Effects of anti-diabetic drugs on bone metabolism

Abstract

An increased fracture risk is observed in Type 1 and Type 2 diabetic patients. Although diabetes-related complications are important in the etiology of bone fracture in diabetes, the effect of anti-diabetic medications should not be neglected. Indeed, many drugs used commonly to treat diabetes can interfere with bone physiology, resulting in a positive or negative impact on skeletal health. The aim of the present review is to summarize the current evidence on the effects of anti-diabetic drugs on bone.

Keywords:

• bone fracture
• diabetes
• DPP-4
• GIP
• GLP-1
• metformin
• SGLT-2 inhibitor
• sulfonylurea
• thiazolidinediones

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.

Key issues

• Patients suffering with Type 1 and Type 2 diabetes mellitus are at high risk of bone fracture and anti-diabetic drugs may interfere with skeletal physiology.

• Metformin has been associated in vitro with beneficial effects on bone health but in vivo demonstration of this effect is lacking.

• Thiazolidinediones have a negative impact on bone by promoting adipogenesis at the expense of osteoblastogenesis. However, early data with new selective peroxisome proliferator-activated receptor γ modulators seem to suggest that adverse effects on bone are no longer an issue.

• Sulfonylureas, and related meglitinides, are often considered as a control group in the assessment of bone effect of new oral anti-diabetic agent but data are scarce to ensure that these oral agents do not alter bone physiology.

• Glucagon-like peptide 1 receptor agonists and dipeptidyl peptidase 4 inhibitors do not seem to reduce fracture risk in clinical trials, despite promising effects in vitro.

• Due to their mechanisms of action and recent evidence from clinical studies, the use of sodium–glucose co-transporter 2 inhibitors should be cautiously considered in patients with high fracture risk.

Notes