With diabetes now reaching epidemic proportions, unearthing an innovative way to tackle the condition is pressing. A new study investigates whether vitamin D might provide a new route to treatment.
Obesity, one of the major risk factors, is steadily rising, meaning that the number of people with type 2 diabetes is likely to follow suit.
The condition is caused by faulty beta cells in the pancreas. These cells manufacture and release insulin, the hormone essential for controlling glucose levels in the blood.
If beta cells produce too little insulin, or none at all, glucose can accumulate in the blood at levels that are toxic to cells and tissues.
A recent study, now published in the journal Cell, looked into a novel way of protecting beta cells, thereby slowing the onset of diabetes. The researchers, from the Salk Institute in La Jolla, CA, concentrated on a well-known compound: vitamin D.
Vitamin D is often referred to as the sunshine vitamin because it is created in our skin in response to direct sunlight. Previous studies have found a connection between low vitamin D levels and a higher risk of diabetes, but the mechanisms involved have been challenging to unravel.
This is due, in part, to the wide-reaching physiological functions of vitamin D; for instance, vitamin D is involved in cell growth, bone maintenance, neuromuscular activity, and the immune system. Also, importantly for this study, it has been implicated in inflammation.
“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.”
Senior study author Ronald Evans
To reach these conclusions, the researchers created beta cells using embryonic stem cells. Then, they tested a battery of compounds to investigate what effects they had on them.
The researchers found that a particular compound — called iBRD9 — boosted the activity of vitamin D receptors when they were bound to vitamin D molecules. This had a protective effect on the beta cells.
They demonstrated that, in a mouse model of diabetes, iBRD9 brought glucose levels back down into the normal range.
“This study started out by looking at the role of vitamin D in beta cells,” says first study author Zong Wei. “Epidemiological studies in patients,” he reports, “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.”
He continues, “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.”
They identified a way in which vitamin D might protect beta cells. It seems to involve transcription, or how genes are decoded to produce proteins. The introduction of iBRD9 caused genes with a protective effect to be transcribed at higher rates, protecting the beta cells.
“Activating the vitamin D receptor,” notes co-corresponding study author Michael Downes, “can trigger the anti-inflammatory function of genes 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.”
While the findings have clear implications for scientists trying to design new drugs to treat diabetes, there are further-reaching possibilities.
As study co-author Ruth Yu explains, “[B]ecause this is an important receptor, it could potentially be universal for any treatments where you need to boost the effect of vitamin D. For example, we are especially interested in looking at it in pancreatic cancer.”
Of course, before any drug can be used in humans, there are many essential hoops to be jumped through. Although there were no notable side effects in mice, only time will tell if it is safe for humans, too.