Chitin provides important exoskeletal structure and protection to soft-bodied arthropods such as crustaceans, spiders, and insects, and it may play a surprising role in regulating mammalian metabolism and preventing weight gain. Chitin has been the focus of research into everything from stronger materials to better drug delivery. It has even been used to help fight malaria.
Scientists at Washington University School of Medicine in St. Louis found in studies on mice that chitin triggers an immune system response in the intestines, and that inhibiting enzymes in the body that fight the breakdown of chitin could provide a new way to treat obesity.
Steven Van Dyken, assistant professor of pathology and immunology, said: "Obesity is an epidemic. What we put into our bodies has a profound impact on our physiology and how we metabolize food. Profound effects. We are investigating ways to fight obesity based on what we are learning about how diet affects the immune system. "
When chitin is ingested, stomach cells activate the production of chitinase, an enzyme that breaks down polysaccharides. There are two chitinases in the human body, chitinotriosidase 1 (CHIT1) and acid mammalian chitinase (AMCase), which have long fought against pathogens that contain chitin in their cell walls, including virulent fungi and the intestinal lining of parasitic nematodes. They are also associated with inflammation caused by asthma and other dysregulated immune responses.
In the study, three groups of mice were fed a high-fat diet; one group had an inhibited chitinase enzyme that was unable to break down chitin, another group had normal chitinase production, and a third group did not consume any chitin. Animals that ate but could not break down chitin gained the least weight and had the lowest body fat compared to animals that did not eat chitin or that did but could break down chitin.
Scientists believe that the immune response triggered by animals unable to degrade chitin is the key to their ability to resist dietary obesity.
"We believe that the digestion of chitin relies primarily on the host's own chitinases," says Van-Dyken. "Gastric cells change their enzyme output through a process we call adaptation. But surprisingly, this process occurs without microbial input, because bacteria in the gastrointestinal tract are also the source of the chitinase enzyme that degrades chitin."
The researchers now hope to use this finding in human studies to see whether adding chitin to the diet, while blocking the production of chitinase, can have similar weight-control effects.
Fortunately, while some adventurous eaters don’t mind eating a bowl of crunchy crickets, chitin is also found in yeast and algae, as well as common edible fungi, and can easily be modified into tastier dietary supplements.
"We have several methods of inhibiting chitinase in the stomach. Pairing these with chitin-containing foods could have very real metabolic benefits," VanDyken said.
The study was published in the journal Science.