Diabetes-related impairment in bone strength is established early in the life course

Casazza, Krista; Hanks, Lynae J.; Clines, Gregory A.; Tse, Hubert M.; Eberhardt, Alan W.

doi:10.4239/wjd.v4.i4.145

Cited by 2 publications

(2 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We expand on our previous reports regarding the positive relationship between BMC and REE in children 4–12y (38) (39) and BMC and insulin in animal models (40). Here we report a positive association of BMC with REE among both black and white boys and fasting insulin apparent only in black boys.…”

Section: Discussionsupporting

confidence: 52%

Bone Mineral Content as a Driver of Energy Expenditure in Prepubertal and Early Pubertal Boys

Hanks¹,

Gutiérrez²,

Ashraf³

et al. 2015

The Journal of Pediatrics

Self Cite

View full text Add to dashboard Cite

Objective To examine the associations of bone and bone-secreted factors with measures of energy metabolism in prepubertal boys. Study design Participants in this cross-sectional, observational study included 37 (69% black, 31% white) boys, 7–12y (Tanner stage<3). DXA was used to measure bone mineral content (BMC) and percent body fat. Indirect calorimetry was used to assess resting energy expenditure (REE). Fasting blood measures of osteocalcin (OCN), fibroblast growth factor-23 (FGF23), insulin, glucose, pre-cursor product of type-1 collagen (N-terminal pro-peptide; P1NP) and type-I collagen, C-terminal cross-linked telopeptide (CTX) were obtained. Pearson correlations were performed to evaluate relationships among BMC, OCN, FGF23, fasting insulin and glucose, and REE. Multiple linear regression models were used to test associations between OCN and BMC (independent variables) with fasting insulin and glucose, and REE, adjusting for bone turnover markers, and further adjusted for percent body fat. Results BMC was correlated with REE and insulin. OCN was correlated with glucose in blacks only (r=0.45, P<0.05). FGF23 was not correlated with any markers of energy metabolism. BMC was associated with insulin in blacks (β =0.95, P=0.001); which was attenuated by percent body fat (β=0.47, P=0.081). BMC was associated with REE in whites (β=0.496.7, P<0.05) and blacks (β=619.5, P<0.0001); but accounting for percent body fat attenuated the association in whites (β=413.2, P=0.078). Conclusions Our findings suggest that BMC is a determinant of fasting insulin and REE, and the contribution of body fat appears to be race-specific. An endocrine effect of FGF23 and OCN on energy metabolism was not apparent.

show abstract

Section: Discussionsupporting

confidence: 52%

Bone Mineral Content as a Driver of Energy Expenditure in Prepubertal and Early Pubertal Boys

Hanks¹,

Gutiérrez²,

Ashraf³

et al. 2015

The Journal of Pediatrics

Self Cite

View full text Add to dashboard Cite

show abstract

“…The bone union at fracture site was quantified according to the X-ray scoring system described by Lane and Sandhu with modifications [54] . For analysis of the 3D microarchitecture of the healing bone, the femurs were scanned by the Scanco μCT40 desktop cone-beam micro-CT scanner [55] . In brief, the femurs were placed vertically in the scanning holder with diameter of 12 µm.…”

Section: Methodsmentioning

confidence: 99%

EPO Promotes Bone Repair through Enhanced Cartilaginous Callus Formation and Angiogenesis

Lin

Zhang

et al. 2014

PLoS ONE

View full text Add to dashboard Cite

Erythropoietin (EPO)/erythropoietin receptor (EPOR) signaling is involved in the development and regeneration of several non-hematopoietic tissues including the skeleton. EPO is identified as a downstream target of the hypoxia inducible factor-α (HIF-α) pathway. It is shown that EPO exerts a positive role in bone repair, however, the underlying cellular and molecular mechanisms remain unclear. In the present study we show that EPO and EPOR are expressed in the proliferating, pre-hypertrophic and hypertrophic zone of the developing mouse growth plates as well as in the cartilaginous callus of the healing bone. The proliferation rate of chondrocytes is increased under EPO treatment, while this effect is decreased following siRNA mediated knockdown of EPOR in chondrocytes. EPO treatment increases biosynthesis of proteoglycan, accompanied by up-regulation of chondrogenic marker genes including SOX9, SOX5, SOX6, collagen type 2, and aggrecan. The effects are inhibited by knockdown of EPOR. Blockage of the endogenous EPO in chondrocytes also impaired the chondrogenic differentiation. In addition, EPO promotes metatarsal endothelial sprouting in vitro. This coincides with the in vivo data that local delivery of EPO increases vascularity at the mid-stage of bone healing (day 14). In a mouse femoral fracture model, EPO promotes cartilaginous callus formation at days 7 and 14, and enhances bone healing at day 28 indexed by improved X-ray score and micro-CT analysis of microstructure of new bone regenerates, which results in improved biomechanical properties. Our results indicate that EPO enhances chondrogenic and angiogenic responses during bone repair. EPO's function on chondrocyte proliferation and differentiation is at least partially mediated by its receptor EPOR. EPO may serve as a therapeutic agent to facilitate skeletal regeneration.

show abstract

Diabetes-related impairment in bone strength is established early in the life course

Cited by 2 publications

References 20 publications

Bone Mineral Content as a Driver of Energy Expenditure in Prepubertal and Early Pubertal Boys

Bone Mineral Content as a Driver of Energy Expenditure in Prepubertal and Early Pubertal Boys

EPO Promotes Bone Repair through Enhanced Cartilaginous Callus Formation and Angiogenesis

Contact Info

Product

Resources

About