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

机译:兔模型中的高饮食脂肪和骨关节炎的发展

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Objective: Osteoarthritis (OA) is associated with obesity, although this relationship remains unclear. Proposed etiologies of OA in obesity include mechanical loading of malaligned joints and possible toxicity of dietary fat. The hypothesis tested in the present study was that increased dietary fat worsens OA in both malaligned and normal joints, detected by biochemical and histological cartilage markers. Method: 83 New Zealand white rabbits were divided among two conditions related to OA: bowing of the knee and a 14%. kcal vs 47.8%. kcal fat diet. Rabbit weights and knee angles were compared throughout the experiment. At 28 and 38 weeks, intra-articular forces were measured, animals sacrificed, and knee cartilage examined for histological changes, glycosaminoglycan content, 35S uptake, and aggrecanase-1 expression. Results: There were no differences in animal weights or intra-articular forces between the two diets. Despite increased fat content in their diet, animals on the 47.8%. kcal fat diet did not gain excess weight. Representative histology showed atypical shearing of articular cartilage among animals on the high fat diet. Animals on the 47.8%. kcal fat diet had suppression of protein synthesis compared to the 14%. kcal fat diet: lower glycosaminoglycan content and aggrecanase-1 expression in all knee compartments at both times, and lower 35S uptake at 38 weeks. Conclusion: 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.
机译:目的:骨关节炎(OA)与肥胖有关,尽管这种关系尚不清楚。肥胖症中OA的拟议病因包括关节畸形的机械负荷和膳食脂肪的可能毒性。在本研究中测试的假设是,通过生化和组织软骨标记物检测到,膳食脂肪增加会导致畸形和正常关节中的OA恶化。方法:将83只新西兰白兔分为与OA相关的两种情况:膝弓和14%。大卡vs 47.8%。大卡脂肪饮食。在整个实验中比较了兔子的体重和膝盖角度。在28和38周时,测量关节内力,处死动物,并检查膝软骨的组织学变化,糖胺聚糖含量,35S摄取和聚集蛋白聚糖酶-1的表达。结果:两种饮食之间的动物体重或关节内力没有差异。尽管饮食中脂肪含量增加,但动物中的脂肪含量为47.8%。大卡脂肪饮食没有增加体重。代表性的组织学表明,高脂饮食对动物的关节软骨具有非典型的剪切作用。动物占47.8%。大卡脂肪饮食具有抑制蛋白质合成的作用,而后者为14%。大卡脂肪饮食:在所有时间,所有膝关节室的糖胺聚糖含量和聚集蛋白聚糖酶-1表达均降低,而38周时的35S摄取降低。结论:这些结果表明,饮食脂肪与动物体重无关,会导致软骨细胞功能改变。饮食中脂肪的增加与体内兔软骨的变化有关,并且似乎是OA发生的危险因素。

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