4.6 Article

Deficits in Trabecular Bone Microarchitecture in Young Women With Type 1 Diabetes Mellitus

Journal

JOURNAL OF BONE AND MINERAL RESEARCH
Volume 30, Issue 8, Pages 1386-1393

Publisher

WILEY
DOI: 10.1002/jbmr.2465

Keywords

ADIPOSITY; BONE HEALTH; BONE MARROW; GLYCEMIA; MRI

Funding

  1. University of Glasgow
  2. Government of Libya
  3. Scottish Academic Health Sciences Collaboration
  4. MRC [MR/N003403/1] Funding Source: UKRI

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The pathophysiological mechanism of increased fractures in young adults with type 1 diabetes mellitus (T1DM) is unclear. We conducted a case-control study of trabecular bone microarchitecture and vertebral marrow adiposity in young women with T1DM. Thirty women with T1DM with a median age (range) age of 22.0 years (16.9, 36.1) attending one outpatient clinic with a median age at diagnosis of 9.7 years (0.46, 14.8) were compared with 28 age-matched healthy women who acted as controls. Measurements included MRI-based assessment of proximal tibial bone volume/total volume (appBV/TV), trabecular separation (appTb.Sp), vertebral bone marrow adiposity (BMA), and abdominal adipose tissue and biochemical markers of GH/IGF-1 axis (IGF-1, IGFBP3, ALS) and bone turnover. Median appBV/TV in cases and controls was 0.3 (0.22, 0.37) and 0.33 (0.26, 0.4), respectively (p=0.018) and median appTb.Sp in T1DM was 2.59 (2.24, 3.38) and 2.32 (2.03, 2.97), respectively (p=0.012). The median appBV/TV was 0.28 (0.22, 0.33) in those cases with retinopathy (n=15) compared with 0.33 (0.25, 0.37) in those without retinopathy (p=0.02). Although median visceral adipose tissue in cases was higher than in controls at 5733 mm(3) (2030, 11,144) and 3460 mm(3) (1808, 6832), respectively (p=0.012), there was no difference in median BMA, which was 31.1% (9.9, 59.9) and 26.3% (8.5, 49.8) in cases and controls, respectively (p=0.2). Serum IGF-1 and ALS were also lower in cases, and the latter showed an inverse association to appTbSp (r=-0.30, p=0.04). Detailed MRI studies in young women with childhood-onset T1DM have shown clear deficits in trabecular microarchitecture of the tibia. Underlying pathophysiological mechanisms may include a microvasculopathy. (c) 2015 American Society for Bone and Mineral Research.

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