scholarly journals Calcium- and Phosphorus-Supplemented Diet Increases Bone Volume After Four Weeks of High-Speed Treadmill Exercise in Adult Mice

2020 ◽  
Author(s):  
Michael A. Friedman ◽  
David H. Kohn

ABSTRACTExercise has long-lasting benefits to bone health. Bone mass and the ability to exercise both decline with age, making it ideal to exercise earlier in life and to maximize gains in bone mass. Increasing strain on bone and frequency of loading during exercise can increase bone formation rate and cross-sectional area. Combining a short-term exercise program with a calcium- and phosphorus-supplemented diet increases cortical bone tissue mineral content (TMC) and area more than exercise alone in adult mice. It was hypothesized that combining high-speed running with a mineral-supplemented diet would lead to greater cortical TMC and area than high-speed running on a standard diet and low-speed running on a supplemented diet after 4 weeks. Male, 15-week old mice were assigned to 7 groups – a baseline group, non-exercised groups fed a control or supplemented diet, low-speed exercised groups fed a control or supplemented diet, and high-speed exercised groups fed a control or supplemented diet. Exercise consisted of 4 weeks of daily treadmill running for 20 min/day at 12 m/min or 20 m/min for low- and high-speed exercise, respectively. High-speed exercised mice had significantly lower body weight and lower tibial length after 4 weeks. Cortical TMC and area were significantly higher in high-speed exercised mice on the supplemented diet than high-speed exercised mice on the control diet. Trabecular bone volume (BV) and bone density were significantly higher in all groups on the supplemented diet than groups on the control diet, regardless of exercise. For mice on the control diet, non-exercised mice had significantly lower trabecular BV than baseline, while both speeds of exercise prevented this decline. There were few effects of exercise or diet on mechanical properties. For mice on the control diet, exercise significantly decreased serum PINP/CTX ratio on day 9 which may be preventing exercise from increasing bone mass or strength after only 4 weeks. For non-exercised mice on the supplemented diet, the serum PINP/CTX ratio on day 30 was significantly greater than for exercised mice, suggesting the supplemented diet may also lead to significantly greater bone mass in non-exercised mice if these interventions were extended beyond 4 weeks. Increasing treadmill speed can lower body weight while maintaining cortical and trabecular bone mass. A mineral-supplemented diet increases cortical and trabecular bone mass with high-speed exercise.

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2200
Author(s):  
Weirong Xing ◽  
Sheila Pourteymoor ◽  
Gustavo A. Gomez ◽  
Yian Chen ◽  
Subburaman Mohan

We previously showed that conditional disruption of the Phd2 gene in chondrocytes led to a massive increase in long bone trabecular bone mass. Loss of Phd2 gene expression or inhibition of PHD2 activity by a specific inhibitor resulted in a several-fold compensatory increase in Phd3 expression in chondrocytes. To determine if expression of PHD3 plays a role in endochondral bone formation, we conditionally disrupted the Phd3 gene in chondrocytes by crossing Phd3 floxed (Phd3flox/flox) mice with Col2α1-Cre mice. Loss of Phd3 expression in the chondrocytes of Cre+; Phd3flox/flox conditional knockout (cKO) mice was confirmed by real time PCR. At 16 weeks of age, neither body weight nor body length was significantly different in the Phd3 cKO mice compared to Cre−; Phd3flox/flox wild-type (WT) mice. Areal BMD measurements of total body as well as femur, tibia, and lumbar skeletal sites were not significantly different between the cKO and WT mice at 16 weeks of age. Micro-CT measurements revealed significant gender differences in the trabecular bone volume adjusted for tissue volume at the secondary spongiosa of the femur and the tibia for both genotypes, but no genotype difference was found for any of the trabecular bone measurements of either the femur or the tibia. Trabecular bone volume of distal femur epiphysis was not different between cKO and WT mice. Histology analyses revealed Phd3 cKO mice exhibited a comparable chondrocyte differentiation and proliferation, as evidenced by no changes in cartilage thickness and area in the cKO mice as compared to WT littermates. Consistent with the in vivo data, lentiviral shRNA-mediated knockdown of Phd3 expression in chondrocytes did not affect the expression of markers of chondrocyte differentiation (Col2, Col10, Acan, Sox9). Our study found that Phd2 but not Phd3 expressed in chondrocytes regulates endochondral bone formation, and the compensatory increase in Phd3 expression in the chondrocytes of Phd2 cKO mice is not the cause for increased trabecular bone mass in Phd2 cKO mice.


