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Bone Tissue Collagen Maturity and Mineral Content Increase With Sustained Hyperglycemia in the KK‐Ay Murine Model of Type 2 Diabetes
Author(s) -
Hunt Heather B,
Pearl Jared C,
Diaz David R,
King Karen B,
Donnelly Eve
Publication year - 2018
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.3365
Subject(s) - pyridinoline , pentosidine , medicine , endocrinology , bone mineral , chemistry , glycation , advanced glycation end product , bone remodeling , diabetes mellitus , type i collagen , cortical bone , osteoporosis , osteocalcin , biochemistry , enzyme , anatomy , alkaline phosphatase
Type 2 diabetes mellitus (T2DM) increases fracture risk for a given bone mineral density (BMD), which suggests that T2DM changes bone tissue properties independently of bone mass. In this study, we assessed the effects of hyperglycemia on bone tissue compositional properties, enzymatic collagen crosslinks, and advanced glycation end‐products (AGEs) in the KK‐Ay murine model of T2DM using Fourier transform infrared (FTIR) imaging and high‐performance liquid chromatography (HPLC). Compared to KK‐aa littermate controls ( n = 8), proximal femoral bone tissue of KK‐Ay mice ( n = 14) exhibited increased collagen maturity, increased mineral content, and less heterogeneous mineral properties. AGE accumulation assessed by the concentration of pentosidine, as well as the concentrations of the nonenzymatic crosslinks hydroxylysylpyridinoline (HP) and lysyl pyridinoline (LP), did not differ in the proximal femurs of KK‐Ay mice compared to controls. The observed differences in tissue‐level compositional properties in the KK‐Ay mice are consistent with bone that is older and echo observations of reduced remodeling in T2DM. © 2017 American Society for Bone and Mineral Research.