HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Thrailkill, K. M. Articles by Lumpkin, C. K. Search for Related Content PubMed PubMed Citation Articles by Thrailkill, K. M. Articles by Lumpkin, C. K. Social Bookmarking                What's this?

Bone Formation Is Impaired in a Model of Type 1 Diabetes

¹ Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, Arkansas
² Arkansas Children’s Hospital, Little Rock, Arkansas
³ Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, Arkansas
⁴ Center for Orthopedic Research, University of Arkansas for Medical Sciences, Little Rock, Arkansas
⁵ Department of Orthopedics, University of Arkansas for Medical Sciences, Little Rock, Arkansas

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.

Abbreviations: BMD, bone mineral density; DO, distraction osteogenesis; FIZ, fibrous interzone; µCT, microcomputed tomography; PMF, primary matrix front; ROI, region of interest

CiteULike    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				K. Fulzele, D. J. DiGirolamo, Z. Liu, J. Xu, J. L. Messina, and T. L. Clemens Disruption of the Insulin-like Growth Factor Type 1 Receptor in Osteoblasts Enhances Insulin Signaling and Action J. Biol. Chem., August 31, 2007; 282(35): 25649 - 25658. [Abstract] [Full Text] [PDF]

				S. Botolin and L. R. McCabe Bone Loss and Increased Bone Adiposity in Spontaneous and Pharmacologically Induced Diabetic Mice Endocrinology, January 1, 2007; 148(1): 198 - 205. [Abstract] [Full Text] [PDF]

				R. Irwin, H. V. Lin, K. J. Motyl, and L. R. McCabe Normal Bone Density Obtained in the Absence of Insulin Receptor Expression in Bone Endocrinology, December 1, 2006; 147(12): 5760 - 5767. [Abstract] [Full Text] [PDF]