Reversibility of pancreatic β-cells dysfunction after vitamin D and calcium supplementation: a pilot study in a population of obese and prepubescent North-African children

补充维生素D和钙后胰岛β细胞功能障碍的可逆性:一项针对北非肥胖青春期前儿童的初步研究

阅读:2

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/m(2), 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.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。