Nishimura Fusanori, Iwamoto Yoshihiro, Mineshiba Junji, Shimizu Akemi, Soga Yoshihiko, Murayama Yoji
Department of Periodontal Science, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan.
J Periodontol. 2003 Jan;74(1):97-102. doi: 10.1902/jop.2003.74.1.97.
It is generally accepted that obesity is associated with many other multiple-risk factor syndromes such as hypertension, hyperlipidemia, type 2 diabetes mellitus, and periodontal disease. The number of obese people is increasing rapidly in both western and eastern countries. Adipocytes in the adipose tissues of obese people produce large quantities of biologically active molecules such as leptin, an important molecule regulating energy expenditure and body weight. Therefore, adipocyte-derived active molecules, named adipocytokines, are candidate molecules accounting for the close association between obesity and other multiple-risk factor syndromes. The proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) is produced by adipocytes, and its blood concentration is elevated in obese patients and declines with weight loss. Studies have demonstrated that TNF-alpha suppresses insulin action via its specific receptor; hence, it exacerbates insulin resistance. In addition to adipocytes, monocytes/macrophages produce large quantities of TNF-alpha. Thus, TNF-alpha, produced from monocytic cells due to inflammatory diseases, may have an additive influence on insulin sensitivity to adipocyte-derived TNF-alpha. Here, we hypothesized that 1) TNF-alpha produced by the adipose tissues of obese patients acts as a risk factor for periodontal inflammation, and 2) TNF-alpha produced due to periodontal inflammation may be an additional important factor influencing insulin sensitivity in both obese and type 2 diabetic patients. We believe that this interaction is a possible mechanism accounting for a 2-way relationship between type 2 diabetes and periodontal disease.
人们普遍认为，肥胖与许多其他多危险因素综合征相关，如高血压、高脂血症、2型糖尿病和牙周病。肥胖人群的数量在西方国家和东方国家都在迅速增加。肥胖者脂肪组织中的脂肪细胞会产生大量生物活性分子，如瘦素，这是一种调节能量消耗和体重的重要分子。因此，源自脂肪细胞的活性分子，即脂肪细胞因子，是解释肥胖与其他多危险因素综合征之间密切关联的候选分子。促炎细胞因子肿瘤坏死因子-α（TNF-α）由脂肪细胞产生，肥胖患者血液中其浓度升高，且随体重减轻而下降。研究表明，TNF-α通过其特异性受体抑制胰岛素作用；因此，它会加剧胰岛素抵抗。除了脂肪细胞外，单核细胞/巨噬细胞也会产生大量TNF-α。因此，由于炎症性疾病由单核细胞产生的TNF-α，可能会对脂肪细胞源性TNF-α的胰岛素敏感性产生叠加影响。在此，我们假设：1）肥胖患者脂肪组织产生的TNF-α是牙周炎症的危险因素；2）牙周炎症产生的TNF-α可能是影响肥胖和2型糖尿病患者胰岛素敏感性的另一个重要因素。我们认为这种相互作用是解释2型糖尿病与牙周病双向关系的一种可能机制。
