Baseline serum VD possibly influences the effect of VD repletion on inflammatory markers .
Risk of bias was present in most studies , thus supporting the need for higher quality studies in this area to more conclusively underst and the role VD supplementation has on inflammatory pathways
BACKGROUND Obesity induced low- grade chronic inflammation disrupts proper immune and metabolic function .
Vitamin D deficiency increases inflammation , which is associated with cardiometabolic risk .
This systematic review examines the association between oral vitamin D ( VD ) supplementation and circulating inflammatory biomarkers and glycemic outcomes from r and omized controlled trials ( RCTs ) of overweight and /or obese adults .
Long-term bioavailability after a single oral or intramuscular administration of 600,000 IU of ergocalciferol or cholecalciferol: implications for treatment and prophylaxis.
CONTEXT We previously showed that a single high dose of oral ( po ) cholecalciferol ( D₃ ) sharply increases serum 25-hydroxyvitamin D [ 25(OH)D ] . OBJECTIVE We evaluated the long-term bioavailability and metabolism of a single po or intramuscular ( i m ) high dose of ergocalciferol ( D₂ ) or D₃. DESIGN This was a prospect i ve intervention study . SETTING The study was conducted in an ambulatory care setting . PATIENTS Participants were 24 subjects with hypovitaminosis D. INTERVENTIONS A single dose of 600,000 IU of po or i m D₂ or D₃ was administered . MAIN OUTCOME MEASURES Serum 25(OH)D and 1,25-dihydroxyvitamin D [ 1,25(OH)₂D ] were measured at baseline and at days 30 , 60 , 90 , and 120 by RIA . Serum 1,25(OH)₂D₂ , 1,25-dihydroxyvitamin D₃ [ 1,25(OH)₂D₃ ] , 24,25-hydroxyvitamin D₂ [ 24,25(OH)D₂ ] , and 24,25-hydroxyvitamin D₃ [ 24,25(OH)D₃ ] were measured by liquid chromatography-t and em mass spectrometry in a subgroup of patients receiving the po formulations . RESULTS The areas under the curve of 25(OH)D after D₃ were significantly higher than those after D₂ ( P < .0001 ) . Serum 25(OH)D basal difference significantly increased at day 30 with po D₂ and D₃ ( P < .01 and P < .0001 ) and up to day 90 with po D₃ ( P < .01 ) . The i m formulations produced a slow increased , and values peaked at day 120 relative to the other time points ( P < .0001 ) . We found a decrease in 1,25(OH)₂D at day 30 ( P < .05 ) and up to day 120 ( P < .001 ) and an increase in 1,25(OH)₂D₂ at day 30 ( P < .01 ) and up to day 120 ( P < .01 ) after po D₂. Oral D₂ and D₃ produced increases in 24,25(OH)D₂ and 24,25(OH)D₃ , respectively , at day 30 ( P < .001 ) . CONCLUSIONS A po dose of 600,000 IU of D₂ or D₃ is initially more effective in increasing serum 25(OH)D than the equivalent i m dose and is rapidly metabolized . Our RIA assay for 1,25(OH)₂D may not recognize
Baseline serum VD possibly influences the effect of VD repletion on inflammatory markers .
Risk of bias was present in most studies , thus supporting the need for higher quality studies in this area to more conclusively underst and the role VD supplementation has on inflammatory pathways
BACKGROUND Obesity induced low- grade chronic inflammation disrupts proper immune and metabolic function .
Vitamin D deficiency increases inflammation , which is associated with cardiometabolic risk .
This systematic review examines the association between oral vitamin D ( VD ) supplementation and circulating inflammatory biomarkers and glycemic outcomes from r and omized controlled trials ( RCTs ) of overweight and /or obese adults .