IGF‐1 and IGF‐Binding Proteins and Bone Mass, Geometry, and Strength: Relation to Metabolic Control in Adolescent Girls With Type 1 Diabetes

• Published in: Journal of bone and mineral research Vol. 23; no. 12; pp. 1884 - 1891
• Main Authors: Moyer‐Mileur, Laurie J, Slater, Hillarie, Jordan, Kristine C, Murray, Mary A
• Format: Journal Article
• Language: English
• Published: Washington, DC John Wiley and Sons and The American Society for Bone and Mineral Research (ASBMR) 01.12.2008
• Subjects: adolescence; Adolescent; bone; Bone and Bones - metabolism; Child; Cohort Studies; diabetes; Diabetes Mellitus, Type 1 - blood; Diabetes Mellitus, Type 1 - metabolism; Female; Glucose - metabolism; Glycated Hemoglobin A - metabolism; Growth Hormone - metabolism; Humans; Insulin-Like Growth Factor Binding Protein 1 - blood; Insulin-Like Growth Factor Binding Protein 1 - physiology; Insulin-Like Growth Factor Binding Protein 5 - blood; Insulin-Like Growth Factor Binding Protein 5 - physiology; Insulin-Like Growth Factor I - metabolism; Magnesium - urine; metabolic control; Models, Biological
• ISSN: 0884-0431; 1523-4681; 1523-4681
• DOI: 10.1359/jbmr.080713

Children and adolescents with poorly controlled type 1 diabetes mellitus (T1DM) are at risk for decreased bone mass. Growth hormone (GH) and its mediator, IGF‐1, promote skeletal growth. Recent observations have suggested that children and adolescents with T1DM are at risk for decreased bone mineral acquisition. We examined the relationships between metabolic control, IGF‐1 and its binding proteins (IGFBP‐1, ‐3, ‐5), and bone mass in T1DM in adolescent girls 12–15 yr of age with T1DM (n = 11) and matched controls (n = 10). Subjects were admitted overnight and given a standardized diet. Periodic blood samples were obtained, and bone measurements were performed. Serum GH, IGFBP‐1 and ‐5, glycosylated hemoglobin (HbA1c), glucose, and urine magnesium levels were higher and IGF‐1 values were lower in T1DM compared with controls (p < 0.05). Whole body BMC/bone area (BA), femoral neck areal BMD (aBMD) and bone mineral apparent density (BMAD), and tibia cortical BMC were lower in T1DM (p < 0.05). Poor diabetes control predicted lower IGF‐1 (r2 = 0.21) and greater IGFBP‐1 (r2 = 0.39), IGFBP‐5 (r2 = 0.38), and bone‐specific alkaline phosphatase (BALP; r2 = 0.41, p < 0.05). Higher urine magnesium excretion predicted an overall shorter, lighter skeleton, and lower tibia cortical bone size, mineral, and density (r2 = 0.44–0.75, p < 0.05). In the T1DM cohort, earlier age at diagnosis was predictive of lower IGF‐1, higher urine magnesium excretion, and lighter, thinner cortical bone (r2 ⩽ 0.45, p < 0.01). We conclude that poor metabolic control alters the GH/IGF‐1 axis, whereas greater urine magnesium excretion may reflect subtle changes in renal function and/or glucosuria leading to altered bone size and density in adolescent girls with T1DM.