Endocrine Abstracts

Background: Vitamin D insufficiency (VDI) was reported to be associated with decreased insulin sensitivity (IS). Individuals with higher osteocalcin (OC) were shown to have better IS. Vitamin D regulates OC synthesis. Obese children carry an abnormal glucose homeostasis risk. Whether correction of VDI improves IS in obese children and mediates such effect via OC are unclear. We, therefore, studied glucose homeostasis, IS, vitamin D status and serum OC concentration in 230 obese children and examined vitamin D treatment effect on those parameters in 42 obese children with VDI.

Methods: Serum 25-hydroxyvitamin D (25-OHD) and OC levels were measured. An oral glucose tolerance test (OGTT) was performed. IS indices including HOMA-IR, Matsuda index and QUICKI and β-cell function, insulinogenic index (IGI) were calculated. Patients with VDI (25-OHD <30 ng/ml) were treated with 560 000 units of vitamin D2 and underwent the second OGTT after treatment completion.

Results: Of 230 patients, 58 (25%) had impaired glucose tolerance, impaired FPG and diabetes. One hundred and fifty-nine (69%) had VDI (25-OHD 22.3 (4.5) ng/ml), while the remaining 69 patients had adequate 25-OHD level of 34.6 (2.9) ng/ml. Comparing between patients with vitamin D sufficiency and insufficiency, there were no differences in BMI Z-score, OC, IS and β-cell function. However, 42 VDI patients who had 25-OHD increased to 55.5 (14.8) ng/ml after treatment completion had Matsuda index and QUICKI significantly increased from the pre-treatment values. Furthermore, the percentage of patients with abnormal OGTT was reduced from 33 to 19%. There were no changes in IGI and OC. OC was positively correlated with IGI (r=0.218, P=0.001) but not with IS.

Conclusion: Correction of VDI in obese children could enhance IS but not β-cell function. Critical level of 25-OHD may be needed to augment IS. IS enhancement seems not to be mediated by OC.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details are unavailable.