Prof. João Manuel R. S. Tavares, Faculdade de Engenharia da Universidade do Porto, Rua Dr. Roberto Frias, s/n, 4200-465 Porto, Portugal, email:
J Nutr Health Aging. 2017;21(10):1337-1343. doi: 10.1007/s12603-017-0871-x.
The relationship between obesity and bone tissue remains contradictory, especially when the effect of high-fat diet is assessed in experimental models. The aim of this study was to evaluate the effects of high-fat diet on bone metabolism of growing rats.
Twenty weaned female Wistar rats were equally divided into two groups: SD (standard diet) and HFD (high-fat diet with 60 % of energy as fat). After five weeks of the two diets, the rats were euthanized, and the liver, blood and bones extracted. The liver was analysed for malondialdehyde (MDA) and reduced glutathione (GSH) concentrations. Blood was analysed by the ELISA method for osteoprotegerin (OPG) and tumour necrosis factor ligand superfamily member 11 (TNFSF11/RANKL). The bone tissue was analysed by dual-energy X-ray absorptiometry (DXA), mechanical tests, computed microtomography, histological quantitative analysis and scanning electron microscopy. The gene expressions of PPAR-γ Runx-2, RANKL and Cathepsin-K were also evaluated.
HFD caused an increase in the MDA concentration, indicating oxidative stress. It also increased the expression of PPAR-γ, which is the gene that is related to adipocyte differentiation. There was an increase in BMD of the tibia of animals fed with the HFD, but other microstructural and mechanical properties were maintained unaltered. In addition, there were no changes in the gene expressions related to the differentiation of osteoblasts and osteoclasts, as well as no changes to the biochemical markers of bone formation and bone resorption.
Liver and gene parameters are changed in response to the HFD. However, although there was an increase in BMD, the microstructure and function of the bone did not change after a 5-week HFD.
肥胖与骨组织之间的关系仍存在争议,尤其是在评估高脂肪饮食对实验模型的影响时。本研究旨在评估高脂肪饮食对生长大鼠骨代谢的影响。
将 20 只断奶雌性 Wistar 大鼠等分为两组:SD(标准饮食)和 HFD(高脂肪饮食,脂肪提供 60%的能量)。两种饮食 5 周后,处死大鼠,提取肝脏、血液和骨骼。分析肝脏中的丙二醛(MDA)和还原型谷胱甘肽(GSH)浓度。通过 ELISA 法分析血液中的骨保护素(OPG)和肿瘤坏死因子配体超家族成员 11(TNFSF11/RANKL)。通过双能 X 射线吸收法(DXA)、力学试验、计算微断层扫描、组织学定量分析和扫描电子显微镜分析骨组织。还评估了 PPAR-γ、Runx-2、RANKL 和组织蛋白酶 K 的基因表达。
HFD 导致 MDA 浓度升高,表明存在氧化应激。它还增加了与脂肪细胞分化相关的基因 PPAR-γ 的表达。HFD 喂养的动物的胫骨 BMD 增加,但其他微观结构和力学性能保持不变。此外,与成骨细胞和破骨细胞分化相关的基因表达没有变化,骨形成和骨吸收的生化标志物也没有变化。
HFD 会引起肝脏和基因参数的变化。然而,尽管 BMD 增加,但在 HFD 5 周后,骨的微观结构和功能没有改变。