title: IMPROVEMENT IN PANCREATIC β-CELL FUNCTION WITH VITAMIN D AND CALCIUM SUPPLEMENTATION IN VITAMIN D-DEFICIENT NONDIABETIC SUBJECTS.
abstract: OBJECTIVE
  There are varied reports on the effect of vitamin D supplementation on β-cell function and plasma glucose levels. The objective of this study was to examine the effect of vitamin D and calcium supplementation on β-cell function and plasma glucose levels in subjects with vitamin D deficiency.
  
  
  METHODS
  Nondiabetic subjects (N = 48) were screened for their serum 25-hydroxyvitamin D (25-OHD), albumin, creatinine, calcium, phosphorus, alkaline phosphatase, and intact parathyroid hormone (PTH) status. Subjects with 25-OHD deficiency underwent a 2-hour oral glucose tolerance test. Cholecalciferol (9,570 international units [IU]/day; tolerable upper intake level, 10,000 IU/day; according to the Endocrine Society guidelines for vitamin D supplementation) and calcium (1 g/day) were supplemented.
  
  
  RESULTS
  Thirty-seven patients with 25-OHD deficiency participated in the study. The baseline and post-vitamin D/calcium supplementation and the difference (corrected) were: serum calcium, 9 ± 0.33 and 8.33 ± 1.09 mg/dL (-0.66 ± 1.11 mg/dL); 25-OHD, 8.75 ± 4.75 and 36.83 ± 18.68 ng/mL (28.00 ± 18.33 ng/mL); PTH, 57.9 ± 29.3 and 36.33 ± 22.48 pg/mL (-20.25 ± 22.45 pg/mL); fasting plasma glucose, 78.23 ± 7.60 and 73.47 ± 9.82 mg/dL (-4.88 ± 10.65 mg/dL); and homeostasis model assessment-2-percent β-cell function C-peptide secretion (HOMA-2-%B C-PEP), 183.17 ± 88.74 and 194.67 ± 54.71 (11.38 ± 94.27). Significant differences were observed between baseline and post-vitamin D/calcium supplementation serum levels of corrected calcium (Z, -3.751; P<.0001), 25-OHD (Z, -4.9; P<.0001), intact PTH (Z, -4.04; P<.0001), fasting plasma glucose (Z, -2.7; P<.007), and HOMA-2-%B C-PEP (Z, -1.923; P<.05) as determined by Wilcoxon signed rank test. Insulin resistance as measured by HOMA was unchanged.
  
  
  CONCLUSIONS
  Optimizing serum 25-OHD concentrations and supplementation with calcium improves fasting plasma glucose levels and β-cell secretory reserve. Larger randomized control studies are needed to determine if correction of 25-OHD deficiency will improve insulin secretion and prevent abnormalities of glucose homeostasis.
authors.forename: Chittari Venkata
authors.initials: CV
authors.lastname: Harinarayan
authors.forename: Shalini
authors.initials: S
authors.lastname: Arvind
authors.forename: Shalini
authors.initials: S
authors.lastname: Joshi
authors.forename: Kandavel
authors.initials: K
authors.lastname: Thennarasu
authors.forename: Vasanthi
authors.initials: V
authors.lastname: Vedavyas
authors.forename: Anushka
authors.initials: A
authors.lastname: Baindur
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D002136:Calcium, Dietary / Q000008:administration & dosage*; D019587:Dietary Supplements; D005260:Female; D006801:Humans; D050417:Insulin-Secreting Cells / Q000502:physiology*; D008297:Male; D014807:Vitamin D / Q000008:administration & dosage* / Q000031:analogs & derivatives / Q000097:blood; D014808:Vitamin D Deficiency / Q000188:drug therapy* / Q000503:physiopathology
chemical_list: D001786:Blood Glucose; D002136:Calcium, Dietary; D014807:Vitamin D; C104450:25-hydroxyvitamin D