Further analysis showed that the intervertebral discs of diabetic rats exhibited stiffening of collagen fibrils with higher concentrations of non-enzymatic crosslinks. Increased collagen cross-linking induced by hyperglycemia limited plastic deformation due to fibril sliding. These findings highlight that fibril reorientation, straightening, stretching, and gliding are important mechanisms promoting overall disc compression. Type 2 diabetes disrupts these efficient deformation mechanisms, altering the biomechanics of the entire disc and causing a more fragile (low-energy) behavior.
The team published their results in the December 2023 issue of PNAS Nexus.
This research was supported by the UCSF Research Allocation Committee (AJF), ​​the UCSF Musculoskeletal Biology and Medicine Core Center (AJF), ​​the University of California Office of the President (PJH), and the National Institutes of Health (R01 DK095980, R01 HL107256, R01 HL121324, P30 AR066262 , R01 AR070198), University of Utah (JLR), and Advanced Light Sources (ALS07392; TNA, CA).
