Study finds that type 2 diabetes changes the behavior of spinal discs

In type 2 diabetes, the behavior of the intervertebral discs in the spinal column changes, making them stiffer and changing their shape more quickly than normal. As a result, the disc’s ability to withstand pressure is compromised. That’s one of the results of a new study in rodents by a team of engineers and doctors from UC San Diego, UC Davis, UCSF, and the University of Utah.

Low back pain is a major cause of disability and is often associated with disc degeneration. People with type 2 diabetes are at increased risk for lower back pain and disc-related problems. However, the exact mechanism of disc degeneration remains unclear.

Investigating the biomechanical properties of intervertebral discs is critical to understanding the disease and developing effective strategies to manage low back pain. The research team was co-led by Claire Acevedo, a faculty member in the Department of Mechanical and Aerospace Engineering at the University of California, San Diego, and Aaron Fields, a faculty member in the Department of Orthopedics at the University of California, San Francisco.

The research will be published in a journal PNAS Nexus.

“These findings provide new insights into the potential mechanisms underlying diabetes-associated disc tissue damage and may aid in the development of prevention and treatment strategies for this debilitating disease,” the researchers said. are writing.

This study highlights that the nanoscale deformation mechanism of collagen fibrils adapts to the compressive loading of the intervertebral disc. In type 2 diabetes, these mechanisms are compromised, leading to weakened collagen. These findings provide new insights into the potential mechanisms underlying diabetes-associated disc tissue damage and may inform the development of prevention and treatment strategies for this debilitating condition.

The researchers employed synchrotron small-angle X-ray scattering (SAXS), an experimental technique to observe the deformation and orientation of collagen fibrils at the nanoscale. They wanted to investigate how changes in collagen behavior contribute to changes in the disc’s ability to withstand compression.

They compared discs from healthy rats to discs from rats with type 2 diabetes (UC Davis rat model). Healthy rats showed that when the disc is compressed, the collagen fibrils rotate and elongate, allowing the disc to dissipate energy effectively.

“In diabetic rats, the way discs dissipate energy under pressure is severely impaired. Diabetes reduces the rotation and stretching of collagen fibrils, indicating that their ability to cope with pressure is impaired. “There is,” the researchers wrote.

Further analysis showed that discs from diabetic rats exhibited stiffening of collagen fibrils with higher concentrations of non-enzymatic crosslinks. The increased collagen cross-linking caused by hyperglycemia limited the plastic deformation due to fibril sliding.

These findings highlight that fibril reorientation, straightening, elongation, and sliding are important mechanisms promoting compression across the intervertebral disc. Type 2 diabetes disrupts these efficient deformation mechanisms, altering the biomechanics of the entire disc and causing a more fragile (low-energy) behavior.