ArticleDisease models & mechanisms2018
Dietary advanced glycation end-product consumption leads to mechanical stiffening of murine intervertebral discs.
Article in Disease models & mechanisms, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Pooled it
- Causal relationships between dietary factors and spinal diseases: a univariable and multivariable Mendelian randomization study.Frontiers in nutrition · 2025Article
- Ipriflavone ameliorates intervertebral disc degeneration by inhibiting osteoporosis of vertebral body and pyroptosis of the nucleus pulposus in instability of lumbar spine and diabetic mice.Frontiers in bioengineering and biotechnology · 2025Article
- Targeting advanced glycation end products: potential therapeutic approaches for mitigating diabetic intervertebral disc degeneration?Frontiers in endocrinology · 2025Review
- Non-enzymatic glycation reduces glucose transport in the human cartilage endplate independently of matrix porosity or proteoglycan content.JOR spine · 2024Article
- Understanding the etiopathogenesis of lumbar intervertebral disc herniation: From clinical evidence to basic scientific research.JOR spine · 2024Review
- From hyperglycemia to intervertebral disc damage: exploring diabetic-induced disc degeneration.Frontiers in immunology · 2024Review
- Causal association of leisure sedentary behavior and cervical spondylosis, sciatica, intervertebral disk disorders, and low back pain: a Mendelian randomization study.Frontiers in public health · 2024Article
- Article
- Sex differences in the biomechanical and biochemical responses of caudal rat intervertebral discs to injury.JOR spine · 2023Article
- Advanced-Glycation Endproducts: How cross-linking properties affect the collagen fibril behavior.Journal of the mechanical behavior of biomedical materials · 2023Article
- The influence of AGEs and enzymatic cross-links on the mechanical properties of collagen fibrils.Journal of the mechanical behavior of biomedical materials · 2023Article
- Galectin-3 and RAGE differentially control advanced glycation endproduct-induced collagen damage in murine intervertebral disc organ culture.JOR spine · 2023Article
- The Chemistry and Biology of Collagen Hybridization.Journal of the American Chemical Society · 2023Review
- Effects of Sex and Obesity onInternational journal of molecular sciences · 2022Article
- High fat diet causes inferior vertebral structure and function without disc degeneration in RAGE-KO mice.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2022Article
- The degenerative impact of hyperglycemia on the structure and mechanics of developing murine intervertebral discs.JOR spine · 2022Article
- Role of Advanced Glycation End Products in Intervertebral Disc Degeneration: Mechanism and Therapeutic Potential.Oxidative medicine and cellular longevity · 2022Review
- Review
- Association of Novel Advanced Glycation End-Product (AGE10) with Complications of Diabetes as Measured by Enzyme-Linked Immunosorbent Assay.Journal of clinical medicine · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Back pain is a leading cause of disability and is strongly associated with intervertebral disc (IVD) degeneration. Reducing structural disruption and catabolism in IVD degeneration remains an important clinical challenge. Pro-oxidant and structure-modifying advanced glycation end-products (AGEs) contribute to obesity and diabetes, which are associated with increased back pain, and accumulate in tissues due to hyperglycemia or ingestion of foods processed at high heat. Collagen-rich IVDs are particularly susceptible to AGE accumulation due to their slow metabolic rates, yet it is unclear whether dietary AGEs can cross the endplates to accumulate in IVDs. A dietary mouse model was used to test the hypothesis that chronic consumption of high AGE diets results in sex-specific IVD structural disruption and functional changes. High AGE diet resulted in AGE accumulation in IVDs and increased IVD compressive stiffness, torque range and failure torque, particularly for females. These biomechanical changes were likely caused by significantly increased AGE crosslinking in the annulus fibrosus, measured by multiphoton imaging. Increased collagen damage measured with collagen hybridizing peptide did not appear to influence biomechanical properties and may be a risk factor as these animals age. The greater influence of high AGE diet on females is an important area of future investigation that may involve AGE receptors known to interact with estrogen. We conclude that high AGE diets can be a source for IVD crosslinking and collagen damage known to be important in IVD degeneration. Dietary modifications and interventions that reduce AGEs warrant further investigation and may be particularly important for diabetics, in whom AGEs accumulate more rapidly.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.