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  • People with type 2 diabetes are at high risk for several diseases and health complications, including back pain.
  • Researchers from the University of California San Diego and the University of Utah report that type 2 diabetes negatively impacts the vertebral discs that form the spine, via an animal model.
  • This finding could explain why people with type 2 diabetes often experience chronic body pain, including back pain.

Researchers estimate about 508 million people around the world have type 2 diabetes — a condition where the body stops using insulin properly.

A person who has type 2 diabetes is at a higher risk for heart disease, stroke, high blood pressure, kidney disease, and dementia.

Type 2 diabetes can cause several health complications, including nerve damage, eye diseases, skin problems, sleeping issues, and chronic body pain, including back pain.

Now, researchers from the University of California San Diego and the University of Utah report that type 2 diabetes negatively impacts the vertebral discs that form the spine.

Via an animal model, scientists found that type 2 diabetes causes the collagen fibrils within discs to become inflexible, comprising their ability to withstand pressure.

The new study was recently published in the journal PNAS Nexus.

Past studies show that type 2 diabetes can adversely affect the body’s spine and back.

For example, people with type 2 diabetes are at an increased risk of developing diffuse idiopathic skeletal hyperostosis (DISH). DISH is a type of arthritis that hardens the tendons and ligaments around the spine, causing stiffness, decreased motion, and pain.

A study published in March 2022 found that people with type 2 diabetes are at a higher risk for lumbar disc degeneration disease.

Other studies have linked type 2 diabetes with an increased risk for other spinal diseases, including spinal stenosis and vertebral osteomyelitis.

Previous research has also associated type 2 diabetes disease progression with chronic back pain.

Prior studies have shown that people with diabetes have a 35% increased risk of experiencing low back pain and a 24% heightened risk of having neck pain compared to those who do not have the disease.

“We wanted to see if the effects of diabetes we were seeing in the bones were also present in the vertebral discs, which could explain disc degeneration and low back pain in these populations,” Dr. Claire Acevedo, assistant professor in the Department of Mechanical and Aerospace Engineering at the University of California San Diego, adjunct assistant professor of biomedical engineering and mechanical engineering at the University of Utah, and co-lead author of this study explained to Medical News Today when asked why they decided to focus on the vertebral column for their study.

For this study, researchers used a rat model of type 2 diabetes. Vertebral discs from rats with type 2 diabetes were compared to healthy rats to look for any collagen fibril deformation in the discs. The outer portion of vertebral discs is made from layers of collagen and proteins.

The researchers discovered in rats with type 2 diabetes, the compression ability of the disc collagen fibrils became compromised, causing the collagen to become stiff and brittle and making it difficult for the collagen to handle being compressed like it would when healthy.

“Type 2 diabetes and the associated hyperglycemia (cross-links) the collagen fibrils more than usual, like a fast aging process.”
— Dr. Claire Acevedo

“This increase in cross-linking limits the usual compression mechanisms — energy dissipation mechanisms — in the discs via one, limitation of the collagen fibrils deformation making the collagen more stiff and brittle, (and) two, limitation of the lamellar rotation,” Dr. Acevedo explained.

“Future treatment can target the cross-link removal to restore the disc’s ability to deform normally,” she added.

Scientists used an experimental technique called synchrotron small-angle x-ray scattering (SAXS) to look for any change in disc collagen behavior on a nanoscale.

“Small angle X-ray scattering is an X-ray diffraction technique that enables (us) to measure the collagen fibril periodicity (67 nm). When we perform a tensile test in front of the X-ray beam, the collagen periodicity increases,” Dr. Acevedo said.

“We can capture this change in collagen periodicity, which allows us to calculate the collagen deformation or strain and measure the whole-disc deformation or strain at the same time,” she continued. “Therefore, we can see how much disc strain is transferred to the collagen level at the nanoscale.”

For the next steps in this research, Dr. Acevedo said they will be looking at ways to find a proxy for advanced glycation end-products (AGEs) crosslink assessment. AGEs are a biomarker associated with aging and both the development and worsening of degenerative conditions like diabetes.

“Assessing AGEs content in discs or bones is complicated and intrusive while assessing AGEs crosslink increase in (the) skin might be a good way to assess the same increase in discs and bones, even though the absolute content value will differ between tissues,” she said.

MNT also spoke about this study with Dr. Neel Anand, an orthopedic surgeon and co-director of spine trauma at Cedars-Sinai Spine Center in Los Angeles.

Dr. Anand said he was not surprised by this study’s findings.

“Type 2 diabetes affects collagen — it’s a collagen disease and discs (are) collagen,” he explained. “The ring of the disc on the outside is made of collagen fibers. So it’s not surprising that it will affect the disc in some form, shape, or fashion.”

“Type 2 diabetes affects collagen all over the body. The collagen will get affected just like it affects the blood vessels in the body. That’s what type 2 diabetes does — that’s why you get vascular problems, you get heart problems, you get kidney problems. You get a million problems with type 2 diabetes, including eye problems, so it affects a lot of things.”
— Dr. Neel Anand

However, Dr. Anand did point out this research was conducted through a rat model.

“Humans are not rats,” he continued. “Is (this) true in humans? (It) probably is — there’s probably some element to it. Someone’s got to prove that’s true in humans at some point. Ultimately, it has to translate to humans.”

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