TY - JOUR
T1 - Bone formation is impaired in a model of type 1 diabetes
AU - Thrailkill, Kathryn M.
AU - Liu, Lichu
AU - Wahl, Elizabeth C.
AU - Bunn, Robert C.
AU - Perrien, Daniel S.
AU - Cockrell, Gael E.
AU - Skinner, Robert A.
AU - Hogue, William R.
AU - Carver, Adam A.
AU - Fowlkes, John L.
AU - Aronson, James
AU - Lumpkin, Charles K.
PY - 2005/10
Y1 - 2005/10
N2 - The effects of type 1 diabetes on de novo bone formation during tibial distraction osteogenesis (DO) and on intact trabecular and cortical bone were studied using nonobese diabetic (NOD) mice and comparably aged nondiabetic NOD mice. Diabetic mice received treatment with insulin, vehicle, or no treatment during a 14-day DO procedure. Distracted tibiae were analyzed radiographically, histologically, and by microcomputed tomography (μCT). Contralateral tibiae were analyzed using μCT. Serum levels of insulin, osteocalcin, and cross-linked C-telopeptide of type I collagen were measured. Total new bone in the DO gap was reduced histologically (P ≤ 0.001) and radiographically (P ≤ 0.05) in diabetic mice compared with nondiabetic mice but preserved by insulin treatment. Serum osteocalcin concentrations were also reduced in diabetic mice (P ≤ 0.001) and normalized with insulin treatment. Evaluation of the contralateral tibiae by μCT and mechanical testing demonstrated reductions in trabecular bone volume and thickness, cortical thickness, cortical strength, and an increase in endosteal perimeter in diabetic animals, which were prevented by insulin treatment. These studies demonstrate that bone formation during DO is impaired in a model of type 1 diabetes and preserved by systemic insulin administration.
AB - The effects of type 1 diabetes on de novo bone formation during tibial distraction osteogenesis (DO) and on intact trabecular and cortical bone were studied using nonobese diabetic (NOD) mice and comparably aged nondiabetic NOD mice. Diabetic mice received treatment with insulin, vehicle, or no treatment during a 14-day DO procedure. Distracted tibiae were analyzed radiographically, histologically, and by microcomputed tomography (μCT). Contralateral tibiae were analyzed using μCT. Serum levels of insulin, osteocalcin, and cross-linked C-telopeptide of type I collagen were measured. Total new bone in the DO gap was reduced histologically (P ≤ 0.001) and radiographically (P ≤ 0.05) in diabetic mice compared with nondiabetic mice but preserved by insulin treatment. Serum osteocalcin concentrations were also reduced in diabetic mice (P ≤ 0.001) and normalized with insulin treatment. Evaluation of the contralateral tibiae by μCT and mechanical testing demonstrated reductions in trabecular bone volume and thickness, cortical thickness, cortical strength, and an increase in endosteal perimeter in diabetic animals, which were prevented by insulin treatment. These studies demonstrate that bone formation during DO is impaired in a model of type 1 diabetes and preserved by systemic insulin administration.
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U2 - 10.2337/diabetes.54.10.2875
DO - 10.2337/diabetes.54.10.2875
M3 - Article
C2 - 16186388
AN - SCOPUS:25844492123
SN - 0012-1797
VL - 54
SP - 2875
EP - 2881
JO - Diabetes
JF - Diabetes
IS - 10
ER -
