Key result
1,25(OH)2D3 and 25(OH)D3 reduce murine myoblast proliferation and stimulate VDR expression without altering myotube size.
Why the study?
Whether vitamin D directly reduces muscle fiber atrophy or stimulates muscle fiber hypertrophy remains subject of debate, and the role of local conversion of 25(OH)D to 1,25(OH)2D in muscle fiber size regulation is unclear.
Skeletal muscle cells respond to and metabolize both 1,25(OH)2D3 and 25(OH)D3, affecting proliferation and differentiation but not myotube size in vitro.
Answers are grounded in this paper and cite their sources.
Vitamin D metabolites directly affect myoblast proliferation and differentiation in vitro; leaves open whether this regulates human muscle fiber size.
An adequate vitamin D status is essential to optimize muscle strength. However, whether vitamin D directly reduces muscle fiber atrophy or stimulates muscle fiber hypertrophy remains subject of debate. A mechanism that may affect the role of vitamin D in the regulation of muscle fiber size is the local conversion of 25(OH)D to 1,25(OH)2 D by 1α-hydroxylase. Therefore, we investigated in a murine C2C12 myoblast culture whether both 1,25(OH)2 D3 and 25(OH)D3 affect myoblast proliferation, differentiation, and myotube size and whether these cells are able to metabolize 25(OH)D3 and 1,25(OH)2 D3 . We show that myoblasts not only responded to 1,25(OH)2 D3 , but also to the precursor 25(OH)D3 by increasing their VDR mRNA expression and reducing their proliferation. In differentiating myoblasts and myotubes 1,25(OH)2 D3 as well as 25(OH)D3 stimulated VDR mRNA expression and in myotubes 1,25(OH)2 D3 also stimulated MHC mRNA expression. However, this occurred without notable effects on myotube size. Moreover, no effects on the Akt/mTOR signaling pathway as well as MyoD and myogenin mRNA levels were observed. Interestingly, both myoblasts and myotubes expressed CYP27B1 and CYP24 mRNA which are required for vitamin D3 metabolism. Although 1α-hydroxylase activity could not be shown in myotubes, after treatment with 1,25(OH)2 D3 or 25(OH)D3 myotubes showed strongly elevated CYP24 mRNA levels compared to untreated cells. Moreover, myotubes were able to convert 25(OH)D3 to 24R,25(OH)2 D3 which may play a role in myoblast proliferation and differentiation. These data suggest that skeletal muscle is not only a direct target for vitamin D3 metabolites, but is also able to metabolize 25(OH)D3 and 1,25(OH)2 D3 . J. Cell. Physiol. 231: 2517-2528, 2016.
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Meijden et al. (2016) studied Murine C2C12 myoblast culture. 1,25(OH)2D3 and 25(OH)D3 vs. Untreated cells was evaluated on Myoblast proliferation, differentiation, and myotube size. Treatment of murine C2C12 myoblasts with 1,25(OH)2D3 and 25(OH)D3 reduced proliferation and stimulated VDR mRNA expression, but had no notable effects on myotube size.
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