Study2018

[Sustained serum 25-hydroxyvitamin D concentrations for one year with cholecalciferol supplementation improves glycaemic control and slows the decline of residual β cell function in children with type 1 diabetes]

Panjiyar RP, Dayal D, Attri SV, Sachdeva N, Sharma R, Bhalla AK

Pediatric endocrinology, diabetes, and metabolism · 22 citations

Review labels

Funding not disclosed

Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.

How it was studied

Design
Controlled clinical trial (classified by our AI screen)
Studied in
People
Main outcome
Health markers and function

Who paid for it

Funding
Funding not disclosed

Publication

Published
2018-01-01 · Pediatr Endocrinol Diabetes Metab · vol. 24 · issue 3 · pp. 111–117
Cited
38 citations · more than 87% of similar papers · 2.1× the field average
References
31 works
Access
Open access (free to publish) · CC-BY-NC-SA
Research areas
Vitamin D Research Studies · Diabetes and associated disorders · Celiac Disease Research and Management
Keywords
Cholecalciferol, Vitamin D and neurology, Type 2 diabetes, Internal medicine, Endocrinology, Medicine, Residual, Diabetes mellitus, Mathematics
MeSH
humans, diabetes mellitus, type 1, vitamin d deficiency, cholecalciferol, vitamin d, dietary supplements, child, female, male

6 authors

From IN

  • Ram Prakash PanjiyarPost Graduate Institute of Medical Education and Research
  • Devi Dayal · correspondingPost Graduate Institute of Medical Education and Research
  • Savita Verma AttriPost Graduate Institute of Medical Education and Research
  • Naresh Kumar SachdevaPost Graduate Institute of Medical Education and Research
  • Romesh SharmaPost Graduate Institute of Medical Education and Research
  • Anil Kumar BhallaPost Graduate Institute of Medical Education and Research

Abstract

Introduction

Studies using vitamin D for preservation of residual b-cell function (RBCF) and improvement of glycaemic control in type 1 diabetes (T1D) have shown inconsistent results. The possible causes of the discrepancies in the results are related to the dosage, type, and duration of vitamin D supplementation, C-peptide concentration at entry into the study, and the influence of glycaemic control on RBCF during supplementation.

Aim of the study

To evaluate the effect of cholecalciferol supplementation on RBCF and glycaemic control in children with T1D.

Material and methods

Forty-two children aged 6-12 years and within 1-2 years of diagnosis of T1D received cholecalciferol 3000 IU/day for one year (Group A). Thirty patients were recruited as controls (Group B). The mean changes in stimulated C-peptide levels, HbA1c, fasting blood glucose (FBG), mean blood glucose (MBG), and mean total daily insulin (TDI) dose from baseline to the study endpoint were calculated.

Results

Children in Group A showed lower mean FBG, MBG, HbA1c, and lesser TDI as compared to Group B at all follow-up visits. However, the differences in these parameters between the two groups reached statistical significance towards the study endpoint. Within group A, the decline in C-peptide levels from baseline to the endpoint was minor (-0.13 ±0.11, p-value = 0.16) as compared to a substantial decline in Group B (-0.41 ±0.07, p-value = 0.00). Comparison of the mean decrease in stimulated C-peptide levels from baseline to the endpoint between the two groups was also statistically significant (-0.13 ±0.11 vs. -0.41 ±0.07, p-value = 0.00). The mean decrease in FBG and MBG in Group A were greater, whereas the comparison of the mean decrease in HbA1c between the groups reached statistical significance at the study endpoint (p-value = 0.04). The decrease in the TDI was, however, similar in the two groups (p-value = 0.10).

Conclusions

Sustained serum 25-(OH)D concentrations with cholecalciferol supplementation for one year improves metabolic control and slows the decline of RBCF in children with T1D. Larger studies with longer duration and cholecalciferol dosage stratification are suggested.

Abstract via Europe PMC. Copyright remains with the authors or publisher.

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