Background Obesity has a strong influence on T2D in children and adolescents, by increasing the insulin resistance and damaging β-cell function. A growing number of studies suggest a link between vitamin D and type 2 diabetes

Aim of Study This study aimed to determine the impact of vitamin D and calcium supplementation on pancreatic β-cells function in terms of insulin secretion and sensitivity.

Methods This was a quasi-experimental study involving 30 obese and prepubescent Tunisian children (57% boys). During three months, the children received calcium and vitamin D supplementation at therapeutic doses. An oral glucose tolerance test (OGTT) was performed at the beginning and at the end of the study. The following metabolic definitions were applied: i) hyperinsulinism: insulinemia sum > 300 μ UI/ml during OGTT, ii) insulin-resistance: homeostatic model assessment of insulin- resistance > 2, iii) normal glycaemic profile: normal plasma levels during OGTT without any spike, and iv) pancreatic β-cells dysfunction reversibility: disappearance of the aforementioned disorders

Results The means ± standard-deviation of age and body mass index were 10.87 ± 1.9 years, and 30.17 ± 4.99 kg/m2, respectively. As risk factors, we identified a family type 2 diabetes in all cases, and family obesity in 48.57%. All the children had hypovitaminosis D, with insufficiency in 77.1% cases and deficiency in 22.9%.

Moreover, all of them were at the stage of hyperinsulinism associated with insulin-resistance. These disturbances were noted even in children having a normal glycaemic profile at OGTT. After calcium and vitamin D supplementation, glycaemic profile as well as insulin-secretion improved significantly (p < 0.0001). Hyperinsulinism and insulin-resistance decreased significantly by 56.67% (p < 0.0001) and 70.00% (p < 0.0001), respectively. Complete reversibility of these two disorders was noted in 26.6% of children

Conclusion(s) To conclude, in obese and prepubescent children, vitamin D and calcium supplementation led to the reversibility of the pancreatic β-cells dysfunction.