TY - JOUR
T1 - Advanced glycation endproducts and bone quality
T2 - Practical implications for people with type 2 diabetes
AU - Moseley, Kendall F.
AU - Du, Zexu
AU - Sacher, Sara E.
AU - Ferguson, Virginia L.
AU - Donnelly, Eve
N1 - Publisher Copyright:
© 2021 Lippincott Williams and Wilkins. All rights reserved.
PY - 2021/8/1
Y1 - 2021/8/1
N2 - Purpose of reviewIndividuals with type 2 diabetes (T2D) are at increased risk of fracture, often despite normal bone density. This observation suggests deficits in bone quality in the setting of abnormal glucose homeostasis. The goal of this article is to review recent developments in our understanding of how advanced glycation end products (AGEs) are incorporated into the skeleton with resultant deleterious effects on bone health and structural integrity in patients with T2D.Recent findingsThe adverse effects of skeletal AGE accumulation on bone remodeling and the ability of the bone to deform and absorb energy prior to fracture have been demonstrated both at the bench as well as in small human studies; however, questions remain as to how these findings might be better explored in large, population-based investigations.SummaryHyperglycemia drives systemic, circulating AGE formation with subsequent accumulation in the bone tissue. In those with T2D, studies suggest that AGEs diminish fracture resistance, though larger clinical studies are needed to better define the direct role of longstanding AGE accumulation on bone strength in humans as well as to motivate potential interventions to reverse or disrupt skeletal AGE deposition with the goal of fracture prevention.
AB - Purpose of reviewIndividuals with type 2 diabetes (T2D) are at increased risk of fracture, often despite normal bone density. This observation suggests deficits in bone quality in the setting of abnormal glucose homeostasis. The goal of this article is to review recent developments in our understanding of how advanced glycation end products (AGEs) are incorporated into the skeleton with resultant deleterious effects on bone health and structural integrity in patients with T2D.Recent findingsThe adverse effects of skeletal AGE accumulation on bone remodeling and the ability of the bone to deform and absorb energy prior to fracture have been demonstrated both at the bench as well as in small human studies; however, questions remain as to how these findings might be better explored in large, population-based investigations.SummaryHyperglycemia drives systemic, circulating AGE formation with subsequent accumulation in the bone tissue. In those with T2D, studies suggest that AGEs diminish fracture resistance, though larger clinical studies are needed to better define the direct role of longstanding AGE accumulation on bone strength in humans as well as to motivate potential interventions to reverse or disrupt skeletal AGE deposition with the goal of fracture prevention.
KW - advanced glycation end products
KW - bone remodeling
KW - nonenzymatic glycation
KW - type 2 diabetes
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U2 - 10.1097/MED.0000000000000641
DO - 10.1097/MED.0000000000000641
M3 - Review article
C2 - 34183538
AN - SCOPUS:85109732100
SN - 1752-296X
VL - 28
SP - 360
EP - 370
JO - Current Opinion in Endocrinology, Diabetes and Obesity
JF - Current Opinion in Endocrinology, Diabetes and Obesity
IS - 4
ER -