Department of Anatomy, Cell Biology, Physiology and Biophysics, Institute of Biology, State University of Campinas, Campinas, Brazil.
Connect Tissue Res. 2010 Jun;51(3):171-8. doi: 10.3109/03008200903191312.
Obesity is currently considered to be a world epidemic and one of the major public health problems in many countries, whose incidence is increasing at alarming rates. Genetically obese Zucker rats are used as a model of obesity and were employed in the present study. Tendons transmit contractile force from muscles to bone, thus permitting articular movement. The objective of our study was to analyze the ultrastructural, biochemical, and biomechanical alterations that occur in the deep digital flexor tendon of obese Zucker rats compared to lean animals. Ultrastructural analysis showed differences in collagen fibril diameter distribution and mass-average diameter between obese and lean animals. Regarding mechanical parameters, there was a significant difference in maximum displacement and strain. Hydroxyproline content was higher in obese animals. In view of the excess weight and peculiar conditions to which the tendon of obese animals is submitted, we concluded that obesity provokes alterations in the composition and organization of tendon extracellular matrix components. These alterations might be related to organizational and structural modifications in the collagen bundles, influencing the mechanical properties of the tendon and the progression to a pathological state.
肥胖目前被认为是一种世界范围内的流行疾病,也是许多国家主要的公共卫生问题之一,其发病率正在以惊人的速度增长。肥胖 Zucker 大鼠被用作肥胖模型,并在本研究中使用。肌腱将收缩力从肌肉传递到骨骼,从而允许关节运动。我们的研究目的是分析肥胖 Zucker 大鼠与瘦型动物相比,深屈趾肌腱的超微结构、生化和生物力学变化。超微结构分析显示肥胖和瘦型动物胶原纤维直径分布和质量平均直径存在差异。关于力学参数,最大位移和应变有显著差异。肥胖动物的羟脯氨酸含量较高。鉴于肥胖动物的肌腱承受的额外重量和特殊条件,我们得出结论,肥胖引起肌腱细胞外基质成分的组成和组织发生变化。这些变化可能与胶原束的组织和结构改变有关,影响肌腱的力学性能,并导致向病理状态发展。