OBJECTIVE: We aimed to investigate whether vitamin D supplementation modulates peripheral blood mononuclear cell (PBMC) telomerase activity in overweight African Americans. DESIGN: A double blind, randomized and placebo-controlled clinical trial (#NCT01141192) was recently conducted. SUBJECTS AND METHODS: African-American adults were randomly assigned to either the placebo, or the vitamin Dgroup (60,000 IU per month (equivalent to ~2000 IU per day) oral vitamin D3 supplementation). Fresh PBMCs were collected from 37 subjects (18 in theplacebo group and 19 in the vitamin D group), both at baseline and 16 weeks. PBMC telomerase activity was measured by the telomeric repeat amplification protocol. RESULTS:Serum 25 hydroxyvitamin D levels increased from 40.7±15.7 at baseline to 48.1±17.5 nmol l(-1) at posttest (P=0.004) in the placebo group, and from 35.4±11.3 at baseline to 103.7±31.5 nmol l(-1) at posttests (P<0.0001) in the vitamin D group. In the vitamin D group, PBMC telomerase activity increased by 19.2% from baseline (1.56±0.29 absorbance reading unit (AU)) to posttest (1.86±0.42 AU, P<0.0001). The significance persisted after controlling for age, sex and body mass index (P=0.039). PBMC telomerase activity in the placebo group did not change from baseline (1.43±0.26 AU) to posttest (1.46±0.27 AU, P=0.157). CONCLUSION:Vitamin D supplementation significantly increased PBMC telomerase activity in overweight African Americans. Our data suggest that vitamin D may improve telomere maintenance and prevent cell senescence and counteract obesity-induced acceleration of cellular aging.
RCT Entities:
OBJECTIVE: We aimed to investigate whether vitamin D supplementation modulates peripheral blood mononuclear cell (PBMC) telomerase activity in overweight African Americans. DESIGN: A double blind, randomized and placebo-controlled clinical trial (#NCT01141192) was recently conducted. SUBJECTS AND METHODS: African-American adults were randomly assigned to either the placebo, or the vitamin D group (60,000 IU per month (equivalent to ~2000 IU per day) oral vitamin D3 supplementation). Fresh PBMCs were collected from 37 subjects (18 in the placebo group and 19 in the vitamin D group), both at baseline and 16 weeks. PBMC telomerase activity was measured by the telomeric repeat amplification protocol. RESULTS: Serum 25 hydroxyvitamin D levels increased from 40.7±15.7 at baseline to 48.1±17.5 nmol l(-1) at posttest (P=0.004) in the placebo group, and from 35.4±11.3 at baseline to 103.7±31.5 nmol l(-1) at posttests (P<0.0001) in the vitamin D group. In the vitamin D group, PBMC telomerase activity increased by 19.2% from baseline (1.56±0.29 absorbance reading unit (AU)) to posttest (1.86±0.42 AU, P<0.0001). The significance persisted after controlling for age, sex and body mass index (P=0.039). PBMC telomerase activity in the placebo group did not change from baseline (1.43±0.26 AU) to posttest (1.46±0.27 AU, P=0.157). CONCLUSION:Vitamin D supplementation significantly increased PBMC telomerase activity in overweight African Americans. Our data suggest that vitamin D may improve telomere maintenance and prevent cell senescence and counteract obesity-induced acceleration of cellular aging.
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