High dietary fat and the development of osteoarthritis in a rabbit model

Brunner, Andreas; Henn, Curtis M; Drewniak, Elizabeth I.; Lesieur-Brooks, Anne M.; Machan, Jason T.; Crisco, Joseph J.; Ehrlich, Michael G.

doi:10.1016/j.joca.2012.02.007

Cited by 51 publications

(46 citation statements)

References 41 publications

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“…Sulfated GAG content was not significantly different between young RD, HF, and HFv mice in either the medial and lateral compartments, as determined by Hexabrix staining intensity, although previous studies have reported decreased sGAG content with high fat diet, and increased sGAG production with moderate exercise . Although sGAG content did not vary between groups, RT‐PCR analysis showed that aggrecan gene expression within the knee was reduced in both HF and HFv groups (short‐term study), suggesting that high fat diet suppressed anabolic processes in joint tissue, and LIV was unable to mitigate this effect.…”

Section: Resultsmentioning

confidence: 77%

Low‐intensity vibration increases cartilage thickness in obese mice

Pamon

Bhandal

Adler

et al. 2017

Journal Orthopaedic Research

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Obesity is associated with an elevated risk of osteoarthritis (OA). We examined here whether high fat diet administered in young mice, compromised the attainment of articular cartilage thickness. Further, we sought to determine if low-intensity vibration (LIV) could protect the retention of articular cartilage in a mouse model of diet-induced obesity. Five-week-old, male, C57BL/6 mice were separated into three groups (n = 10): Regular diet (RD), High fat diet (HF), and HF + LIV (HFv; 90 Hz, 0.2g, 30 min/d, 5 d/w) administered for 6 weeks. Additionally, an extended HF diet study was run for 6 months (LIV at 15 m/d). Articular cartilage and subchondral bone morphology, and sulfated GAG content were quantified using contrast agent enhanced μCT and histology. Gene expression within femoral condyles was quantified using real-time polymerase chain reaction. Contrary to our hypothesis, HF cartilage thickness was not statistically different from RD. However, LIV increased cartilage thickness compared to HF, and the elevated thickness was maintained when diet and LIV were extended into adulthood. RT-PCR analysis showed a reduction of aggrecan expression with high fat diet, while application of LIV reduced the expression of degradative MMP-13. Further, long-term HF diet resulted in subchondral bone thickening, compared to RD, providing early evidence of OA pathology-LIV suppressed the thickening, such that levels were not significantly different from RD. These data suggest that dynamic loading, via LIV, protected the retention of cartilage thickness, potentially resulting in joint surfaces better suited to endure the risks of elevated loading that parallel obesity. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:751-759, 2018.

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Section: Resultsmentioning

confidence: 77%

Low‐intensity vibration increases cartilage thickness in obese mice

Pamon

Bhandal

Adler

et al. 2017

Journal Orthopaedic Research

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“…Numerous studies indicate an important role of the adipose tissue in the pathogenesis of OA [24,25]. A correlation was reported between obesity and increased stiffness of knee joints, accompanied by pain [26,27], and it was shown that the percentage of total body fat favours exacerbation of the inflammatory processes and acceleration of the disease progress [28].…”

Section: Discussionmentioning

confidence: 99%

Correlations between serum adipocytokine concentrations, disease stage, radiological status and total body fat content in the patients with primary knee osteoarthritis

Richter

Trzeciak

Rybka

et al. 2016

International Orthopaedics (SICOT)

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Purpose The study was designed to investigate whether serum concentrations of leptin, resistin and adiponectin in obese and normal-weight patients with primary knee osteoarthritis (OA) correlate with clinical and radiological stages of the disease and percentage of total body fat. Methods Seventy-three patients with knee OA, divided into obese and normal-weight groups, were clinically evaluated according to the Knee Society Score (KSS), and radiologically assessed using Kellgren and Lawrence scale. The percentage of total body fat and some anthropometric data were also given. Serum leptin, resistin and adiponectin concentrations were measured by Elisa and were correlated with the clinical, radiological and anthropometric parameters. Results Leptin concentrations were significantly higher (p = 0.001) in the obese patients and positively correlated (R = 0.63) with radiologically assessed OA grade, but only in the normal-weight group. Resistin and adiponectin concentrations were identical in obese and normal-weight patients and negatively correlated (R = −0.41) with the clinical status of obese patients. In both groups, percentage of total body fat positively correlated (R = 0.29 and R = 0.53 for obese and normal-weight respectively) with radiologically assessed OA grade. However, no correlations were found with clinical status of the patients. Conclusions It was found that in the obese patients with knee OA, increased percentage of total body fat and elevated serum leptin concentration might favour the advancement of clinical but not radiologically assessed changes in the joint structures, while in normal-weight patients it correlates only with radiologically assessed changes but does not affect to an appreciable extent the clinical status of the patients.

