Collins K H, Hart D A, Seerattan R A, Reimer R A, Herzog W
Human Performance Laboratory, McCaig Institute for Bone and Joint Health, and Biomedical Engineering Program, University of Calgary, Calgary, Canada.
Human Performance Laboratory, McCaig Institute for Bone and Joint Health, Biomedical Engineering Program, and Department of Biochemistry and Molecular Biology, University of Calgary, and Alberta Health Services Bone & Joint Health Strategic Clinical Network, Calgary, Canada.
Bone Joint Res. 2018 May 5;7(4):274-281. doi: 10.1302/2046-3758.74.BJR-2017-0201.R2. eCollection 2018 Apr.
Metabolic syndrome and low-grade systemic inflammation are associated with knee osteoarthritis (OA), but the relationships between these factors and OA in other synovial joints are unclear. The aim of this study was to determine if a high-fat/high-sucrose (HFS) diet results in OA-like joint damage in the shoulders, knees, and hips of rats after induction of obesity, and to identify potential joint-specific risks for OA-like changes.
A total of 16 male Sprague-Dawley rats were allocated to either the diet-induced obesity group (DIO, 40% fat, 45% sucrose, n = 9) or a chow control diet (n = 7) for 12 weeks. At sacrifice, histological assessments of the shoulder, hip, and knee joints were performed. Serum inflammatory mediators and body composition were also evaluated. The total Mankin score for each animal was assessed by adding together the individual Modified Mankin scores across all three joints. Linear regression modelling was conducted to evaluate predictive relationships between serum mediators and total joint damage.
The HFS diet, in the absence of trauma, resulted in increased joint damage in the shoulder and knee joints of rats. Hip joint damage, however, was not significantly affected by DIO, consistent with findings in human studies. The total Mankin score was increased in DIO animals compared with the chow group, and was associated with percentage of body fat. Positive significant predictive relationships for total Mankin score were found between body fat and two serum mediators (interleukin 1 alpha (IL-1α) and vascular endothelial growth factor (VEGF)).
Systemic inflammatory alterations from DIO in this model system may result in a higher risk for development of knee, shoulder, and multi-joint damage with a HFS diet.: K. H. Collins, D. A. Hart, R. A. Seerattan, R. A. Reimer, W. Herzog. High-fat/high-sucrose diet-induced obesity results in joint-specific development of osteoarthritis-like degeneration in a rat model. 2018;7:274-281. DOI: 10.1302/2046-3758.74.BJR-2017-0201.R2.
代谢综合征和低度全身炎症与膝关节骨关节炎（OA）相关，但这些因素与其他滑膜关节OA之间的关系尚不清楚。本研究的目的是确定高脂/高糖（HFS）饮食在诱导大鼠肥胖后是否会导致肩部、膝部和髋部出现类似OA的关节损伤，并确定OA样改变的潜在关节特异性风险因素。
将16只雄性Sprague-Dawley大鼠分为饮食诱导肥胖组（DIO，40%脂肪，45%蔗糖，n = 9）或普通对照饮食组（n = 7），为期12周。处死后，对肩部、髋部和膝关节进行组织学评估。还评估了血清炎症介质和身体组成。通过将所有三个关节的个体改良曼金评分相加来评估每只动物的总曼金评分。进行线性回归建模以评估血清介质与总关节损伤之间的预测关系。
在没有创伤的情况下，HFS饮食导致大鼠肩部和膝关节的关节损伤增加。然而，髋关节损伤并未受到DIO的显著影响，这与人体研究结果一致。与普通饮食组相比，DIO组动物的总曼金评分增加，且与体脂百分比相关。在体脂与两种血清介质（白细胞介素1α（IL-1α）和血管内皮生长因子（VEGF））之间发现了总曼金评分的正显著预测关系。
在该模型系统中，DIO引起的全身炎症改变可能导致在HFS饮食情况下膝关节、肩关节和多关节损伤发生的风险更高。：K. H. 柯林斯、D. A. 哈特、R. A. 西拉坦、R. A. 赖默、W. 赫尔佐格。高脂/高糖饮食诱导的肥胖导致大鼠模型中骨关节炎样退变的关节特异性发展。2018；7：274 - 281。DOI：10.1302/2046 - 3758.74.BJR - 2017 - 0201.R2
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