Research conducted in mice suggests that engaging certain types of fiber with the immune system may help prevent obesity.

Who can forget the stomach-churning moment when contestants on “Survivor” ate crunchy insects and other unpalatable foods for a chance to win $1 million? The TV show featured contestants demonstrating their gastronomic courage by trying their hand at cooking, leaving viewers feeling uncomfortable.

Digestion in a crunchy creature begins with the sound of its hard protective covering, the exoskeleton. It may be unpalatable, but hardcovers may be good for your metabolism, according to a new study in mice from Washington University School of Medicine in St. Louis.

Immune system activation and dietary fiber

Researchers led by Dr. Stephen Van Dyken, assistant professor of pathology and immunology, have discovered that the immune system is involved in digesting chitin, a dietary fiber found abundantly in insect exoskeletons, mushrooms, and crustacean shells. A vigorous immune response was associated with less weight gain, less body fat, and resistance to obesity.

“Obesity is an epidemic,” Van Dyken said. “What we put into our bodies has a huge impact on our physiology and how we metabolize food. Based on this, we are researching ways to combat obesity.”

This study was recently published in the journal science.

The immune system is well known for protecting the body from a variety of threats such as bacteria, viruses, allergens, and even cancer. Researchers have discovered that specific departments of the immune system are also involved in chitin digestion. Stomach distension after chitin ingestion activates the immune response, causing gastric cells to increase production of enzymes known as chitinases, which break down chitin. Notably, chitin is insoluble and cannot be dissolved in liquids, so enzymes and harsh acidic conditions are required for digestion.

Research methods and findings

Dr. Do-hyun Kim, a postdoctoral fellow and lead author of the study, conducted experiments on germ-free mice lacking gut bacteria. His results show that chitin activates the immune response in the absence of bacteria.

“We believe that chitin digestion relies primarily on the host’s own chitinases,” van Dijken said. “The cells of the stomach change their enzyme output through a process called adaptation. However, bacteria in the gastrointestinal tract are also a source of chitinase, which breaks down chitin, so it is unlikely that this process is occurring without microbial input. Dr. van Dijken noted that in mice with gut bacteria, dietary chitin altered the bacterial composition of the lower gastrointestinal tract, suggesting that after the gut bacteria left the stomach, This also suggests that they can also adapt to chitin-containing foods.

The researchers found that chitin, which activates the immune system but is not digested, had the greatest effect on obesity in mice. Mice fed a high-fat diet were also given chitin. Some mice lacked the ability to produce chitinase, which breaks down chitin. Mice that ate but were unable to break down chitin gained the least weight, had the lowest body fat measurements, and were resistant to obesity compared to mice that did not eat chitin or mice that ate chitin but were able to break it down. did.

Although mice could still break down chitin, which would give them a metabolic advantage, they adapted by overproducing chitinases to extract nutrients from chitin.

Van Dijken and his team will next follow up on the results of the human study to determine whether chitin can be added to the human diet to help control obesity.

“There are several ways to inhibit gastric chitinases,” he says. “Combining these approaches with chitin-containing foods could have enormous metabolic benefits.”

Reference: “The gastric type 2 immune circuit controls mammalian adaptation to dietary chitin” Do-Hyun Kim, Yilin Wang, Haerin Jung, Rachael L. Field, Xinya Zhang, Ta-Chiang Liu, Changqing Ma, James Written by S. Fraser, Jonathan R. Brestoff and Stephen J. Van Dyken, September 7, 2023. science.
DOI: 10.1126/science.add5649

This study was supported by the Children’s Discovery Institute, Barnes-Jewish Hospital Foundation, Rheumatic Disease Research Resource Base Center, National Institutes of Healthand Burroughs Wellcome Fund.

Source: scitechdaily.com