OBJECTIVE: To determine the associations between body adiposity and change in serum 25-(OH)D levels over 2.6 years, and if these associations are mediated by metabolic and inflammatory factors in older adults. METHODS: This is a longitudinal study of 859 randomly selected subjects (mean 62 years, range 51-80, 49% women). Serum 25-hydroxyvitamin D [25-(OH)D] was assessed by radioimmunoassay at baseline and 2.6 years later. Baseline serum level of leptin was assessed by radioimmunoassay and interleukin (IL)-6 by a chemiluminescent immunoassay in the first 183 subjects. RESULTS: In multivariable analyses, body mass index, trunk fat percentage and waist-to-hip ratio were significant predictors of increased incident vitamin D deficiency [a 25-(OH)D < 50 nmol L⁻¹ at follow-up when ≥50 nmol L⁻¹ at baseline] and decreased recovery of vitamin D deficiency [a 25-(OH)D ≥ 50 nmol L⁻¹ at follow-up when < 50 nmol L⁻¹ at baseline]. Change in 25-(OH)D levels per annum was also independently predicted by baseline leptin (β: -0.09/unit, 95% CI: -0.17, -0.03), IL-6 (β: -0.68/quartile, 95% CI: -1.35, -0.02) and total cholesterol/high-density lipoprotein (HDL) ratio (β: -0.51, 95% CI: -0.88, -0.14). The associations between body adiposity measures and change in 25-(OH)D completely disappeared after adjustment for leptin, diminished after adjustment for IL-6, but remained unchanged after adjustment for total cholesterol/HDL ratio. All associations were independent of season and sun exposure. CONCLUSIONS: Body fat is not simply a passive reservoir for 25-(OH)D. In addition to season and sun exposure, 25-(OH)D levels appear to be determined by metabolic and, to a lesser extent, inflammatory factors, and these appear to mediate the effects of adiposity on change in 25-(OH)D.
OBJECTIVE: To determine the associations between body adiposity and change in serum 25-(OH)D levels over 2.6 years, and if these associations are mediated by metabolic and inflammatory factors in older adults. METHODS: This is a longitudinal study of 859 randomly selected subjects (mean 62 years, range 51-80, 49% women). Serum 25-hydroxyvitamin D [25-(OH)D] was assessed by radioimmunoassay at baseline and 2.6 years later. Baseline serum level of leptin was assessed by radioimmunoassay and interleukin (IL)-6 by a chemiluminescent immunoassay in the first 183 subjects. RESULTS: In multivariable analyses, body mass index, trunk fat percentage and waist-to-hip ratio were significant predictors of increased incident vitamin D deficiency [a 25-(OH)D < 50 nmol L⁻¹ at follow-up when ≥50 nmol L⁻¹ at baseline] and decreased recovery of vitamin D deficiency [a 25-(OH)D ≥ 50 nmol L⁻¹ at follow-up when < 50 nmol L⁻¹ at baseline]. Change in 25-(OH)D levels per annum was also independently predicted by baseline leptin (β: -0.09/unit, 95% CI: -0.17, -0.03), IL-6 (β: -0.68/quartile, 95% CI: -1.35, -0.02) and total cholesterol/high-density lipoprotein (HDL) ratio (β: -0.51, 95% CI: -0.88, -0.14). The associations between body adiposity measures and change in 25-(OH)D completely disappeared after adjustment for leptin, diminished after adjustment for IL-6, but remained unchanged after adjustment for total cholesterol/HDL ratio. All associations were independent of season and sun exposure. CONCLUSIONS: Body fat is not simply a passive reservoir for 25-(OH)D. In addition to season and sun exposure, 25-(OH)D levels appear to be determined by metabolic and, to a lesser extent, inflammatory factors, and these appear to mediate the effects of adiposity on change in 25-(OH)D.
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