Contributors to impaired bone health in type 2 diabetes

Angela Sheu; Jerry R Greenfield; Christopher P White; Jacqueline R Center

doi:10.1016/j.tem.2022.11.003

Contributors to impaired bone health in type 2 diabetes

Trends Endocrinol Metab. 2023 Jan;34(1):34-48. doi: 10.1016/j.tem.2022.11.003. Epub 2022 Nov 23.

Authors

Angela Sheu¹, Jerry R Greenfield², Christopher P White³, Jacqueline R Center⁴

Affiliations

¹ Bone Biology Division, Garvan Institute of Medical Research, Sydney, Australia; Clinical School, St Vincent's Hospital, Faculty of Medicine, University of New South Wales Sydney, Sydney, Australia; Department of Endocrinology and Diabetes, St Vincent's Hospital, Sydney, Australia. Electronic address: a.sheu@garvan.org.au.
² Clinical School, St Vincent's Hospital, Faculty of Medicine, University of New South Wales Sydney, Sydney, Australia; Department of Endocrinology and Diabetes, St Vincent's Hospital, Sydney, Australia; Diabetes and Metabolism, Garvan Institute of Medical Research, Sydney, Australia.
³ Clinical School, Prince of Wales Hospital, Faculty of Medicine, University of New South Wales Sydney, Sydney, Australia; Department of Endocrinology and Metabolism, Prince of Wales Hospital, Sydney, Australia.
⁴ Bone Biology Division, Garvan Institute of Medical Research, Sydney, Australia; Clinical School, St Vincent's Hospital, Faculty of Medicine, University of New South Wales Sydney, Sydney, Australia; Department of Endocrinology and Diabetes, St Vincent's Hospital, Sydney, Australia.

PMID: 36435679
DOI: 10.1016/j.tem.2022.11.003

Abstract

Type 2 diabetes (T2D) is associated with numerous complications, including increased risk of fragility fractures, despite seemingly protective factors [e.g., normal bone mineral density and increased body mass index(BMI)]. However, fracture risk in T2D is underestimated by current fracture risk calculators. Importantly, post-fracture mortality is worse in T2D following any fracture, highlighting the importance of identifying high-risk patients that may benefit from targeted management. Several diabetes-related factors are associated with increased fracture risk, including exogenous insulin therapy, vascular complications, and poor glycaemic control, although detailed comprehensive studies to identify the independent contributions of these factors are lacking. The underlying pathophysiological mechanisms are complex and multifactorial, with different factors contributing during the course of T2D disease. These include obesity, hyperinsulinaemia, hyperglycaemia, accumulation of advanced glycation end products, and vascular supply affecting bone-cell function and survival and bone-matrix composition. This review summarises the current understanding of the contributors to impaired bone health in T2D, and proposes an updated approach to managing these patients.

Keywords: bone; diabetes; fractures; insulin resistance; osteoporosis.

Publication types

Review
Research Support, Non-U.S. Gov't

MeSH terms

Bone Density / physiology
Bone and Bones
Diabetes Mellitus, Type 2* / complications
Fractures, Bone* / etiology
Glycation End Products, Advanced
Humans
Hyperglycemia*

Substances

Glycation End Products, Advanced