Promotion of osteoporosis by high-salt dietary through activation of osteoclasts in mice

YANG Yang, WU Wen-bin, LIU Bin, ZHANG Liang-ming, LUO Chun-xiao, RONG Li-min

Chinese Journal of Clinical Anatomy ›› 2019, Vol. 37 ›› Issue (3) : 267-272.

Chinese Journal of Clinical Anatomy ›› 2019, Vol. 37 ›› Issue (3) : 267-272. DOI: 10.13418/j.issn.1001-165x.2019.03.006

Promotion of osteoporosis by high-salt dietary through activation of osteoclasts in mice

  • YANG Yang, WU Wen-bin, LIU Bin, ZHANG Liang-ming, LUO Chun-xiao, RONG Li-min
Author information +
History +

Abstract

Objective To clarify the promotion effect of mouse osteoclast differentiation and osteoporosis by high-salt dietary. Methods Bone marrow mononuclear cells of C57 mice were obtained and induced to differentiate into osteoclasts. During this procedure, cells were cultured in each of 3 kinds of medium: no salt addition (control group), addition of 20 mmol/L salt (low-dose group), and addition of 40 mmol/L salt (high-dose group). The quantity of formed osteoclasts was acquired and compared among all 3 groups. In in-vivo study, a total of 24 C57 mice were divided into 3 groups randomly and equally: a normal group (regular feeding), an ovariectomy group (removal of ovary and regular feeding), and a high-salt group (removal of ovary, fed with 8% salt and drinking normal saline). At 6 weeks after administration, in all 3 cohorts, the number of generated osteoclasts in left femurs, as well as indicators associated with bone resorption and protection in serum were acquired. Moreover, bone histomorphometric parameters in right femurs were obtained and compared between each group using micro-CT. Results High-salt medium ex vitro enhanced the formation of osteoclasts significantly. Similarly, in vivo study found the largest number of osteoclasts in the high-salt group in comparison with the other 2 cohorts. Also in this group, C-telopeptide of type I collagen and receptor activator of nuclear factor-κ B ligand increased at different levels, while osteoprotegerin decreased remarkably. With respect to bone histomorphometric parameters in the high-salt group,  bone volume/total volume, cortical wall thickness, trabecular number and trabecular thickness were significantly increased whereas bone surface area/ bone volume, trabecular spacing and trabecular pattern factor were increased at various levels. Conclusions High-salt dietary enables the occurrence of osteoporosis through activating differentiation of bone marrow mononuclear cells into osteoclasts and strengthening of overall bone-resorption potential.

Key words

High-salt dietary /  Osteoclast /  Bone-resorption /  Osteoporosis

Cite this article

Download Citations
YANG Yang, WU Wen-bin, LIU Bin, ZHANG Liang-ming, LUO Chun-xiao, RONG Li-min. Promotion of osteoporosis by high-salt dietary through activation of osteoclasts in mice[J]. Chinese Journal of Clinical Anatomy. 2019, 37(3): 267-272 https://doi.org/10.13418/j.issn.1001-165x.2019.03.006

References

[1]  Lewiecki EM. New and emerging concepts in the use of denosumab for the treatment of osteoporosis[J]. Ther Adv Musculoskelet Dis, 2018, 10(11): 209-223.
[2] Baccaro LF, Conde DM, Costa-Paiva L, et al. The epidemiology and management of postmenopausal osteoporosis: a viewpoint from Brazil[J]. Clin Interv Aging, 2015, 10: 583-591.
[3]  Tella SH, Gallagher JC. Prevention and treatment of postmenopausal osteoporosis[J]. J Steroid Biochem Mol Biol, 2014, 142:155-170.
[4] Park SM, Joung JY, Cho YY, et al. Effect of high dietary sodium on bone turnover markers and urinary calcium excretion in Korean postmenopausal women with low bone mass[J]. Eur J Clin Nutr, 2015, 69(3):361-366.
[5] Wu L, Luthringer BJC, Feyerabend F, et al. Increased levels of sodium chloride directly increase osteoclastic differentiation and resorption in mice and men[J]. Osteoporos Int, 2017, 28(11): 3215-3228.
[6]  Iwasa Y, Shimoyama K, Aoki K, et al. The effect of high salt intake on the mandibular bone loss in Dahl-Iwai salt-sensitive rat[J]. J Med Dent Sci, 2000, 47(3): 187-195.
[7] Hernandez AL, Kitz A, Wu C, et al. Sodium chloride inhibits the suppressive function of FOXP3+ regulatory T cells[J]. J Clin Invest, 2015, 125(11): 4212-4222.
[8] Cho JH, Zhang R, Kilfoil PJ, et al. Delayed repolarization underlies ventricular arrhythmias in rats with heart failure and preserved ejection fraction[J]. Circulation, 2017, 136(21): 2037- 2050.
[9] Teucher B, Dainty JR, Spinks CA, et al. Sodium and bone health: impact of moderately high and low salt intakes on calcium metabolism in postmenopausal women[J]. J Bone Miner Res, 2008, 23(9): 1477-1485.
[10]Frings-Meuthen P, Buehlmeier J, Baecker N, et al. High sodium chloride intake exacerbates immobilization-induced bone resorption and protein losses[J]. J Appl Physiol (1985), 2011, 111(2): 537-542.
[11]Creedon A, Cashman KD. The effect of high salt and high protein intake on calcium metabolism, bone composition and bone resorption in the rat[J]. Br J Nutr, 2000, 84(1): 49-56.
[12]Buehlmeier J, Remer T, Frings-Meuthen P, et al. Glucocorticoid activity and metabolism with NaCl-induced low-grade metabolic acidosis and oral alkalization: results of two randomized controlled trials[J]. Endocrine, 2016, 52(1): 139-147.
[13]Buehlmeier J, Frings-Meuthen P, Remer T, et al. Alkaline salts to counteract bone resorption and protein wasting induced by high salt intake: results of a randomized controlled trial[J]. J Clin Endocrinol Metab, 2012, 97(12): 4789-4797.
[14]Robey IF. Examining the relationship between diet-induced acidosis and cancer[J]. Nutr Metab (Lond), 2012, 9(1): 72-82.
[15]Frings-Meuthen P, Baecker N, Heer M. Low-grade metabolic acidosis may be the cause of sodium chloride-induced exaggerated bone resorption[J]. J Bone Miner Res, 2008, 23(4): 517-524.
[16]Frick KK, LaPlante K, Bushinsky DA. RANK ligand and TNF-alpha mediate acid-induced bone calcium efflux in vitro[J]. Am J Physiol Renal Physiol, 2005, 289(5): F1005-F1011.
[17]Krieger NS, Frick KK, Bushinsky DA. Mechanism of acid-induced bone resorption[J]. Curr Opin Nephrol Hypertens, 2004, 13(4): 423-436.
[18]Albano G, Dolder S, Siegrist M, et al. Increased bone resorption by osteoclast-specific deletion of the sodium/calcium exchanger isoform 1 (NCX1)[J]. Pflugers Arch, 2017, 469(2): 225-233.

Accesses

Citation

Detail

Sections
Recommended

/