Diabetes is estimated to affect more than 29 million people in the United States.

Type 2 diabetes accounts for around 90 to 95 percent of all diagnosed cases, and this arises when the beta cells of the pancreas fail to produce enough insulin - the hormone that regulates blood glucose - or when the body is no longer able to use insulin effectively.

Type 1 diabetes, which accounts for the remaining 5 percent of cases, occurs when the immune system destroys beta cells, hampering insulin production.

In a new study - recently reported in the Endocrine Journal - researchers from the United Kingdom and Sweden discovered that there are large quantities of vitamin A receptors on the surface of beta cells, called GPRC5C.

"When we discovered that insulin cells have a cell surface expressed 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," says study co-author Albert Salehi, of the University of Lund in Sweden.

On partially blocking the vitamin A receptors in beta cells from mice - eliminating the ability of vitamin A to bind to these cells - the team found that their ability to secrete insulin was reduced in response to sugar.

Vitamin A deficiency may destroy beta cells

For their study, Salehi and colleagues also tested beta cells derived from humans with and without type 2 diabetes.

Again, the researchers partially blocked GPRC5C in these beta cells. When sugar was applied to these cells, the team found that their insulin-secreting ability decreased by almost 30 percent.

Since impaired insulin secretion is a major cause of type 2 diabetes, the researchers believe that this finding indicates that a lack of vitamin A - found in liver, fish oils, and various fruits and vegetables - may play a role in the disease.

What is more, the team discovered that a lack of vitamin A led to a reduction in beta cells' ability to stave off inflammation, while a complete deficiency of vitamin A caused beta cells to die.

This finding suggests that vitamin A deficiency may also be involved in type 1 diabetes, which is caused by the destruction of beta cells.

"In animal experiments it is known that newborn mice need vitamin A to develop their beta cells in a normal way. Most likely, the same applies to human beings. Children must absorb a sufficient amount of vitamin A through their diet," notes Salehi.

Compounds targeting GPRC5C may lead to new diabetes treatments

While these findings indicate that vitamin A may be beneficial for diabetes, the researchers stress that increasing the intake of this vitamin, particularly through supplements, may be too risky.

They note that excess vitamin A levels have been associated with osteoporosis and other health problems. However, they say that it is unlikely that one could get too much vitamin A from dietary sources alone.

Still, the team is now on the hunt for small molecules or peptides that can activate GPRC5C on the surface beta cells, but which do not cause the side effects associated with vitamin A.

The authors conclude:

"These observations therefore raise the exciting possibility that agents targeting GPRC5C may represent a novel therapeutic means of increasing the functional beta cell mass and also modestly boost insulin secretion."