Relationship of serum GDF11 levels with bone mineral density and bone turnover markers in postmenopausal Chinese women

Yusi Chen , Qi Guo , Min Zhang , Shumin Song , Tonggui Quan , Tiepeng Zhao , Hongliang Li , Lijuan Guo , Tiejian Jiang , Guangwei Wang

Bone Research ›› 2016, Vol. 4 ›› Issue (1) : 16012

PDF
Bone Research ›› 2016, Vol. 4 ›› Issue (1) : 16012 DOI: 10.1038/boneres.2016.12
Article

Relationship of serum GDF11 levels with bone mineral density and bone turnover markers in postmenopausal Chinese women

Author information +
History +
PDF

Abstract

Growth differentiation factor 11 (GDF11) is an important circulating factor that regulates aging. However, the role of GDF11 in bone metabolism remains unclear. The present study was undertaken to investigate the relationship between serum GDF11 level, bone mass, and bone turnover markers in postmenopausal Chinese women. Serum GDF11 level, bone turnover biochemical markers, and bone mineral density (BMD) were determined in 169 postmenopausal Chinese women (47–78 years old). GDF11 serum levels increased with aging. There were negative correlations between GDF11 and BMD at the various skeletal sites. After adjusting for age and body mass index (BMI), the correlations remained statistically significant. In the multiple linear stepwise regression analysis, age or years since menopause, BMI, GDF11, and estradiol were independent predictors of BMD. A significant negative correlation between GDF11 and bone alkaline phosphatase (BAP) was identified and remained significant after adjusting for age and BMI. No significant correlation was noted between cross-linked N-telopeptides of type I collagen (NTX) and GDF11. In conclusion, GDF11 is an independent negative predictor of BMD and correlates with a biomarker of bone formation, BAP, in postmenopausal Chinese women. GDF11 potentially exerts a negative effect on bone mass by regulating bone formation.

Osteoporosis: A biomarker for age-dependent bone loss

A study in Chinese women reveals that levels of a protein circulating in the blood correlate with age-dependent bone loss. Although there is compelling evidence suggesting that growth differentiation factor 11 (GDF11) levels increase with age, different groups have obtained contradictory findings on its role in osteoporosis. Researchers led by GuangWei Wang at the Hunan University of Medicine and TieJian Jiang at the Xiangya Hospital of Central South University have now obtained evidence that this protein is linked with skeletal degeneration. After analyzing blood samples from 169 postmenopausal women, the researchers determined that elevated GDF11 levels correlated with reduced hip bone density and lower levels of an established protein biomarker of new bone formation. These findings offer additional support for GDF11 involvement in osteoporosis progression, although further research will be needed to clarify the mechanism.

Cite this article

Download citation ▾
Yusi Chen, Qi Guo, Min Zhang, Shumin Song, Tonggui Quan, Tiepeng Zhao, Hongliang Li, Lijuan Guo, Tiejian Jiang, Guangwei Wang. Relationship of serum GDF11 levels with bone mineral density and bone turnover markers in postmenopausal Chinese women. Bone Research, 2016, 4(1): 16012 DOI:10.1038/boneres.2016.12

登录浏览全文

4963

注册一个新账户 忘记密码

References

[1]

Harvey N, Dennison E, Cooper C. Osteoporosis: a lifecourse approach. J Bone Miner Res, 2014, 29: 1917-1925

[2]

Liu Z, Piao J, Pang L et al The diagnostic criteria for primary osteoporosis and the incidence of osteoporosis in China. J Bone Miner Metab, 2002, 20: 181-189

[3]

Li H, Xie H, Liu W et al A novel microRNA targeting HDAC5 regulates osteoblast differentiation in mice and contributes to primary osteoporosis in humans. J Clin Invest, 2009, 119: 3666-3677

[4]

Li CJ, Cheng P, Liang MK et al MicroRNA-188 regulates age-related switch between osteoblast and adipocyte differentiation. J Clin Invest, 2015, 125: 1509-1522

[5]

