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Vitamin D supplementation increases true fractional calcium absorption in the absence of caloric restriction
Author(s) -
Shapses Sue A,
Sukumar Deeptha,
Schlussel Yvette,
Schneider Stephen H,
Ambia-Sobhan Hasina
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.386.6
Subject(s) - vitamin d and neurology , medicine , endocrinology , multivitamin , placebo , calcitriol , vitamin d deficiency , cholecalciferol , calcium , weight loss , vitamin , chemistry , obesity , alternative medicine , pathology
Caloric restriction is associated with a decrease in true fractional calcium absorption (TFCA). We examined whether vitamin D supplementation would attenuate the decrease in TFCA associated with weight loss (WL). Seventy‐seven women (58 ± 5.9 years of age; BMI of 30.2 ± 3.6 kg/m2; serum 25‐hydroxyvitamin D [25OHD] = 24.8 ± 5.7 ng/mL) were randomized into 4 groups (n=18–20/group) to receive either vitamin D supplementation (D) or placebo (Pl) and undergo WL or maintain their body weight (WM) over 6 weeks. The women received either 2500 IU/d [2100 IU D3 plus 400 IU from multivitamin (MV)] or 400 IU/d [Placebo plus 400 IU from MV] of vitamin D3 with 1.2 g Ca/d in all groups. Subjects in the WL group lost 3.8 ± 1.2% body weight with no differences between the D or Pl groups. Vitamin D did not influence calcitriol (1,25OH2D) but increased 25OHD. The 25OHD rise was greater during WL (WL‐D, +8 ± 6 ng/mL) vs. WM‐D (+3 ± 4 ng/m) (p < 0.01). WL decreased TFCA (p<0.01). D treatment suppressed PTH and increased TFCA (p<0.02). The TFCA change from baseline was greater (p < 0.01) in WM‐D (+0.037 ± 0.052) than WL‐D (−0.006 ± 0.036). TFCA change in the WL‐D group did not differ significantly from the WL‐Pl group (−0.026 ± 0.039). Since the rise in 25OHD in the WL‐D was more than double the WM‐D group and there was no rise in 1,25OH2D, other mechanisms are likely also contributing to the regulation of TFCA during caloric restriction. Supported by NIH‐AG12161.