Possible participation of advanced glycation end products in the pathogenesis of osteoporosis in diabetic patients.

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Osteoporosis, one of the most prevalent metabolic bone diseases in developed countries, is a major public health problem through its association with fragility fractures. Several epidemiological studies have reported moderately increased risks of osteoporotic bone fractures in diabetic patients compared with general population. However, the underlying molecular link between diabetes and osteoporosis remains to be elucidated. In diabetes mellitus, the formation and accumulation of advanced glycation end products (AGEs) progress. There is a growing body of evidence to show that AGEs-their receptor (RAGE) interactions are involved in the development of atherosclerosis and diabetic microangiopathy. AGEs enhance osteoclast-induced bone resorption in cultured mouse unfractionated bone cells. Furthermore, we have recently found that AGEs-RAGE interactions induced human mesenchymal stem cell apoptosis and subsequently prevented cognate differentiation into adipose tissue, cartilage, and bone. In vivo, serum levels of AGEs are elevated in patients with osteoporosis as well. These observations let us to hypothesize that AGEs could explain the molecular link between diabetes and osteoporosis. In this paper, we would like to propose the possible ways of testing our hypotheses. Does treatment with metformin, which has a potential effect on the inhibition of glycation reactions in vivo, decr

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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