Abstract
Diabetic bone disease, a form of secondary osteoporosis, is characterized by weakened bones and an increased risk of fractures, especially in patients with type 2 diabetes (T2D). This review explores the key mechanisms driving this condition, including hyperglycemia, insulin resistance, advanced glycation end products (AGEs), and proinflammatory cytokines, all of which disturb normal bone turnover by disrupting the functions of osteoblasts and osteoclasts. We examine the roles of bone turnover and mineralization, as well as how microvascular complications affect bone microarchitecture. Additionally, the influence of gut hormones, such as GLP-1 and GIP, and gut microbiota, particularly species like Akkermansia muciniphila, on the gut-bone axis is discussed, as these factors play a role in regulating bone density and structure. While T2D patients may show normal or even elevated bone mineral density (BMD), the underlying quality of bone is often compromised, leading to increased fragility. This review integrates current knowledge on the molecular, hormonal, and microbial interactions contributing to diabetic bone disease. By highlighting these pathways, we aim to offer insights into potential therapeutic strategies and inform future research aimed at improving the diagnosis, treatment, and overall management of this condition.
Published Version
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