'Unusual' diabetes approach: Vitamin D may boost insulin cell survival, finds study

By Will Chu

- Last updated on GMT

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©iStock
Vitamin D appears to play a role in the preservation of the beta cells that produce, store and release the hormone insulin, opening up possibilities of harnessing this benefit to tackle type 2 diabetes, say researchers.

The discovery was made by Salk Institute researchers, who describe the activation of vitamin D receptors (VDR) at enhanced levels, which appear to dampen the inflammation process – one of the triggers for the condition.

“This study started out by looking at the role of vitamin D in beta cells," ​said first study author Dr Zong Wei, a research associate in Salk's Gene Expression Laboratory.

"Studies 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."

Vitamin D’s expanded role

T2D is already at epidemic proportions, with prospects for keeping the condition at bay or under control limited.

Triggered by insulin resistance, β cell malfunction is typified by reduced insulin secretion, later β cell loss, and progression of the disease.

Vitamin D is better known for its benefits to bone health but recent interest has focused on its anti-inflammatory potential.

Epidemiological and human genetic research associating vitamin D and the VDR to type 1 and T2D has led to possibilities that there may be a therapeutic role in the future.

Intriguingly, researchers​ claimed that vitamin D supplements reversed a number of diabetic phenotypes in T1D rodent models suppressing the auto-immunity process involved in diabetic onset.

Despite these findings, a therapeutic benefit in type 2 diabetic patients (or rodents) has yet to be established.

Study details

Along with colleagues from the University of Sydney, the team began using mice to test their theories by first using β cells created from embryonic stem cells,

Here, the team identified a compound, iBRD9 that appeared to enhance the activation of the vitamin D receptor when combined with vitamin D to improve the survival of beta cells.

The team achieved this by carrying a screening test to identify compounds that improved the survival chances of beta cells in a dish.

They then tested the combination in a mouse model of diabetes and demonstrated its ability to glucose back to normal levels in the animals.

The underlying process has to do with the method that genes are translated into proteins, the study said.

By combining the new compound with vitamin D certain protective genes could be expressed at much higher levels than they were in diseased cells.

‘An unusual therapeutic strategy’

“We uncover an unusual therapeutic strategy to suppress inflammation via sustained receptor activation in β cells,” ​the study said.

“This strategy demonstrates the power of genomic reprogramming, tackling the problem at the genome-wide level.

“As this is a natural way in which β cells normally limit chronic inflammation, exploiting the power of the VDR, its acetylation, and the safety of its ligands offer a very different approach in the treatment of T2D.”

Michael Downes, a Salk senior staff scientist and co-corresponding author added that by activating the vitamin D receptor the anti-inflammatory function of genes could be triggered to help cells survive under stressed conditions.

"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 commented.

The investigators added that, although the new compound did not appear to cause any side effects in the mice, further testing would needed before clinical trials could begin.

Source: Cell

Published online ahead of print: doi.org/10.1016/j.cell.2018.04.013

“Vitamin D Switches BAF Complexes to Protect β Cells.”

Authors: Zong Wei et al.

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