The new study shows that maintaining vitamin D receptor (VDR) levels in insulin-producing cells which synthesizes and secretes insulin contributes to protect against diabetes and counteract the pancreatic cell damage caused by the progression of diabetes.
Researchers at the CIBER’S area of Diabetes and Associated Metabolic Diseases (CIBERDEM) and the Universitat Autònoma de Barcelona (UAB) have demonstrated that VDR is a potential therapeutic target in prevention and treatment of diabetes.
Vitamin D deficiency has been linked to a greater prevalence of Type 1 and Type 2 diabetes and the relation of diabetes with variations in the receptor gene of vitamin D has also been explained.
The specific participation of Vitamin D receptor in the development of diabetes, particularly in the β cells is still unknown. Because of this reason, researchers have focused their efforts on understanding the role of Vitamin D receptor of the pancreatic cells in diabetes development, by conducting experiments in mice.
According to the statistics of the American Diabetes Association, around 34.2 million people in the United States have diabetes. 1.5 million Americans are diagnosed with diabetes every year. It was the seventh leading cause of deaths in the U.S. in 2017 based on the 83,564 death certificates in which diabetes was mentioned as the cause of death. It was mentioned as a cause of death in a total of 270,702 death certificates.
According to the CDC’s 2020 report about diabetes statistics, 88 million adults in America have prediabetes. New cases of both Type 1 and Type 2 diabetes have significantly increased among youth.
Researchers found lower expression of VDR in the pancreatic cells of mice in both types of diabetes. They demonstrated that overexpression of VDR in pancreatic β cells of diabetic mice counteracted the damage caused by diabetes and proved that sustained levels of VRD in the β cells could preserve their function and mass and protect against diabetes.
The study outcomes suggest that maintaining VDR levels might be essential for counteracting the damage caused by the disease to the β cells and protect against the progression of diabetes.
CIBERDEM researcher at the Centre for Animal Biotechnology and Gene Therapy at the Universitat Autònoma de Barcelona and the coauthor, Alba Casellas said that sustained levels of VDR protected transgenic mice from hyperglycemia and also partially preserved the mass of β cells so that reducing inflammation and diabetes.
These findings reveal that vitamin D receptor plays an unprecedented role in the pathophysiology of diabetes.
The study also confirmed that the expression of vitamin D receptor was negatively correlated with the levels of circulating sugar, glucose stimulates VDR.
Casellas shared that unexpectedly they found that VDR decreases when the levels of circulating sugar are physiologically low such as after fasting. Relating these findings to the characteristics of insulin-producing cells in diabetic individuals, they found that these findings could be explained because of the fact that diabetes is correlated with low intracellular levels of circulating sugar.
Although the benefits of vitamin D in preventing diabetes have been widely reported clinical data on the effectiveness of vitamin D in improving diabetes are controversial.
Dr. Casellas said that discrepancies in ineffectiveness of supplements of vitamin D may be due to negative regulation of vitamin D receptor during diabetes.
Study authors suggested that for gaining positive results, the dosage of vitamin D supplements must be scheduled in the absence of expression of VDR decrease.
Researchers conclude that future strategies for diabetes treatment should be based on a better understanding of the mechanisms underlying the negative regulation of vitamin D receptor during diabetes and must focus on restoring its levels.