Periodontal disease and hypertriglyceridemia in Japanese subjects: potential association with enhanced lipolysis

Nakarai, Hideo; Yamashita, Akiko; Takagi, Mikimasa; Adachi, Masataka; Sugiyama, Masaharu; Noda, Haruhiko; Katano, Masafumi; Yamakawa, Ryuji; Nakayama, Keiji; Takumiya, Hitomi; Nakai, Yoshikatsu; Taniguchi, Ataru; Nishimura, Fusanori

doi:10.1016/j.metabol.2010.07.034

Cited by 32 publications

(30 citation statements)

References 26 publications

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“…Thus, observed high triglycerides in severe periodontitis subjects may also indicate enhanced lipolysis in such subjects. 27,28 Interestingly, elevated SAA in association with periodontitis has recently been reported, although this report did not indicate the source of SAA in such periodontitis patients. 29 …”

Section: Discussioncontrasting

confidence: 56%

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Adipocyte-macrophage interaction may mediate LPS-induced low-grade inflammation: Potential link with metabolic complications

et al. 2011

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Chronic low-grade infection has been suggested to be associated with metabolic disorder such as diabetes. However, the molecular mechanism underlying this important association is largely unknown. The only clue established so far is that many subjects exhibit elevated levels of C-reactive protein as measured by highly sensitive assay. Here, we hypothesized that adipocyte-macrophage interaction plays a key role in amplifying such low grade infection to the level of influencing metabolic disorders. The presence of macrophages in abdominal adipose tissues was investigated by immunohistochemistry. To see whether molecules associated with acute phase protein, LPS signaling, and persistent recruitment of monocytes, are produced at higher amounts in adipocytes co-cultured with macrophages stimulated with low concentration of LPS (1 ng/ml), we measured serum amyloid A (SAA), LPS binding protein (LBP), soluble CD14 (sCD14), and RANTES levels in culture supernatant of co-cultures. Lastly, we investigated in vivo effect of low-grade LPS infusion on the production of these molecules using obese model mice. The macrophages were certainly identified in abdominal adipose tissues. Investigated molecules, especially LBP, SAA, and RANTES were produced at higher amounts in co-cultures stimulated with LPS compared with the cells without LPS. The ob/ob, and high-fat diet-induced obesity mice produced higher amounts of LBP, SAA, and RANTES one day after LPS infusion (1 ng/ml/g body weight) compared with ob/- and normal-fat fed control mice. Thus, adipocytes and infiltrated macrophages, and their interaction with low endotoxin stimulation appear to play an important role in amplifying and maintaining LPS-induced low-grade inflammation.

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Section: Discussioncontrasting

confidence: 56%

“…25,26 A recent report indicated significant association between clinical severity of periodontitis and serum triglyceride level. 27 Furthermore, as mentioned above, obesity and/or overweight are associated with periodontitis. 12 Triglycerides are mainly synthesized in the liver from FFA following lipolysis.…”

Section: Discussionmentioning

confidence: 96%

Adipocyte-macrophage interaction may mediate LPS-induced low-grade inflammation: Potential link with metabolic complications

et al. 2011

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“…Studies have shown positive association between dyslipidemia and periodontal disease [21,29,30]. In our previous animal study, feeding with a high-cholesterol diet increased serum lipid peroxidation and the number of TRAP-positive osteoclasts, with an increase in RANKL expression [14].…”

Section: Discussionmentioning

confidence: 99%

Involvement of toll-like receptor 2 and 4 in association between dyslipidemia and osteoclast differentiation in apolipoprotein E deficient rat periodontium

