In:
European Journal of Endocrinology, Oxford University Press (OUP), Vol. 181, No. 4 ( 2019-10), p. 439-450
Abstract:
Vitamin D may potentially play a central role in glucose homeostasis and β-cell function (BCF), although studies are not consistent. Aim of our study was to test the hypotheses of a direct relationship between vitamin D, insulin sensitivity (IS) and BCF in overweight and obese non-diabetic children. Design and methods Cross-sectional study carried out at the Childhood Obesity Outpatient Clinic, University Hospital of Verona. One hundred twenty-two Caucasian overweight and obese children (age: 12.8 ± 0.2 years) were enrolled. Exclusion criteria: genetic or endocrine causes of obesity, chronic diseases or therapies. Patients underwent oral glucose tolerance test. HOMA-IR, Matsuda index and insulinogenic index were calculated. BCF was reconstructed by mathematical modeling and described by Derivative and Proportional Control. Total 25-hydroxyvitamin D and vitamin D-binding protein (VDBP) were measured. Two SNPs (rs4588 and rs7041) in the VDBP gene were studied, and bioavailable vitamin D (BVD) was calculated. Results Hypovitaminosis D was documented in 90% of patients. Forty-seven subjects were homozygous for both SNPs. Total vitamin D was positively correlated with Matsuda index ( P = 0.002), VDBP ( P = 0.045), and negatively with BMI SDS ( P = 0.043), HOMA-IR ( P = 0.008), HOMA-B ( P = 0.001), IGI ( P = 0.007), derivative control ( P = 0.036) and proportional control ( P = 0.018). Total vitamin D, adjusted for age, gender, BMI SDS, puberty and seasonality of vitamin D measurement, was a predictor of Matsuda index, HOMA-IR, HOMA-B, IGI, proportional control (all P 〈 0.05). BVD was positively correlated with total vitamin D ( P 〈 0.001) and negatively with BMI SDS ( P = 0.041). Conclusions Hypovitaminosis D negatively influences BCF and IS, suggesting that vitamin D levels might be implicated in glucose metabolism impairment in overweight and obese individuals.
Type of Medium:
Online Resource
ISSN:
0804-4643
,
1479-683X
Language:
Unknown
Publisher:
Oxford University Press (OUP)
Publication Date:
2019
detail.hit.zdb_id:
1485160-X
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