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Diet Enhancing Gut Microbes Shown to Slow Type 1 Diabetes

Eliana Mariño and Charles MacKay

Eliana Mariño, left, and Charles MacKay (Monash University)

28 March 2017. A diet that produces certain short-chain fatty acids in the gut is shown in lab mice to support the immune system and slow the onset of type 1 diabetes. An international team led by researchers at Monash University in Clayton, Australia published its findings in the 27 March issue of the journal Nature Immunology (paid subscription required).

Type 1 diabetes is an autoimmune disorder where the body does not produce insulin, and is diagnosed primarily in children or young adults. Autoimmune disorders are conditions where the immune system is tricked into attacking healthy cells and tissue as if they were foreign invaders, in this case, insulin-producing beta cells in the pancreas. About 5 percent of people with diabetes have this type of the disease.

Caring for type 1 diabetes requires constant management of the condition with tracking blood glucose levels and food intake, even for children. Advances in technology, such as closed-loop glucose measurement and and insulin-pump devices, make the management task easier. The team led by Monash immunology researcher and first author Eliana Mariño, however, is seeking ways of slowing or preventing development of type 1 diabetes itself through harnessing beneficial gut microbes, bacteria in the colon.

The Monash team — with associates from Australia, Germany, and Brazil — investigated the role of certain short-chain fatty acids to influence the immune system and protect against the auto-reactive immune system cells from attacking insulin-producing beta cells in the pancreas. Short-chain fatty acids are produced by supportive gut bacteria from the fermentation of fiber that survives the digestive system long enough to enter the colon.

Mariño and colleagues looked particularly at resistant starches that, as the name implies, resist digestion and are not broken down or absorbed in the stomach or small intestine, allowing them to be metabolized by bacteria in the gut into short-chain fatty acids. The team focused on two specific fatty acids from resistant starches, acetate and butyrate.

The researchers tested effects of acetate and butyrate on the immune systems in lab mice induced with the underlying genetic conditions supporting type 1 diabetes. Blood and stool samples show these diabetes-susceptible mice have lower concentrations of these fatty acids than comparable mice without the conditions supporting diabetes. When the susceptible mice were given diets rich in resistant starches to yield larger quantities of acetate and butyrate, however, the mice were protected against developing diabetes.

In addition, the team discovered acetate and butyrate worked differently in the immune systems of mice. Acetate was found to reduce the production of auto-reactive T-cells, white blood cells in the immune system erroneously programmed to attack healthy cells, in this case beta cells in the pancreas. Butyrate, on the other hand, was shown to help produce more functioning regulatory T-cells that help keep the auto-reactive T-cells under control.

Both fatty acids also help protect overall gut health and reduce enzymes that support development of diabetes. “Our research found that feeding mice that spontaneously develop type 1 autoimmune diabetes,” says Mariño in a Monash statement, “diets that release high levels of natural metabolites such as acetate or butyrate, improved the integrity of the gut lining, reduced pro-inflammatory factors, and promoted immune tolerance.”

“The findings illustrate the dawn of a new era in treating human disease with medicinal foods,” adds molecular biologist and senior author Charles MacKay. “The key next steps will be to understand, through proper clinical studies, how these results might be translated to patients at-risk or living with type 1 diabetes to prevent or delay progression.”

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