The spine in diabetes

Hillson, Rowan

doi:10.1002/pdi.2149

Cited by 7 publications

(4 citation statements)

References 20 publications

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“…DM and obesity are increasing at alarming rates, making this a growing high-risk population. Furthermore, DM and obesity contribute to chronic inflammation, catabolism and altered biomechanics on the spine (Fields et al, 2015; Hillson, 2018; Illien-Jünger et al, 2013), and we believe that understanding risk factors for DM and obesity will also help elucidate novel risk factors for spinal diseases in the general population. Interestingly, sex differences in obesity and DM prevalence exist, with DM women having increased risks for cardiovascular disease, myocardial infarction and stroke mortality compared to DM men (Kautzky-Willer et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Dietary advanced glycation end-product consumption leads to mechanical stiffening of murine intervertebral discs

Krishnamoorthy

Hoy

Natelson

et al. 2018

Disease Models &Amp; Mechanisms

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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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Section: Introductionmentioning

confidence: 99%

Dietary advanced glycation end-product consumption leads to mechanical stiffening of murine intervertebral discs

Krishnamoorthy

Hoy

Natelson

et al. 2018

Disease Models &Amp; Mechanisms

View full text Add to dashboard Cite

show abstract

“…Furthermore, DM and obesity contribute to chronic inflammation, catabolism, and altered biomechanics on the spine (Fields et al, 2015, Hillson, 2018, Illien-Junger et al, 2013, and we believe understanding risk factors for DM and obesity will also help elucidate novel risk factors for spinal diseases in the general population. Interestingly, sex differences in obesity and DM prevalence exist with DM women having increased risks for cardiovascular disease, myocardial infarction, and stroke mortality compared to DM men (Kautzky-Willer et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Dietary Advanced Glycation End-Product Consumption Leads to Mechanical Stiffening of Murine Intervertebral Discs

Krishnamoorthy

Hoy

Natelson

et al. 2018

Preprint

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StatementDietary advanced glycation end-products (AGE) lead to sex-specific intervertebral disc structural and functional changes and may be targeted for promoting spinal health especially in diabetes where AGEs form rapidly. ABSTRACTBack pain is a leading cause of disability strongly associated with intervertebral disc (IVD) degeneration. Reducing structural disruption and catabolism in IVD degeneration remains an important clinical challenge. Pro-oxidant and structuremodifying 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 if dietary AGEs can cross the endplates to accumulate in IVDs. We apply a dietary mouse model 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 may be a risk factor for IVD degeneration 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 high AGE diets can be a source for IVD crosslinking and collagen damage known to be important in IVD degeneration. This suggests dietary and other interventions that modify AGEs warrant further investigation and may be particularly important for diabetics where AGEs accumulate more rapidly.

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“…Some uncommon causes of back pain are more frequent among people with diabetes than in those without. These include spinal infections, vertebral fractures, spinal stenosis, and spinal cord injury 8 …”

Section: Musculoskeletal Painmentioning

confidence: 99%