Molecular and cellular endocrinology · 2026
Activation of AGEs-RAGE axis impairs bone repair in a metabolic syndrome model.
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Wanionok N E, Molinuevo M S, Streckwall L, Fernández J M, McCarthy A D
Аннотация
INTRODUCTION: Metabolic Syndrome (MetS) is a heterogeneous and multifactorial disorder associated with an increased risk of cardiovascular diseases. Preclinical and clinical studies have reported a negative correlation between MetS and bone tissue integrity and repair; however, a consensus remains elusive, likely due to the variability observed among individuals with MetS.
MATERIALS AND METHODS: Young male Wistar rats were randomly assigned to two groups (n = 5). One group received 20% fructose in their drinking water, while the control group received water alone, for three months. One month prior to euthanasia, a 1 mm bur hole injury was surgically created in the right parietal bones of all animals. Following euthanasia, blood samples were collected, and parietal bones were dissected and processed for histomorphometry and immunohistochemistry to evaluate accumulation of carboxy-methyl-lysine, a prevalent advanced glycation end-product (AGEs). Humeral bone marrow progenitor cells (BMPCs) were also isolated to assess their osteogenic potential and expression of receptor for AGEs (RAGE).
RESULTS: Fructose treatment induced metabolic alterations compatible with MetS; and significantly decreased newly formed bone in calvarial injuries, indicating impaired BMPC-mediated bone repair. Furthermore, fructose-rich diet increased the expression of RAGE in BMPCs, increased the accumulation of AGEs in bones and reduced osteogenic potential.
CONCLUSION: Oral administration of fructose for three months can impair bone repair in rats, possibly associated with activation of the AGEs-RAGE axis in bone.
MATERIALS AND METHODS: Young male Wistar rats were randomly assigned to two groups (n = 5). One group received 20% fructose in their drinking water, while the control group received water alone, for three months. One month prior to euthanasia, a 1 mm bur hole injury was surgically created in the right parietal bones of all animals. Following euthanasia, blood samples were collected, and parietal bones were dissected and processed for histomorphometry and immunohistochemistry to evaluate accumulation of carboxy-methyl-lysine, a prevalent advanced glycation end-product (AGEs). Humeral bone marrow progenitor cells (BMPCs) were also isolated to assess their osteogenic potential and expression of receptor for AGEs (RAGE).
RESULTS: Fructose treatment induced metabolic alterations compatible with MetS; and significantly decreased newly formed bone in calvarial injuries, indicating impaired BMPC-mediated bone repair. Furthermore, fructose-rich diet increased the expression of RAGE in BMPCs, increased the accumulation of AGEs in bones and reduced osteogenic potential.
CONCLUSION: Oral administration of fructose for three months can impair bone repair in rats, possibly associated with activation of the AGEs-RAGE axis in bone.