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“…Previously, we and others have shown that long‐term exposure to high fat or western‐type diets result in OA‐related changes in animal models of diet‐induced obesity . Furthermore, these OA‐related changes may be explained by the inflammatory signatures and metabolic dysfunction resulting from the increased body fat of these animals .…”

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confidence: 86%

Response to diet‐induced obesity produces time‐dependent induction and progression of metabolic osteoarthritis in rat knees

Collins

Hart

Reimer

et al. 2015

Journal Orthopaedic Research

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Obesity, and corresponding chronic-low grade inflammation, is associated with the onset and progression of knee OA. The origin of this inflammation is poorly understood. Here, the effect of high fat, high sucrose (HFS) diet induced obesity (DIO) on local (synovial fluid), and systemic (serum) inflammation is evaluated after a 12-week obesity induction and a further 16-week adaptation period. For 12-weeks of obesity induction, n ¼ 40 DIO male Sprague-Dawley rats consumed a HFS diet while the control group (n ¼ 14) remained on chow. DIO rats were allocated to prone (DIO-P, top 33% based on weight change) or resistant (DIO-R, bottom 33%) groups at 12-weeks. Animals were euthanized at 12-and after an additional 16-weeks on diet (28-weeks). At sacrifice, body composition and knee joints were collected and assessed. Synovial fluid and sera were profiled using cytokine array analysis. At 12-weeks, DIO-P animals demonstrated increased Modified Mankin scores compared to DIO-R and chow (p ¼ 0.026), and DIO-R had higher Mankin scores compared to chow (p ¼ 0.049). While numerous systemic and limited synovial fluid inflammatory markers were increased at 12-weeks in DIO animals compared to chow, by 28-weeks there were limited systemic differences but marked increases in local synovial fluid inflammatory marker concentrations. Metabolic OA may manifest from an initial systemic inflammatory disturbance. Twelve weeks of obesity induction leads to a unique inflammatory profile and induction of metabolic OA which is altered after a further 16-weeks of obesity and HFS diet intake, suggesting that obesity is a dynamic, progressive process. Increasing rates of obesity have been attributed to the consumption of a "western-type" high fat, high sugar diet. 1 Obesity is associated with osteoarthritis (OA)-related changes both clinically and in animal models 2 Likely, metabolic OA may be one subtype of OA with a distinct inflammatory signature, and a unique OA trajectory, when compared with other subtypes (e.g. post-traumatic, genetic). [2][3][4][5] Previously, we and others have shown that longterm exposure to high fat or western-type diets result in OA-related changes in animal models of dietinduced obesity. 6-8 Furthermore, these OA-related changes may be explained by the inflammatory signatures and metabolic dysfunction resulting from the increased body fat of these animals. 3,6,7,9 Moreover, high fat high sucrose diet-induced obesity significantly alters the synovial fluid cytokine, adipokine, and growth factor concentrations in rats after 28-weeks, and many changes are associated with OA-like structural changes. 3,10 However, comparative inflammatory marker profiles from serum and synovial fluid over time, in the context of a high fat, high sucrose dietinduced metabolic OA, are unknown, but are critical to understanding this disease trajectory.Similar to humans, outbred Sprague-Dawley rats demonstrate obesity prone and obesity resistant phenotypes after exposure to a high energy obesity-inducing diet. 11 A diet-induced obe...

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High dietary fat and the development of osteoarthritis in a rabbit model

Abstract: These results suggest dietary fat, independent of animal weight, results in altered chondrocyte function. Increased dietary fat was associated with changes in rabbit cartilage in vivo and appears to be a risk factor for the development of OA.

Cited by 51 publications

References 41 publications

Low‐intensity vibration increases cartilage thickness in obese mice

Low‐intensity vibration increases cartilage thickness in obese mice

Correlations between serum adipocytokine concentrations, disease stage, radiological status and total body fat content in the patients with primary knee osteoarthritis

Response to diet‐induced obesity produces time‐dependent induction and progression of metabolic osteoarthritis in rat knees

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