1988 ◽  
Vol 255 (2) ◽  
pp. R243-R247 ◽  
Author(s):  
L. Vico ◽  
D. Chappard ◽  
S. Palle ◽  
A. V. Bakulin ◽  
V. E. Novikov ◽  
...  

Seven male rats were exposed to 7 days of weightlessness in the Soviet mission COSMOS 1667 and compared with seven control rats by bone histomorphometric methods. In proximal tibial metaphysis, the trabecular bone volume was markedly reduced in flight animals. Trabeculae were decreased in number and thickness; this probably leads to alteration of bone mechanical properties. Formation activity (reflected by measurements of osteoid seams) was decreased at trabecular and endosteal levels. Resorption activity (estimated by count of osteoclast number and active resorption surfaces using a histoenzymologic method) remained unchanged. The imbalance between these cellular activities appears to be responsible for the loss of trabecular bone mass. In proximal femoral metaphysis, measurements were performed in an area located under the muscular insertions. The trabecular bone volume, despite a slight decrease in flight rats, was not significantly different from that of control rats. Furthermore, osteoclastic and osteoid parameters were unchanged. Differential responses between these two long bones need additional investigations. In thoracic and lumbar vertebrae no detectable change in bone mass and bone resorption parameters was found.


1988 ◽  
Vol 29 (6) ◽  
pp. 719-725 ◽  
Author(s):  
M. Nilsson ◽  
O. Johnell ◽  
K. Jonsson ◽  
I. Redlund-Johnell

Bone ◽  
2015 ◽  
Vol 81 ◽  
pp. 459-467 ◽  
Author(s):  
M. Pereira ◽  
J. Jeyabalan ◽  
C.S. Jørgensen ◽  
M. Hopkinson ◽  
A. Al-Jazzar ◽  
...  

2002 ◽  
Vol 17 (1) ◽  
pp. 119-127 ◽  
Author(s):  
Akinori Sakai ◽  
Takeshi Sakata ◽  
Shinya Tanaka ◽  
Ryuji Okazaki ◽  
Naoki Kunugita ◽  
...  

2020 ◽  
Author(s):  
Kevin A. Maupin ◽  
Daniel Dick ◽  
VARI Vivarium ◽  
Transgenics Core ◽  
Bart O. Williams

AbstractThe study of galectin-3 is complicated by its ability to function both intracellularly and extracellularly. While the mechanism of galectin-3 secretion is unclear, studies have shown that the mutation of a highly conserved arginine to a serine in human galectin-3 (LGALS3-R186S) blocks glycan binding and secretion. To gain insight into the roles of extracellular and intracellular functions of galectin-3, we generated mice with the equivalent mutation (Lgals3-R200S) using CRISPR/Cas9-directed homologous recombination. Consistent with a reduction in galectin-3 secretion, we observed significantly reduced galectin-3 protein levels in the plasma of heterozygous and homozygous mutant mice. We observed a similar increased bone mass phenotype in Lgals3-R200S mutant mice at 36 weeks as we previously observed in Lgals3-KO mice with slight variation. Like Lgals3-KO mice, Lgals3-R200S females, but not males, had significantly increased trabecular bone mass. However, only male Lgals3-R200S mice showed increased cortical bone expansion, which we had previously observed in both male and female Lgals3-KO mice and only in female mice using a separate Lgals3 null allele (Lgals3). These results suggest that the trabecular bone phenotype of Lgals3-KO mice was driven primarily by loss of extracellular galectin-3. However, the cortical bone phenotype of Lgals3-KO mice may have also been influenced by loss of intracellular galectin-3. Future analyses of these mice will aid in identifying the cellular and molecular mechanisms that contribute to the Lgals3-deficient bone phenotype as well as aid in distinguishing the extracellular vs. intracellular roles of galectin-3 in various signaling pathways.


Author(s):  
Yongqing Xiang ◽  
Vanessa Yingling ◽  
Jonathan Silverberg ◽  
Mitchell B. Schaffler ◽  
Theodore Raphan

2018 ◽  
Vol 33 (7) ◽  
pp. 1272-1282 ◽  
Author(s):  
Diana Olvera ◽  
Rachel Stolzenfeld ◽  
Joan C Marini ◽  
Michelle S Caird ◽  
Kenneth M Kozloff

2009 ◽  
Vol 12 (1) ◽  
pp. 117
Author(s):  
C. Battista ◽  
I. Chiodini ◽  
S. Muscarella ◽  
G. Guglielmi ◽  
M.L. Mascia ◽  
...  

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