TY - JOUR
T1 - Vestibular dysfunction in vitamin D receptor mutant mice
AU - Minasyan, Anna
AU - Keisala, Tiina
AU - Zou, Jing
AU - Zhang, Ya
AU - Toppila, Esko
AU - Syvälä, Heimo
AU - Lou, Yan Ru
AU - Kalueff, Allan V.
AU - Pyykkö, Ilmari
AU - Tuohimaa, Pentti
PY - 2009/4
Y1 - 2009/4
N2 - The vitamin D endocrine system is essential for calcium and bone homeostasis. Vitamin D deficits are associated with muscle weakness and osteoporosis, whereas vitamin D supplementation may improve muscle function, body sway and frequency of falls, growth and mineral homeostasis of bones. The loss of muscle strength and mass, as well as deficits in bone formation, lead to poor balance. Poor balance is one of the main causes of falls, and may lead to dangerous injuries. Here we examine balance functions in vitamin D receptor deficient (VDR-/-) mice, an animal model of vitamin D-dependent rickets type II, and in 1α-hydroxylase deficient (1α-OHase-/-) mice, an animal model of pseudovitamin D-deficiency rickets. Recently developed methods (tilting box, rotating tube test), swim test, and modified accelerating rotarod protocol were used to examine whether the absence of functional VDR, or the lack of a key vitamin D-activating enzyme, could lead to mouse vestibular dysfunctions. Overall, VDR-/- mice, but not 1α-OHase-/- mice, showed shorter latency to fall from the rotarod, smaller fall angle in the tilting box test, and aberrant poor swimming. These data suggest that VDR deficiency in mice is associated with decreased balance function, and may be relevant to poorer balance/posture control in humans with low levels of vitamin D.
AB - The vitamin D endocrine system is essential for calcium and bone homeostasis. Vitamin D deficits are associated with muscle weakness and osteoporosis, whereas vitamin D supplementation may improve muscle function, body sway and frequency of falls, growth and mineral homeostasis of bones. The loss of muscle strength and mass, as well as deficits in bone formation, lead to poor balance. Poor balance is one of the main causes of falls, and may lead to dangerous injuries. Here we examine balance functions in vitamin D receptor deficient (VDR-/-) mice, an animal model of vitamin D-dependent rickets type II, and in 1α-hydroxylase deficient (1α-OHase-/-) mice, an animal model of pseudovitamin D-deficiency rickets. Recently developed methods (tilting box, rotating tube test), swim test, and modified accelerating rotarod protocol were used to examine whether the absence of functional VDR, or the lack of a key vitamin D-activating enzyme, could lead to mouse vestibular dysfunctions. Overall, VDR-/- mice, but not 1α-OHase-/- mice, showed shorter latency to fall from the rotarod, smaller fall angle in the tilting box test, and aberrant poor swimming. These data suggest that VDR deficiency in mice is associated with decreased balance function, and may be relevant to poorer balance/posture control in humans with low levels of vitamin D.
KW - 1α-hydroxylase
KW - Pseudovitamin D-deficiency rickets
KW - Rickets type II
KW - Rotarod
KW - Rotating tube
KW - Swim test
KW - Tilting box
KW - Vestibular system
KW - Vitamin D
KW - Vitamin D receptor
UR - http://www.scopus.com/inward/record.url?scp=63049084834&partnerID=8YFLogxK
U2 - 10.1016/j.jsbmb.2009.01.020
DO - 10.1016/j.jsbmb.2009.01.020
M3 - Article
C2 - 19429446
AN - SCOPUS:63049084834
SN - 0960-0760
VL - 114
SP - 161
EP - 166
JO - Journal of Steroid Biochemistry and Molecular Biology
JF - Journal of Steroid Biochemistry and Molecular Biology
IS - 3-5
ER -