Insect exoskeletons linked to new weight loss discovery

HONOLULU (KHON2) — Would you eat insects?

A new study has found that the exoskeletons of insects can induce weigh loss in mice. But what about humans?

The study was done by researchers at Washington University School of Medicine in St. Louis. The team was led by Steven Van Dyken, PhD who is an assistant professor of pathology & immunology.

“Digesting a crunchy critter starts with the audible grinding of its rigid protective covering — the exoskeleton,” said the team of researchers. “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.”

Van Dyken’s research team found that in mice digesting chitin, which is 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.”

It has been known for a long time that the human immune system has the capacity to safeguard the body from any number of threats. This includes bacteria, viruses, allergens and even cancer.

This led the team to find that a particular arm of the immune system is also involved in the digestion of chitin. 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.

Something that researchers found of interest is the inability for chitin to dissolved in liquid. It requires enzymes and harsh acidic conditions to digest.

“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.”

A postdoctoral research associate and first author on the study, Do-Hyun Kim, PhD, found that when he give chitin to germ-free mice lacking intestinal bacteria that the chitin activates immune responses in the absence of bacteria.

Hence, the research team found that the greatest impact on obesity in mice occurred when chitin activated the immune system but was not digested.

“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.

In the experiment, Mice were fed a high-fat diet along with chitin. They found that some mice lacked the ability to produce chitinases to break down chitin; and 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. This was compared with mice that didn’t eat chitin and with those that did but could break it down.

But, even for those mice that could break down the chitin still benefited metabolically from the exoskeletons since they adapted by overproducing chitinases to extract nutrients from chitin.

Van Dyken’s team’s research has been published in Science, and his team’s next plan is to follow up on their findings in humans. Their goal will be to determine whether chitin could be added to human diets to help control obesity.

“We have several ways to inhibit stomach chitinases,” Van Dyken concluded. “Pairing those approaches with a chitin-containing food might have a very real metabolic benefit.”