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Abstract
The mechanisms of diabetogenesis in children remain largely obscure. 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. 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. The means ± standard-deviation of age and body mass index were 10.87 ± 1.9 years, and 30.17 ± 4.99 kg/m2, respectively. All children 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. To conclude, in obese and prepubescent children, vitamin D and calcium supplementation led to the reversibility of the pancreatic β-cells dysfunction.
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1 Faculté de Médecine de Sousse, Service de Physiologie et Explorations Fonctionnelles, Université de Sousse, Sousse, Tunisie; University of Sousse, Farhat HACHED Hospital, Departement of physiology and functional explorations, Sousse, Tunisia Sousse
2 Faculté de Médecine de Sousse, Service de Physiologie et Explorations Fonctionnelles, Université de Sousse, Sousse, Tunisie; Laboratoire de recherche LR12SP09 «Insuffisance cardiaque», Université de Sousse, Hôpital Farhat HACHED, Sousse, Tunisie
3 Paediatrics Department, Farhat HACHED Hospital of Sousse, University of Sousse, Sousse, Tunisia
4 Basic Health Center «Sousse Jawhara”, Outpatient consultation, Sousse, Tunisia
5 Epidemiology Department, Farhat HACHED Hospital of Sousse, University of Sousse, Sousse, Tunisia
6 Faculté de Médecine de Sousse, Service de Physiologie et Explorations Fonctionnelles, Université de Sousse, Sousse, Tunisie; University of Sousse, Farhat HACHED Hospital, Departement of physiology and functional explorations, Sousse, Tunisia Sousse; Laboratoire de recherche LR12SP09 «Insuffisance cardiaque», Université de Sousse, Hôpital Farhat HACHED, Sousse, Tunisie