Section of Experimental Dento-Maxillo-Facial Medicine, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Welschnonnenstrasse 17, 53111, Bonn, Germany.
Department of Pathology, University of Bonn, Bonn, Germany.
Clin Oral Investig. 2019 Feb;23(2):937-946. doi: 10.1007/s00784-018-2514-y. Epub 2018 Jun 16.
Obesity is associated with periodontitis, but the mechanisms underlying this association have yet to be unraveled. The present investigation was to evaluate a common rat model, in which obesity is induced by high-fat, high-sucrose diet (HFSD), for its applicability in periodontal research.
Ten male Wistar rats were fed a 3-month HFSD along with a matching control group. Afterwards, the body weight, adipocyte morphology, leptin and adiponectin levels in adipose tissue, gingiva, and serum as well as the serum levels of triglyceride, cholesterol, and glucose were analyzed. For statistical analyses, parametric and non-parametric tests were applied (p < 0.05).
Body weight was significantly higher in the HFSD group after dieting as compared to control. HFSD caused a significant increase in serum triglyceride, low-density lipoprotein cholesterol, and leptin levels and a significant decrease in high-density lipoprotein cholesterol. Furthermore, adipose tissue from HFSD rats exhibited significantly larger adipocytes, displayed a significant upregulation of leptin and, surprisingly, elevated adiponectin levels, which is in contrast to chronic obesity in humans. Although leptin and adiponectin were also observed in gingival biopsies, no obvious differences between the groups were found.
Although this rat diet-induced obesity model is characterized by changes typical of obesity, it also has limitations, which have to be considered when data, especially with regard to adipokines, are extrapolated to humans.
The rodent diet-induced obesity model may be useful for unraveling pathomechanisms underlying the association between obesity and periodontal destruction but conclusions have to be drawn with caution.
肥胖与牙周炎有关,但两者之间的关联机制尚未阐明。本研究旨在评估一种常见的大鼠模型,即高脂肪高蔗糖饮食(HFSD)诱导的肥胖模型,以评估其在牙周研究中的适用性。
10 只雄性 Wistar 大鼠接受 3 个月 HFSD 喂养,同时设立匹配的对照组。之后,分析肥胖大鼠和对照组大鼠的体重、脂肪细胞形态、脂肪组织和血清中的瘦素和脂联素水平以及血清中的甘油三酯、胆固醇和葡萄糖水平。采用参数和非参数检验进行统计学分析(p<0.05)。
与对照组相比,HFSD 组大鼠节食后的体重显著增加。HFSD 导致血清甘油三酯、低密度脂蛋白胆固醇和瘦素水平显著升高,高密度脂蛋白胆固醇水平显著降低。此外,HFSD 大鼠的脂肪组织中脂肪细胞明显增大,瘦素显著上调,令人惊讶的是脂联素水平也升高,这与人类慢性肥胖相反。尽管在牙龈活检组织中也观察到了瘦素和脂联素,但两组之间没有明显差异。
尽管这种大鼠饮食诱导的肥胖模型具有肥胖的典型变化特征,但也存在一定的局限性,在将数据(特别是关于脂肪因子的)外推至人类时必须加以考虑。
啮齿动物饮食诱导的肥胖模型可能有助于阐明肥胖与牙周破坏之间的关联的发病机制,但必须谨慎得出结论。