Anna Damanaki1, Marjan Nokhbehsaim1, Kanishka Hiththetiya2, Svenja Memmert1,3, Jinlong Gao4, Ky-Anh Nguyen4, Werner Götz3, Andreas Jäger3, Gerhard Wahl5, James Deschner6,7,8. 1. Section of Experimental Dento-Maxillo-Facial Medicine, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Welschnonnenstrasse 17, 53111, Bonn, Germany. 2. Department of Pathology, University of Bonn, Bonn, Germany. 3. Department of Orthodontics, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Bonn, Germany. 4. Westmead Institute for Medical Research and Faculty of Dentistry, University of Sydney, Sydney, Australia. 5. Department of Oral Surgery, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Bonn, Germany. 6. Section of Experimental Dento-Maxillo-Facial Medicine, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Welschnonnenstrasse 17, 53111, Bonn, Germany. james.deschner@uni-bonn.de. 7. Noel Martin Visiting Chair, Faculty of Dentistry, University of Sydney, Sydney, Australia. james.deschner@uni-bonn.de. 8. Department of Periodontology and Operative Dentistry, University Medical Center, Johannes Gutenberg University, Augustusplatz 2, 55131, Mainz, Australia. james.deschner@uni-bonn.de.
Abstract
OBJECTIVES: 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. MATERIALS AND METHODS: 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). RESULTS: 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. CONCLUSIONS: 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. CLINICAL RELEVANCE: 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.
OBJECTIVES: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. MATERIALS AND METHODS: 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). RESULTS: 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. CONCLUSIONS: 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. CLINICAL RELEVANCE: 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.
Authors: Gustavo G Nascimento; Fábio R M Leite; Loc G Do; Karen G Peres; Marcos B Correa; Flávio F Demarco; Marco A Peres Journal: J Clin Periodontol Date: 2015-06-02 Impact factor: 8.728
Authors: Anna Damanaki; Svenja Memmert; Marjan Nokhbehsaim; Ali Abedi; Birgit Rath-Deschner; Andressa Nogueira; James Deschner Journal: Int J Mol Sci Date: 2021-12-11 Impact factor: 5.923