been known to have health benefits. It includes a diverse set of strains that have very different properties. Some strains are only found in adults; some are mostly in adolescence. One strain, Bifidobacterium infantis, has been seen predominantly in full-term infants.

The researchers followed 113 premature babies who were born between 24 and 32 weeks' gestation. This study found Bifidobacterium breve (B. breve) only in preemies who had improved gut barrier function within one week after birth. Dr. Ma and her colleagues discovered that Bifidobacterium breve is genetically equipped to digest nutrients within the cell membrane rather than the more typical external digestion process in which bacteria secrete digestive enzymes onto nutrients to break them down.

At the most basic level, the gut microbiome in these breastfed preemies with more B. breve metabolizes carbohydrates differently than it does formula. The researchers say they hypothesize that this process of metabolism then strengthens and matures the intestinal barrier faster, protecting fragile newborns from disease.

"We now know that it is not the breastmilk alone that helps preemies develop their intestinal barrier faster," Dr. Ma said. "We will need to find the best way to prophylactically administer B. breve early in life, rather than rely on transmission from breastmilk or even the mother's gut or vaginal microbiota during the birthing process. This is especially critical in formula-fed preemies."

Dr. Ma said that more studies are needed to determine if the B. breve originated in the breastmilk, gut, mother's vagina, or even environment.

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Thinking with your stomach? The brain may have evolved to regulate digestion

Many life forms use light as an important biological signal, including animals with visual and non-visual systems. But now, researchers from Japan have found that neuronal cells may have initially evolved to regulate digestion according to light information.

In a study published this month in BMC Biology, researchers from the University of Tsukuba have revealed that sea urchins use light to regulate the opening and closing of the pylorus, which is an important component of the digestive tract.

Light-dependent systems often rely on the activity of proteins in the Opsin family, and these are found across the animal kingdom, including in organisms with visual and non-visual systems. Understanding the function of Opsins in animals from different taxonomic groups may provide important clues regarding how visual/non-visual systems evolved in different creatures to use light as an external signal. The function of Opsins in the Ambulacraria groups of animals, which include sea urchins, has not been characterized, something the researchers aimed to address.

"The functions of eyes and visual systems have been well-characterized," says senior author of the study Professor Shunsuke Yaguchi. "However, the way in which light dependent systems were acquired and diversified throughout evolution is unclear especially in deuterostomes because of the lack of data regarding the signaling pathway in the Ambulacraria group."

To address this, the researchers tested whether light exposure caused changes in digestive tract activity in sea urchins. They then conducted micro-surgical and genetic knockdown experiments to test whether Opsin cells in the sea urchin digestive system mediated the effect of light.

"The results provided new information about the role of Opsins in sea urchins," explains Professor Yaguchi. "Specifically, we found that stimulation of sea urchin larvae via light caused changes in digestive system function, even in the absence of food stimuli."

Furthermore, the researchers identified brain serotonergic neurons near the Opsin-expressing cells that were essential for mediating the light-stimulated release of nitric oxide, which acts as a neurotransmitter.

"Our results have important implications for understanding the process of evolution, specifically, that of light-dependent systems controlled via neurotransmitters," says Professor Yaguchi.

Read more at Science Daily