Vitamin A deficiency decreases insulin production capability of pancreatic beta-cells, claims new study in Endocrine Journal.
Partially blocking vitamin A receptors in beta-cells significantly reduced insulin secretions in cells taken from both diabetics and non-diabetics, the multi-centre research team explained.
“We saw close to a 30% reduction,” commented Albert Salehi, senior researcher at Lund University Diabetes Centre, Malmo.
The study also found that without vitamin A, beta-cells were less able to resist inflammation. Where complete deficiency occurred, this resulted in cell death. Researchers propose these findings may be significant in cases of type-1 diabetes where inadequate beta-cells development has occurred in early life.
"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," says Salehi.
Vitamin A receptors
Discovery of a vitamin A receptor (known as the G-protein coupled receptor C5C (GPRC5C)) on the surface of pancreatic beta-cells prompted researchers to investigate their function.
“We thought it was important to find out why and what the purpose is of a cell surface receptor interacting with vitamin A,” explained Saleh.
Study findings suggest GPRC5C’s involvement in regulating genes responsible for insulin production, beta-cell proliferation and survival. In the study, vitamin A increased GPRC5C expression, which may be significant in future disease management.
Findings appear relevant to type 2, as well as type 1 diabetes.
“Levels of GPCR5C protein were reduced in islets from organ donors with type-2 diabetes, which may contribute to the reduction in β-cell mass and insulin secretion associated with type-2 diabetes,” wrote the team.
“Our results demonstrate that agents activating GPRC5C represent a novel modality for the treatment and/or prevention of diabetes by restoring and/or maintaining functional β-cell mass,” they added.
Salehi speculated that the eventual therapy might involve ‘vitamin A – like’ substances, due to risks associated with excessive intake of vitamin A itself.
"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," he concludes.