High-Fiber Diet Protects Against Development of Type 1 Diabetes


A high-fiber diet given to mice with type 1 diabetes almost eliminated their disease.

A diet rich in fiber may help protect against early-onset diabetes, a study suggests.

Investigators created a high-fiber diet that is broken down in the lower intestine into short-chain fatty acids. They believed that the short-chain fatty acids called butyrate and acetate would dampen down the immune system and have the potential to treat various disorders ranging from irritable bowel syndrome to asthma, theGuardianreported.

For latest study published inNature Immunology, investigators monitored the health of mice that had been bred to develop the rodent equivalent of juvenile diabetes.

More than 70% of animals on a normal diet had developed the condition after 30 weeks, whereas the high-fiber diet group was nearly entirely protected from the condition.

“What we saw was dramatic,” said lead investigator Charles Mackay. “When we give the diet to mice that spontaneously develop type 1 diabetes, we could almost completely eliminate their disease.”

Although the findings show promise, it is still too early to know whether such “medicinal foods” could protect individuals from juvenile diabetes, according to the investigators.

“There have been frustrations in the past that findings in these animals have not translated particularly well to human patients, but at other times they do,” Mackay said. “But we think our study established the concept that we can stop a disease with natural medicinal food.”

The diet used in the study is rich in a specific type of fiber derived from the plant product high amylose corn starch. This fiber is resistant to digestion in the upper intestine, and instead is fermented into acetate and butyrate by bacteria in the large intestine or colon.

When tested on mice, the investigators found that acetate and butyrate may work in different ways to cool down the immune reaction that destroys pancreatic cells in type 1 diabetes. Acetate seemed to lower the number of immune cells ready to attack the pancreatic cells, whereas butyrate boosted other cells that dampen the immune reaction.

Next, investigators hope to test the diet in human trials. If the diet proves to be successful in preventing or slowing juvenile diabetes, children may be able to have it as a powder on their food or dissolved in a drink.

“It really reinforces the importance of diet at shaping physiology and offers potential for tailored dietary-based interventions for diabetes,” said John Cryan, professor of anatomy and neuroscience at University College Cork. “It highlights how little we know about short-chain fatty acids despite them being among the most important microbial-mediated dietary breakdown products.”

Cryan noted that more work needs to be done regarding the potential adverse events of diets that boost levels of short-chain fatty acids. In one recent study, investigators found that in the brain, the compounds could affect immune processes that underlie Parkinson’s disease.

“Of course, all diet studies in mice need caution as human diet, the microbiome, and their interactions, are so much more complex,” Cryan said.

Emily Burns at Diabetes UK added, “We know that our immune system and gut work closely together. Understanding how the gut works in more detail could shed light on how to combat conditions that involve an immune attack, like type 1 diabetes. But there’s still a lot we don’t know. The idea that a special medicinal diet could help to regulate the immune system and prevent type 1 diabetes from developing is interesting, but this research is at a very early stage. We won’t know how effective this approach could be in people at risk of type 1 diabetes until research moves into human clinical trials.

“What we currently know is that type 1 diabetes is not linked to diet or lifestyle and it can’t be prevented. Diabetes UK is funding a great deal of research to find ways to stop the immune attack against the pancreas, in order to prevent type 1 diabetes in the future.”

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