Abstract
The interplay between diabetes mellitus and the structural integrity of collagen has significant implications for tissue functionality and disease progression. The aim of this study was to empirically investigate the effects of ribose-induced glycation on the biomechanical properties of collagen fibrils, using atomic force microscopy for precise measurements. Methodology. We used collagen fibrils from the common digital extensor (CDE) and superficial digital flexor (SDF) tendons of an adult bovine model to mimic the glycation processes that occur in diabetic pathology. The samples underwent controlled glycation by incubation with ribose for 24 hours and 14 days compared to phosphate buffered saline treated controls. A Bioscope Catalyst atomic force microscope (Bruker, USA) was used for all atomic force microscopy imaging in this study. Scientific novelty. Our results show a marked increase in the elastic modulus of collagen fibrils after ribose treatment, indicating stiffening with glycation. Notably, SDF fibrils showed a greater increase in stiffness after 24 hours of ribose exposure compared to CDE fibrils, suggesting variations in glycation rates relative to fibril anatomy. Statistical analyses confirmed the significance of these findings and provided a model for understanding similar processes in human diabetes. Conclusions. The different response to glycation observed between CDE and SDF fibrils prompts further investigation into the role of anatomical and structural factors in glycation susceptibility. Identification of tissues at higher risk of glycation-induced damage could lead to the development of targeted prevention strategies for diabetic complications. In addition, the potential for pharmacological intervention to inhibit glycation processes or enhance advanced glycation end products (AGEs) degradation offers a promising avenue for mitigating the progression of diabetes-related complications. The results of this study highlight the potential of ribose-induced changes in collagen as a model for diabetes-related tissue changes and propose a mechanistic framework that could guide the development of interventions aimed at mitigating the effects of collagen-related diabetic complications.
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