Intestinal microflora and metabolic diseases
Abstract Recent advances in molecular sequencing technology have allowed researchers to answer major questions regarding the relationship between a vast genomic diversity—such as found in the intestinal microflora—and host physiology. Over the past few years, it has been established that, in obesity...
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Published in: | Diabetes & metabolism Vol. 35; no. 4; pp. 262 - 272 |
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Main Authors: | , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Paris
Elsevier Masson SAS
01-09-2009
Masson Elsevier Masson |
Subjects: | |
Online Access: | Get full text |
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Summary: | Abstract Recent advances in molecular sequencing technology have allowed researchers to answer major questions regarding the relationship between a vast genomic diversity—such as found in the intestinal microflora—and host physiology. Over the past few years, it has been established that, in obesity, type 1 diabetes and Crohn's disease—to cite but a few—the intestinal microflora play a pathophysiological role and can induce, transfer or prevent the outcome of such conditions. A few of the molecular vectors responsible for this regulatory role have been determined. Some are related to control of the immune, vascular, endocrine and nervous systems located in the intestines. However, more important is the fact that the intestinal microflora-to-host relationship is bidirectional, with evidence of an impact of the host genome on the intestinal microbiome. This means that the ecology shared by the host and gut microflora should now be considered a new player that can be manipulated, using pharmacological and nutritional approaches, to control physiological functions and pathological outcomes. What now remains is to demonstrate the molecular connection between the intestinal microflora and metabolic diseases. We propose here that the proinflammatory lipopolysaccharides play a causal role in the onset of metabolic disorders. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 1262-3636 1878-1780 |
DOI: | 10.1016/j.diabet.2009.03.003 |