PMID- 37531790
OWN - NLM
STAT- Publisher
LR  - 20231014
IS  - 1873-1244 (Electronic)
IS  - 0899-9007 (Linking)
VI  - 115
DP  - 2023 Nov
TI  - Locomotor function of skeletal muscle is regulated by vitamin D via adenosine 
      triphosphate metabolism.
PG  - 112117
LID - S0899-9007(23)00146-6 [pii]
LID - 10.1016/j.nut.2023.112117 [doi]
AB  - OBJECTIVES: During musculoskeletal development, the vitamin D endocrine system is 
      crucial, because vitamin D-dependent calcium absorption is a major regulator of 
      bone growth. Because exercise regimens depend on bone mass, the direct action of 
      active vitamin D (1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)]) on 
      musculoskeletal performance should be determined. METHODS: To evaluate the effect 
      of 1,25(OH)(2)D(3) on muscle tissue, the vitamin D receptor (Vdr) gene was 
      genetically inactivated in mouse skeletal muscle and the role of 
      1,25(OH)(2)D(3)-VDR signaling on locomotor function was assessed. The direct 
      action of 1,25(OH)(2)D(3) on muscle development was determined using cultured 
      C2C12 cells with myogenic differentiation. RESULTS: The lack of Vdr activity in 
      skeletal muscle decreased spontaneous locomotor activity, suggesting that the 
      skeletal muscle performance depended on 1,25(OH)(2)D(3)-VDR signaling. Bone 
      phenotypes, reduced femoral bone mineral density, and accelerated osteoclast bone 
      resorption were confirmed in mice lacking skeletal muscle Vdr activity. In vitro 
      study revealed that the treatment with 1,25(OH)(2)D(3) decreased the cellular 
      adenosine triphosphate (ATP)-to-adenosine monophosphate ratio without reducing 
      ATP production. Remarkably, protein expressions of connexin 43, an ATP releaser 
      to extracellular space, and ATP metabolizing enzyme ectonucleotide 
      pyrophosphatase phosphodiesterase 1 were increased responding to 1,25(OH)(2)D(3) 
      treatment. Furthermore, the concentration of pyrophosphate in the culture medium, 
      which inhibits tissue calcification, was increased with 1,25(OH)(2)D(3) 
      treatment. In the presence of 1,25(OH)(2)D(3)-VDR signaling, calcium accumulation 
      was suppressed in both muscle samples isolated from mice and in cultured C2C12 
      cells. CONCLUSIONS: This study dissected the physiological functions of 
      1,25(OH)(2)D(3)-VDR signaling in muscle and revealed that regulation of ATP 
      dynamics is involved in sustaining locomotor function.
CI  - Copyright (c) 2023 Elsevier Inc. All rights reserved.
FAU - Mori, Risako
AU  - Mori R
AD  - Graduate School of Gastronomy Management, Ritsumeikan University, Kusatsu, Shiga, 
      Japan.
FAU - Mae, Megumi
AU  - Mae M
AD  - Department of Periodontology and Endodontology, Graduate School of Biomedical 
      Sciences, Nagasaki University, Nagasaki, Japan.
FAU - Yamanaka, Hitoki
AU  - Yamanaka H
AD  - Division of Animal Research, Research Center for Advanced Science and Technology, 
      Shinshu University, Matsumoto, Nagano, Japan.
FAU - Kato, Shigeaki
AU  - Kato S
AD  - Health Sciences Research Center, Iryo Sosei University, Iwaki, Fukushima, Japan; 
      Research Institute of Innovative Medicine, Tokiwa Foundation, Iwaki, Fukushima, 
      Japan.
FAU - Masuyama, Ritsuko
AU  - Masuyama R
AD  - Graduate School of Gastronomy Management, Ritsumeikan University, Kusatsu, Shiga, 
      Japan. Electronic address: ritsuko3@fc.ritsumei.ac.jp.
LA  - eng
PT  - Journal Article
DEP - 20230605
PL  - United States
TA  - Nutrition
JT  - Nutrition (Burbank, Los Angeles County, Calif.)
JID - 8802712
SB  - IM
OTO - NOTNLM
OT  - ATP dynamics
OT  - Calcium accumulation
OT  - Locomotor function
OT  - Skeletal muscle
OT  - Vitamin D
COIS- Declaration of Competing Interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2023/08/03 01:06
MHDA- 2023/08/03 01:06
CRDT- 2023/08/02 18:05
PHST- 2023/03/16 00:00 [received]
PHST- 2023/05/25 00:00 [revised]
PHST- 2023/06/01 00:00 [accepted]
PHST- 2023/08/03 01:06 [pubmed]
PHST- 2023/08/03 01:06 [medline]
PHST- 2023/08/02 18:05 [entrez]
AID - S0899-9007(23)00146-6 [pii]
AID - 10.1016/j.nut.2023.112117 [doi]
PST - ppublish
SO  - Nutrition. 2023 Nov;115:112117. doi: 10.1016/j.nut.2023.112117. Epub 2023 Jun 5.