Sun Antonia RuJia, Wu Xiaoxin, Crawford Ross, Li Hongxing, Mei Lin, Luo Yong, Xiao Yin, Mao Xinzhan, Prasadam Indira
School of Mechanical, Medical, and Process Engineering, Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD, Australia.
Center for Translational Medicine Research and Development, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.
Front Med (Lausanne). 2021 Mar 22;8:628843. doi: 10.3389/fmed.2021.628843. eCollection 2021.
Obesogenic diets contribute to the pathology of osteoarthritis (OA) by altering systemic and local metabolic inflammation. Yet, it remains unclear how quickly and reproducibly the body responds to weight loss strategies and improve OA. In this study we tested whether switching obese diet to a normal chow diet can mitigate the detrimental effects of inflammatory pathways that contribute to OA pathology. Male C57BL/6 mice were first fed with obesogenic diet (high fat diet) and switched to normal chow diet (obese diet → normal diet) or continued obese diet or normal diet throughout the experiment. A mouse model of OA was induced by surgical destabilization of the medial meniscus (DMM) model into the knee joint. Outcome measures included changes in metabolic factors such as glucose, insulin, lipid, and serum cytokines levels. Inflammation in synovial biopsies was scored and inflammation was determined using FACs sorted macrophages. Cartilage degeneration was monitored using histopathology. Our results indicate, dietary switching (obese diet → normal diet) reduced body weight and restored metabolic parameters and showed less synovial tissue inflammation. Systemic blood concentrations of pro-inflammatory cytokines IL-1α, IL-6, IL-12p40, and IL-17 were decreased, and anti-inflammatory cytokines IL-4 and IL-13 were increased in dietary switch group compared to mice that were fed with obesogenic diet continuously. Although obese diet worsens the cartilage degeneration in DMM OA model, weight loss induced by dietary switch does not promote the histopathological changes of OA during this study period. Collectively, these data demonstrate that switching obesogenic diet to normal improved metabolic syndrome symptoms and can modulate both systemic and synovium inflammation levels.
致肥胖饮食通过改变全身和局部代谢炎症来促进骨关节炎(OA)的病理发展。然而,目前尚不清楚身体对体重减轻策略的反应速度和可重复性,以及这些策略如何改善OA。在本研究中,我们测试了将肥胖饮食转换为正常饲料饮食是否可以减轻导致OA病理的炎症途径的有害影响。首先给雄性C57BL/6小鼠喂食致肥胖饮食(高脂肪饮食),然后转换为正常饲料饮食(肥胖饮食→正常饮食),或者在整个实验过程中持续喂食肥胖饮食或正常饮食。通过手术使膝关节内侧半月板不稳定(DMM)模型诱导建立OA小鼠模型。结果指标包括代谢因子如葡萄糖、胰岛素、脂质和血清细胞因子水平的变化。对滑膜活检组织中的炎症进行评分,并使用流式细胞术分选的巨噬细胞确定炎症情况。使用组织病理学监测软骨退变。我们的结果表明,饮食转换(肥胖饮食→正常饮食)可降低体重并恢复代谢参数,且滑膜组织炎症较轻。与持续喂食致肥胖饮食的小鼠相比,饮食转换组中促炎细胞因子IL-1α、IL-6、IL-12p40和IL-17的全身血浓度降低,抗炎细胞因子IL-4和IL-13增加。尽管肥胖饮食会使DMM OA模型中的软骨退变恶化,但在本研究期间,饮食转换诱导的体重减轻并未促进OA的组织病理学变化。总体而言,这些数据表明,将致肥胖饮食转换为正常饮食可改善代谢综合征症状,并可调节全身和滑膜炎症水平。