ArticleJournal of periodontal research2019
Upregulation of free fatty acid receptors in periodontal tissues of patients with metabolic syndrome and periodontitis.
Article in Journal of periodontal research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Metabolite sensing receptors in macrophage reprogramming: from inflammation to resolution.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Role of fatty acid metabolism-related genes in periodontitis based on machine learning and bioinformatics analysis.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2024Article
- Sports Diet and Oral Health in Athletes: A Comprehensive Review.Medicina (Kaunas, Lithuania) · 2024Review
- GPR40 deficiency worsens metabolic syndrome-associated periodontitis in mice.Journal of periodontal research · 2023Article
- Obesity, Bone Loss, and Periodontitis: The Interlink.Biomolecules · 2022Review
- Loss of GPR40 in LDL receptor-deficient mice exacerbates high-fat diet-induced hyperlipidemia and nonalcoholic steatohepatitis.PloS one · 2022Article
- GPR40 deficiency is associated with hepatic FAT/CD36 upregulation, steatosis, inflammation, and cell injury in C57BL/6 mice.American journal of physiology. Endocrinology and metabolism · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND AND
objectiveMetabolic syndrome (MetS) exacerbates periodontitis. Since saturated fatty acid (SFA) is increased in MetS and enhances lipopolysaccharide (LPS)-induced proinflammatory cytokine expression in macrophages, it has been considered to play a role in MetS-exacerbated periodontitis. However, it remains unknown how fatty acid receptors, which mediate the interaction of cells with SFA and uptake of SFA, are expressed and regulated in the periodontal tissue. In this study, we tested our hypothesis that the periodontal expression of fatty acid receptors GPR40 and CD36 is increased in patients with both MetS and periodontitis. We also determined the effect of SFA and LPS on GPR40 and CD36 expression in vitro. MATERIAL AND
methodsPeriodontal tissue specimens were collected from 11 participants without MetS and periodontitis, 12 participants with MetS, 11 participants with periodontitis, and 14 participants with both MetS and periodontitis after surgeries. The tissues were processed, and GPR40 and CD36 were detected by immunohistochemistry. Furthermore, cultured macrophages and gingival fibroblasts were treated with LPS, palmitate, a major SFA, or LPS plus palmitate and the expression of GPR40 and CD36 was then quantified.
resultsAnalysis of clinical data showed that age, smoker, gender, and race/ethnicity were not significantly different among 4 groups. Immunohistochemistry showed that GPR40 and CD36 were expressed by epithelial cells, fibroblasts, and immune cells. Quantitative data showed that GPR40 expression is increased in patients with periodontitis, MetS, or both periodontitis and MetS while CD36 expression is increased only in patients with both periodontitis and MetS. The in vitro studies showed that the expression of GPR40 and CD36 in macrophages and fibroblasts was upregulated by the combination of LPS and palmitate.
conclusionPeriodontal expression of GPR40 and CD36 was upregulated in patients with both MetS and periodontitis, and GPR40 and CD36 in macrophages and fibroblasts were upregulated in vitro by the combination of LPS and palmitate, suggesting that GPR40 and CD36 may be involved in MetS-exacerbated periodontitis.
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