title: IGF-1 and IGF-binding proteins and bone mass, geometry, and strength: relation to metabolic control in adolescent girls with type 1 diabetes.
abstract: 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 (HbA(1c)), 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 (r(2) = 0.21) and greater IGFBP-1 (r(2) = 0.39), IGFBP-5 (r(2) = 0.38), and bone-specific alkaline phosphatase (BALP; r(2) = 0.41, p < 0.05). Higher urine magnesium excretion predicted an overall shorter, lighter skeleton, and lower tibia cortical bone size, mineral, and density (r(2) = 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 (r(2) >or=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.
authors.affiliation: Center for Pediatric Nutrition Research, Department of Pediatrics, University of Utah, Salt Lake City, Utah, USA. laurie.moyer-mileur@hsc.utah.edu
authors.forename: Laurie J
authors.initials: LJ
authors.lastname: Moyer-Mileur
authors.forename: Hillarie
authors.initials: H
authors.lastname: Slater
authors.forename: Kristine C
authors.initials: KC
authors.lastname: Jordan
authors.forename: Mary A
authors.initials: MA
authors.lastname: Murray
mesh_terms: D000293:Adolescent; D001842:Bone and Bones / Q000378:metabolism*; D002648:Child; D015331:Cohort Studies; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism; D006442:Glycated Hemoglobin / Q000378:metabolism; D013006:Growth Hormone / Q000378:metabolism; D006801:Humans; D018970:Insulin-Like Growth Factor Binding Protein 1 / Q000097:blood* / Q000502:physiology; D018975:Insulin-Like Growth Factor Binding Protein 5 / Q000097:blood* / Q000502:physiology; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D008274:Magnesium / Q000652:urine; D008954:Models, Biological
chemical_list: D005947:Glucose; D006442:Glycated Hemoglobin; D013006:Growth Hormone; D018970:Insulin-Like Growth Factor Binding Protein 1; D018975:Insulin-Like Growth Factor Binding Protein 5; D007334:Insulin-Like Growth Factor I; D008274:Magnesium