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The role of 1α, 25 dihydroxyvitamin D on muscle hypertrophy and insulin signaling
Author(s) -
Pinkston Catherine Marie,
Teegarden Dorothy
Publication year - 2009
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.23.1_supplement.553.15
Subject(s) - medicine , endocrinology , insulin , insulin receptor , protein kinase b , calcitriol receptor , muscle hypertrophy , myocyte , vitamin d and neurology , skeletal muscle , insulin resistance , basal (medicine) , chemistry , signal transduction , biochemistry
Clinical studies suggest that vitamin D may improve muscle function and insulin sensitivity. The aim of this study was to investigate the effect of the active metabolite of vitamin D, 1α, 25 dihydroxyvitamin D (1,25D), on muscle hypertrophy and insulin signaling in differentiated C2C12 myocytes. Co‐treatment of cells for 72 hr with 1,25D (10 nM) + insulin (100 nM) resulted in an increase in hypertrophy (21.46±0.27 protein/DNA) compared to insulin (15.76±1.09, p=0.005) or 1,25D treated cells (14.27±1.68). 1,25D + insulin treatment also increased basal insulin signaling (phosphorylated AKT/total AKT protein levels, 2.1±0.18 fold) compared to insulin (1.06±0.23, p=0.01) or 1,25D (1.03±0.08, p=0.003). In addition, insulin receptor mRNA expression levels increased following 72 hr treatment with 1,25D (4.73±1.70 fold, p=0.02) compared to vehicle (1.00±0.29). Consistent with this, 1,25D treatment for 72 hrs followed by 20 minute insulin stimulation increased phosphorylated AKT/total AKT (3.41±0.46 fold) compared to vehicle treated cells (1.00±0.91, p=0.03). This study suggests 1,25D enhances muscle hypertrophy as well as basal and insulin‐stimulated insulin signaling, potentially by increasing the expression of the insulin receptor in skeletal muscle cells. These results may, in part, explain the beneficial effects of vitamin D on muscle and insulin resistance. Supported by NIH DK069965. Grant Funding Source NIH DK069965