et al. 2013

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BackgroundDyslipidemia increases circulating levels of oxidized low-density lipoprotein (OxLDL) and this may induce alveolar bone loss through toll-like receptor (TLR) 2 and 4. The purpose of this study was to investigate the effects of dyslipidemia on osteoclast differentiation associated with TLR2 and TLR4 in periodontal tissues using a rat dyslipidemia (apolipoprotein E deficient) model.MethodsLevels of plasma OxLDL, and the cholesterol and phospholipid profiles in plasma lipoproteins were compared between apolipoprotein E-deficient rats (16-week-old males) and wild-type (control) rats. In the periodontal tissue, we evaluated the changes in TLR2, TLR4, receptor activator of nuclear factor kappa B ligand (RANKL) and tartrate resistant acid phosphatase (TRAP) expression.ResultsApolipoprotein E-deficient rats showed higher plasma levels of OxLDL than control rats (p<0.05), with higher plasma levels of total cholesterol (p<0.05) and LDL-cholesterol (p<0.05) and lower plasma levels of high-density lipoprotein cholesterol (p<0.05). Their periodontal tissue also exhibited a higher ratio of RANKL-positive cells and a higher number of TRAP-positive osteoclasts than control rats (p<0.05). Furthermore, periodontal gene expression of TLR2, TLR4 and RANKL was higher in apolipoprotein E-deficient rats than in control rats (p<0.05).ConclusionThese findings underscore the important role for TLR2 and TLR4 in mediating the osteoclast differentiation on alveolar bone response to dyslipidemia.

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“…One of the major adipokines, tumor necrosis factor (TNF)-α, is known to induce lipolysis [10]. Therefore, we hypothesized that adipose-tissue inflammation-derived TNF-α may be associated with elevated levels of triglycerides, as following lipolysis, released free fatty acids are integrated into the liver and triglycerides are re-synthesized afterwards [11]. In fact, we already confirmed that cultured 3T3-L1 adipocytes exhibited higher lipolytic activity when co-cultured with macrophages in the presence of TNF-α- inducing molecule as bacterial endotoxin [11].…”

Section: Discussionmentioning

confidence: 99%

Smoking and adipose tissue inflammation suppress leptin expression in Japanese obese males: Potential mechanism of resistance to weight loss among Japanese obese smokers

Nagayasu¹,

Suzuki²,

Yamashita³

et al. 2012

Tobacco Induced Diseases

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BackgroundThe effect of smoking on leptin regulation is controversial. Smoking may induce low-grade inflammation. Recent series of studies indicated the critical role of macrophage migration in the establishment of adipose tissue inflammation. In this study, we aimed to see the effects of smoking and inflammation on leptin regulation both at cellular and epidemiological levels.MethodsWe compared the concentration of inflammatory markers and serum leptin levels among Japanese male subjects. Additionally, leptin and intercellular adhesion molecule (ICAM) -1 gene expression was assessed in adipocytes co-cultured with or without macrophages in the presence or absence of nicotine and/or lipopolysaccharide (LPS).ResultsIn subjects with BMI below 25 kg/m2, both WBC counts and soluble-ICAM-1 levels are significantly higher in smokers than in non-smokers. However, leptin concentration did not differ according to smoking status. However, in subjects with BMI over 25 kg/m2, smokers exhibited significantly lower serum leptin level as well as higher WBC counts and s-ICAM-1 concentration as compared with non-smokers. Leptin gene expression was markedly suppressed in adipocytes co-cultured with macrophages than in adipocyte culture alone. Furthermore, nicotine further suppressed leptin gene expression. ICAM-1 gene expression was markedly up-regulated in adipocytes co-cultured with macrophages when stimulated with LPS.ConclusionsAdipose tissue inflammation appears to down-regulate leptin expression in adipose tissues. Nicotine further suppresses leptin expression. Thus, both smoking and inflammation may diminish leptin effect in obese subjects. Therefore, obese, but not normal weight, smokers might be more resistant to weight loss than non-smokers.

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Periodontal disease and hypertriglyceridemia in Japanese subjects: potential association with enhanced lipolysis

Cited by 32 publications

References 26 publications

Adipocyte-macrophage interaction may mediate LPS-induced low-grade inflammation: Potential link with metabolic complications

Adipocyte-macrophage interaction may mediate LPS-induced low-grade inflammation: Potential link with metabolic complications

Involvement of toll-like receptor 2 and 4 in association between dyslipidemia and osteoclast differentiation in apolipoprotein E deficient rat periodontium

Smoking and adipose tissue inflammation suppress leptin expression in Japanese obese males: Potential mechanism of resistance to weight loss among Japanese obese smokers

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