Vitamin D found to have a role in diabetes treatment by boosting insulin producing cells

by Barbara Hewitt on June 4, 2018

Scientists in the United States have discovered a potential new approach for treating diabetes by protecting beta cells by using vitamin D to boost their function.

Beta cells in the pancreas produce, store and release the hormone insulin and when they become dysfunctional, the body can’t make insulin to control blood sugar.

Vitamin D

(Kavun Halyna/

Researchers at the Salk Institute in San Diego found that the vitamin D receptor is an important modulator of both inflammation and beta cell survival. Working with mouse models they were able to see how it proved beneficial in treating damaged beta cells.

It also provided new insights about gene regulation that could be applied to developing treatments for other diseases, including cancer.

‘We know that diabetes is a disease caused by inflammation. In this study, we identified the vitamin D receptor as an important modulator of both inflammation and beta cell survival,’ said senior author Ronald Evans.

Using beta cells created from embryonic stem cells, the researchers were able to identify a compound iBRD9 that appeared to enhance the activation of the vitamin D receptor when it was combined with vitamin D to improve the survival of beta cells.

The team accomplished this by conducting a screening test to look for compounds that improved the survival of beta cells in a dish. They then tested the combination in a mouse model of diabetes and showed that it could bring glucose back to normal levels in the animals.

‘Epidemiological studies in patients have suggested a correlation between high vitamin D concentrations in the blood and a lower risk of diabetes, but the underlying mechanism was not well understood. It’s been hard to protect beta cells with the vitamin alone. We now have some ideas about how we might be able to take advantage of this connection,’ said first author Zong Wei.

The underlying process is to do with the way that genes are translated into proteins. Combining the new compound with vitamin D allowed certain protective genes to be expressed at much higher levels than they are in diseased cells.

‘Activating the vitamin D receptor can trigger the anti-inflammatory function of genes to help cells survive under stressed conditions,’ said Michael Downes, a Salk senior staff scientist and co–corresponding author.

‘By using a screening system that we developed in the lab, we’ve been able to identify an important piece of that puzzle that allows for super-activation of the Vitamin D pathway,’ he pointed out.

The discovery could have far reaching implications as it identifies a basic mechanism that can be translated into other areas. ‘In this study, we looked at diabetes, but because this is an important receptor it could potentially be universal for any treatments where you need to boost the effect of vitamin D,’ said Ruth Yu, a Salk staff researcher and one of the study’s authors.

‘For example, we are especially interested in looking at it in pancreatic cancer, which is a disease that our lab already studies,’ she explained, adding that although the new compound did not appear to cause any side effects in the mice, further testing is needed before clinical trials can begin.

The opinions expressed in this article do not necessarily reflect the views of the Community and should not be interpreted as medical advice. Please see your doctor before making any changes to your diabetes management plan.

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