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Review
. 2022 Dec;20(6):379-388.
doi: 10.1007/s11914-022-00747-6. Epub 2022 Oct 10.

Glycemic Control and Bone in Diabetes

David R Weber  1 , Fanxin Long  2 , Babette S Zemel  3   4 , Joseph M Kindler  5
Affiliations
Review

Glycemic Control and Bone in Diabetes

David R Weber et al. Curr Osteoporos Rep. 2022 Dec.

Abstract

Purpose of review: This review summarizes recent developments on the effects of glycemic control and diabetes on bone health. We discuss the foundational cellular mechanisms through which diabetes and impaired glucose control impact bone biology, and how these processes contribute to bone fragility in diabetes.

Recent findings: Glucose is important for osteoblast differentiation and energy consumption of mature osteoblasts. The role of insulin is less clear, but insulin receptor deletion in mouse osteoblasts reduces bone formation. Epidemiologically, type 1 (T1D) and type 2 diabetes (T2D) associate with increased fracture risk, which is greater among people with T1D. Accumulation of cortical bone micro-pores, micro-vascular complications, and AGEs likely contribute to diabetes-related bone fragility. The effects of youth-onset T2D on peak bone mass attainment and subsequent skeletal fragility are of particular concern. Further research is needed to understand the effects of hyperglycemia on skeletal health through the lifecycle, including the related factors of inflammation and microvascular damage.

Keywords: Bone; Diabetes; Dysglycemia; Fracture; Osteoblast; Osteoclast.

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Conflict of interest statement

The authors do not have existing conflicts of Interest.

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