Bone turnover markers and mineral density in type 1 diabetes — A cross-sectional study: DIAFALL

Abstract

Introduction/aim

This study investigated differences in bone turnover markers (BTMs) and their associations with areal bone mineral density (aBMD) in people with type 1 diabetes (T1D) to better understand the mechanisms underlying skeletal fragility, including sex- and hormone-related variations.

Methods

A cohort of 110 Caucasian participants with T1D were matched 1: 1 with age- and sex-matched controls. aBMD at the lumbar spine, femoral neck, legs, and arms was assessed using DXA. BTMs included P1NP, osteocalcin (OC), sclerostin, CTX-1, TRAcP, IGF-1, BASP, and osteopontin (OPN). Group comparisons were conducted using t-tests, and associations between BTMs and aBMD were examined using regression and Spearman correlations. Exploratory subgroup analyses stratified women by menopausal status.

Results

Bone formation markers (P1NP, OC) were significantly lower in T1D men compared to controls (P1NP: p = 0.046; OC: p = 0.002), reflecting suppressed bone formation. IGF-1 was reduced in both sexes (p < 0.001) and correlated positively with aBMD in women (p < 0.05), but not in men. Sclerostin levels were elevated in both sexes (p = 0.002–<0.001) without correlating with aBMD. CTX-1 was reduced in T1D men (p = 0.004), while TRAcP was elevated in both sexes (p = 0.044), correlating negatively with aBMD in women. Men with T1D had significantly lower leg aBMD (p = 0.032) and reduced femoral neck bone mineral content (p = 0.041). No overall differences were observed among women; however, exploratory analyses revealed that postmenopausal women with T1D had higher TRAcP and sclerostin levels and lower femoral neck aBMD compared to premenopausal counterparts.

Conclusion

T1D was associated with significant alterations in certain BTMs and reduced aBMD in men, while skeletal effects in women appeared to be influenced by menopausal status. The weak and mostly non-significant correlations between BTMs and aBMD suggest that impaired bone quality, rather than bone mass alone, may be the primary driver of skeletal fragility in T1D. Hormonal status may further modify these effects in women.