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Diabetes 56:e21 2007
DOI: 10.2337/db07-1262
© 2007 by the American Diabetes Association
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Letter to the Editor

Response to Comment on: Cani et al. (2007) Metabolic Endotoxemia Initiates Obesity and Insulin Resistance: Diabetes 56:1761–1772

Rémy Burcelin1, Patrice D. Cani1, and Jacques Amar2

1 INSERM U858, Institute of Molecular Medicine I2MR, Toulouse, France
2 INSERM U558, Toulouse, France

Address correspondence and reprint requests to Rémy Burcelin, I2MR U858, IFR 31, Hôpital Rangueil, BP 84225, Toulouse 31432 Cedex 4, France. E-mail: burcelin{at}toulouse.inserm.fr

We thank Saito and Reiko (1), who point out an important fact with regard to the potential sources of circulating lipopolysaccharide (LPS) in metabolic endotoxemia and its correlation with obesity. This relationship has been shown in humans and animal models (2,3). In the light of our recent data (4), which causally demonstrate the role of intestinal bacterial LPS on the onset of metabolic diseases, Saito and Reiko remind us that changes in plasma LPS, driven by periodontitis, may be a causative factor of the relationship between periodontitis and metabolic diseases. We agree that, in addition to intestinal microflora, periodontitis could be an important source of endotoxemia. Interestingly, regarding Saito and Reiko’s hypothesis, our group has previously shown an interaction between the soluble CD14 receptor (the main LPS receptor), a CD14 gene polymorphism, and cigarette smoking (5), in which the deleterious role of buccal microbiota and periodontitis have been well established (6). The next step to pursue these hypotheses will be to demonstrate whether a reduction of metabolic endotoxemia, by means of a dietary intervention or treatment of periodontal disease, impact the subsequent risk for metabolic disease.

Received for publication September 5, 2007 and accepted in revised form September 5, 2007

REFERENCES

  1. Saito T, Reiko H: Comment on: Cani et al. (2007) Metabolic endotoxemia initiates obesity and insulin resistance: Diabetes 56:1761–1772. Diabetes 456:e20, 2007. DOI: 10.2337/db07-1181
  2. Saito T, Shimazaki Y, Sakamoto M: Obesity and periodontitis. N Engl J Med 339:482–483, 1998[Free Full Text]
  3. Tomofuji T, Ekni D, Yamanak R, Kusano H, Azuma T, Sanbe T, Tamaki N, Yamamoto T, Watanabe T, Miyauch M, Takat T: Chronic administration of lipopolysaccharide and proteases induces periodontal inflammation and hepatic steatosis in rats. J Periodontol 78:1999–2006, 2007[Medline]
  4. Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, Neyrinck AM, Fava F, Tuohy KM, Chabo C, Waget A, Delmee E, Cousin B, Sulpice T, Chamontin B, Ferrieres J, Tanti JF, Gibson GR, Casteilla L, Delzenne NM, Alessi MC, Burcelin R: Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes 56:1761–1772, 2007[Abstract/Free Full Text]
  5. Gomes SC, Piccinin FB, Oppermann RV, Susin C, Nonnenmacher CI, Mutters R, Marcantonio RA: Periodontal status in smokers and never-smokers: clinical findings and real-time polymerase chain reaction quantification of putative periodontal pathogens. J Periodontol 77:1483–1490, 2006[Medline]
  6. Amar J, Ruidavets JB, Bal dit Sollier C, Bongard V, Boccalon H, Chamontin B, Drouet L, Ferrieres J: CD14 C(-260)T gene polymorphism, circulating soluble CD14 levels and arteriosclerosis. J Hypertens 8:1523–1528, 2004

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This Article
Right arrow Extract Freely available
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Right arrow Articles by Burcelin, R.
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PubMed
Right arrow Articles by Burcelin, R.
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