Abstract
Intervertebral disc (IVD) degeneration and pathological spinal changes are major causes of back pain, which is the top cause of global disability. Obese and diabetic individuals are at increased risk for back pain and musculoskeletal complications. Modern diets contain high levels of advanced glycation end products (AGEs), cyto-toxic components which are known contributors to obesity, diabetes and accelerated aging pathologies. There is little information about potential effects of AGE rich diet on spinal pathology, which may be a contributing cause for back pain which is common in obese and diabetic individuals. This study investigated the role of specific AGE precursors (e.g. methylglyoxal-derivatives (MG)) on IVD and vertebral pathologies in aging C57BL6 mice that were fed isocaloric diets with standard (dMG+) or reduced amounts of MG derivatives (dMG-; containing 60-70% less dMG). dMG+ mice exhibited a pre-diabetic phenotype, as they were insulin resistant but not hyperglycemic. Vertebrae of dMG+ mice displayed increased cortical-thickness and cortical-area, greater MG-AGE accumulation and ectopic calcification in vertebral endplates. IVD morphology of dMG+ mice exhibited ectopic calcification, hypertrophic differentiation and glycosaminoglycan loss relative to dMG- mice. Overall, chronic exposure to dietary AGEs promoted age-accelerated IVD degeneration and vertebral alterations involving ectopic calcification which occurred in parallel with insulin resistance, and which were prevented with dMG- diet. This study described a new mouse model for diet-induced spinal degeneration, and results were in support of the hypothesis that chronic AGE ingestion could be a factor contributing to a pre-diabetic state, ectopic calcifications in spinal tissues, and musculoskeletal complications that are more generally known to occur with chronic diabetic conditions.
Highlights
The etiology of low back pain is multifactorial and often correlated with intervertebral disc (IVD) degeneration
This study described a new mouse model for diet-induced spinal degeneration, and results were in support of the hypothesis that chronic advanced glycation end products (AGEs) ingestion could be a factor contributing to a pre-diabetic state, ectopic calcifications in spinal tissues, and musculoskeletal complications that are more generally known to occur with chronic diabetic conditions
We recently showed that diabetes accelerated degenerative changes to vertebrae and Intervertebral disc (IVD) in a streptozotocin-induced diabetic mice [38], and these degenerative changes were found associated with the accumulation of AGEs in both the IVD and the vertebral bodies
Summary
The etiology of low back pain is multifactorial and often correlated with intervertebral disc (IVD) degeneration. IVD degeneration involves chronic inflammation, which is known to be present in diabetes and other metabolic disorders [4]. In IVD degeneration, chronic inflammation is associated with a catabolic shift of IVD metabolism, increased cell death, and a loss in glycosaminoglycan (GAG) content [5]. These tissue alterations lead to reduced hydration, increased IVD stiffness and loss of overall IVD height [6]. Determining an association of diet, diabetes and spinal pathology, whether causative or correlative, is important in treating complications associated with metabolic disorders and may shed light on mechanisms for pathological IVD degeneration
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