A new study conducted by researchers at the Lund University Diabetes Centre in Sweden has identified a novel link between vitamin A and diabetes. The study – which was published in the Endocrine Journal – found that insulin-producing cells, known as pancreatic β-cells, display many cell surface receptors for vitamin A, suggesting that the compound plays an important role in maintaining proper cell function.
“There are no unnecessary surface receptors in human cells,” said Albert Salehi, senior researcher at the Lund University Diabetes Centre. “They all serve a purpose but which, in many cases, is still unknown and because of that they are called ‘orphan’ receptors. When we discovered that insulin cells have a cell surface expressed a receptor for vitamin A, we thought it was important to find out why and what the purpose is of a cell surface receptor interacting with vitamin A mediating a rapid response to vitamin A.”
The researchers have identified 220 different receptors – including the vitamin A receptor – present on the β-cell surface, however, not all of their functions have been elucidated. Salehi and his team believe that vitamin A is an important component during the development of β-cells and that the compound may also support the healthy functioning of the cells in the presence of inflammatory conditions.
After identifying the vitamin A receptors on the β-cells’ surface, the research team sought to determine whether the compound had an effect on the insulin-secreting ability of the cells. Using pancreatic β-cells collected from mice, and human patients with and without diabetes, the researchers partially blocked the vitamin A receptors and exposed the cells to glucose.
Salehi reported that blocking the vitamin A receptors was associated with an almost 30 percent decrease in insulin secretion. Impaired insulin secretion is a hallmark of type 2 diabetes, and the researchers noted that the β-cells collected from diabetic donors showed the same decreased insulin production, compared to healthy cells.
In the absence of vitamin A, the β-cells also showed decreased resistance to inflammation potentially leading to higher rates of cell death. As well as being applicable to individuals with type 2 diabetes, the findings could have an impact on patients with type 1 diabetes whose β-cells are underdeveloped.
Vitamin A can be found in many foods, including meat and dairy. While vitamin A supplements are available, they carry a risk of overdose which could cause inflammation of the liver. Because of these risks, Salehi says that vitamin A itself may not be an appropriate compound to recommend to diabetic patients, or those looking to promote pancreatic β-cell function.
“In animal experiments, it is known that newborn mice need vitamin A to develop their β-cells in a normal way,” said Salehi. “Most likely, the same applies to human beings. Children must absorb a sufficient amount of vitamin A through their diet. But we’re trying to find substances such as small molecules or peptides that are similar to the vitamin A could activate the newly found receptor while lacking the unwanted effects of vitamin A.”