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).