Targeting vitamin D receptors in insulin-producing cells could be an effective way to prevent type 2 diabetes, suggests a new study.

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Research suggests that targeting vitamin D receptors could protect the insulin-producing function of beta cells.

Researchers found that treating mice with vitamin D, lithocholic acid (LCA) propionate, and other vitamin D receptor agonists stopped dedifferentiation in mouse-derived beta cells, which is a process that has been linked to the development of type 2 diabetes.

Study co-author Fang-Xu Jiang, of the Harry Perkins Institute of Medical Research in Western Australia, and colleagues recently reported their findings in the journal Diabetes & Metabolism.

It is estimated that around 30.3 million people in the United States have diabetes, and around 1.5 million new cases are diagnosed every year.

Type 2 diabetes is the most common form of diabetes, arising when the beta cells of the pancreas are unable to produce sufficient amounts of insulin – the hormone that regulates blood glucose levels – or when the body is unable to use insulin effectively.

Overweight, obesity, hypertension, and high cholesterol are some more well-known risk factors for type 2 diabetes, but previous research has suggested that low levels of vitamin D may also play a role.

According to Jiang, precisely how low vitamin D might fuel the development of type 2 diabetes has been unclear. Their new study sheds light on the process, and it may have identified a way to prevent and treat one of the biggest health burdens in the U.S.

Jiang and colleagues came to their findings by studying the insulin-producing beta cells of mice.

In a high-glucose environment, the expression of vitamin D receptors in the beta cells was reduced. This led to dedifferentiation, wherein the beta cells lost their specialized ability to produce insulin.

The researchers then treated these beta cells with vitamin D, as well as analogs and derivatives of the vitamin, including LCA propionate.

The team found that all of these compounds led to an increase in the expression of vitamin D receptors in the beta cells. This, in turn, increased the expression of genes that encode insulin, protecting the cells against dedifferentiation.

LCA propionate had the strongest effect, the researchers note, suggesting that this molecule could be used to protect the insulin-producing function of beta cells and prevent or treat type 2 diabetes.

“Our investigation uncovered a compound,” explains study co-author Abraham Neelankal John, also of the Harry Perkins Institute of Medical Research, “that appears to prevent the onset and delay the progression of prediabetes and early diabetes.”

More research is needed but if proven in clinical trials, it would certainly become a drug for people at risk of developing type 2 diabetes and/or in the early stages of [it]. Our ultimate aim is to regenerate the health of people who suffer from type 2 diabetes.”

Abraham Neelankal John

Sherl Westlund, the executive director of Diabetes Research WA – a charity in Western Australia that helped to fund the research – hails the team’s findings as “extremely exciting.”

She adds, “It’s vital that research such as this is supported over the long-term because it has huge potential to change the lives of so many people at risk of or affected by type 2 diabetes.”