Xian L, Wu X, Pang L et al Matrix IGF-1 maintains bone mass by activation of mTOR in mesenchymal stem cells. Nat Med, 2012, 18: 1095-1101

[6]

Loffredo FS, Steinhauser ML, Jay SM et al Growth differentiation factor 11 is a circulating factor that reverses age-related cardiac hypertrophy. Cell, 2013, 153: 828-839

[7]

Katsimpardi L, Litterman NK, Schein PA et al Vascular and neurogenic rejuvenation of the aging mouse brain by young systemic factors. Science, 2014, 344: 630-634

[8]

Sinha M, Jang YC, Oh J et al Restoring systemic GDF11 levels reverses age-related dysfunction in mouse skeletal muscle. Science, 2014, 344: 649-652

[9]

Wharton K, Derynck R. TGFbeta family signaling: novel insights in development and disease. Development, 2009, 136: 3691-3697

[10]

Wu MY, Hill CS. Tgf-beta superfamily signaling in embryonic development and homeostasis. Dev Cell, 2009, 16: 329-343

[11]

Sartori R, Sandri M. BMPs and the muscle-bone connection. Bone, 2015, 80: 37-42

[12]

Egerman MA, Cadena SM, Gilbert JA et al GDF11 increases with age and inhibits skeletal muscle regeneration. Cell Metab, 2015, 22: 164-174

[13]

Zhang Y, Shao J, Wang Z et al Growth differentiation factor 11 is a protective factor for osteoblastogenesis by targeting PPARgamma. Gene, 2015, 557: 209-214

[14]

Li Z, Kawasumi M, Zhao B et al Transgenic over-expression of growth differentiation factor 11 propeptide in skeleton results in transformation of the seventh cervical vertebra into a thoracic vertebra. Mol Reprod Dev, 2010, 77: 990-997

[15]

Guo LJ, Jiang TJ, Liao L et al Relationship between serum omentin-1 level and bone mineral density in girls with anorexia nervosa. J Endocrinol Invest, 2013, 36: 190-194

[16]

Wang D, Jiang TJ, Liao L et al Relationships between serum omentin-1 concentration and bone mineral density, and bone biochemical markers in Chinese women. Clin Chim Acta, 2013, 426: 64-67

[17]

Riggs BL, Khosla S, Melton LR. Sex steroids and the construction and conservation of the adult skeleton. Endocr Rev, 2002, 23: 279-302

[18]

Manolagas SC. From estrogen-centric to aging and oxidative stress: a revised perspective of the pathogenesis of osteoporosis. Endocr Rev, 2010, 31: 266-300

[19]

Hamrick MW. Increased bone mineral density in the femora of GDF8 knockout mice. Anat Rec A Discov Mol Cell Evol Biol, 2003, 272: 388-391

[20]

Hamrick MW, Shi X, Zhang W et al Loss of myostatin (GDF8) function increases osteogenic differentiation of bone marrow-derived mesenchymal stem cells but the osteogenic effect is ablated with unloading. Bone, 2007, 40: 1544-1553

[21]

Hamrick MW, McPherron AC, Lovejoy CO. Bone mineral content and density in the humerus of adult myostatin-deficient mice. Calcif Tissue Int, 2002, 71: 63-68

[22]

Gamer LW, Wolfman NM, Celeste AJ et al A novel BMP expressed in developing mouse limb, spinal cord, and tail bud is a potent mesoderm inducer in Xenopus embryos. Dev Biol, 1999, 208: 222-232

[23]

McPherron AC, Lawler AM, Lee SJ. Regulation of anterior/posterior patterning of the axial skeleton by growth/differentiation factor 11. Nat Genet, 1999, 22: 260-264

[24]

Hamrick MW, Arounleut P, Kellum E et al Recombinant myostatin (GDF-8) propeptide enhances the repair and regeneration of both muscle and bone in a model of deep penetrant musculoskeletal injury. J Trauma, 2010, 69: 579-583

AI Summary AI Mindmap
PDF

136

Accesses

0

Citation

Detail

Sections
Recommended

AI思维导图

/