by New research from the University of California San Diego, UC Davis, UCSF, and the University of Utah reveals that type 2 diabetes affects the functioning of disks in the vertebral column. The study shows that individuals with type 2 diabetes experience stiffer disks that change shape earlier than normal. Consequently, the ability of the disks to withstand pressure is compromised. This finding sheds light on the mechanisms behind disk degeneration and low back pain, both of which are prevalent in individuals with diabetes.
Low back pain is a leading cause of disability worldwide, often associated with degeneration of intervertebral disks. People with type 2 diabetes are more susceptible to experiencing low back pain and related disk issues. However, the specific mechanisms contributing to disk degeneration have remained unclear.
Understanding the biomechanical properties of intervertebral disks is crucial for comprehending the disease and developing effective strategies to manage low back pain. The research team, co-led by Claire Acevedo from the Department of Mechanical and Aerospace Engineering at the University of California San Diego and Aaron Fields from the Department of Orthopedic Surgery at UC San Francisco, examined these properties through a study involving rodents.
The study, published in the journal PNAS Nexus, highlights novel insights into the potential mechanisms underlying diabetes-related damage to disk tissue. These findings can inform the development of preventative and therapeutic strategies to address this debilitating condition.
The researchers emphasize that the mechanisms of nanoscale deformation in collagen fibrils accommodate the compressive loading of intervertebral disks. However, in the context of type 2 diabetes, these mechanisms are compromised, resulting in collagen becoming more brittle. This contributes to the tissue damage observed in individuals with diabetes.
To investigate how alterations in collagen behavior impact the disk’s ability to withstand compression, researchers utilized synchrotron small-angle X-ray scattering (SAXS), an experimental technique that examines the deformation and orientation of collagen fibrils at the nanoscale.
The study compared disks from healthy rats to those from rats with type 2 diabetes using a UC Davis rat model. In the healthy rats, collagen fibrils demonstrated rotation and stretching when the disks were compressed, effectively dissipating energy.
However, in the diabetic rats, the ability of vertebral disks to dissipate energy under compression was significantly impaired. The rotation and stretching of collagen fibrils were compromised, indicating a reduced ability to handle pressure.
Further analysis revealed that in disks from diabetic rats, collagen fibrils stiffened, with a higher concentration of non-enzymatic cross-links. This increase in collagen cross-linking, induced by hyperglycemia, restricted plastic deformations through fibrillar sliding.
These findings underscore the importance of fibril reorientation, straightening, stretching, and sliding in facilitating whole-disk compression. The disruption of these efficient deformation mechanisms in type 2 diabetes results in altered whole-disk biomechanics and a more brittle behavior.
This research provides valuable insights into the mechanisms by which type 2 diabetes impacts intervertebral disks and contributes to low back pain. By understanding these mechanisms, researchers can work towards developing preventive measures and effective treatments for individuals with type 2 diabetes who are at a higher risk of experiencing debilitating low back pain.
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1. Source: Coherent Market Insights, Public sources, Desk research
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