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Cited by 282

The DOI matches its Crossref record; 75 of the 75 references it cites were found in a registry or an index.

Gut Microbiota Is a Key Modulator of Insulin Resistance in TLR 2 Knockout Mice

Open access
Caricilli, Andréa M., Picardi, Paty K., de Abreu, Lélia L., Ueno, Mirian, Prada, Patrícia O., Ropelle, Eduardo R., Hirabara, Sandro Massao, Castoldi, Ângela, Vieira, Pedro, Camara, Niels O. S., Curi, Rui, Carvalheira, José B., Saad, Mário J. A.·2011·PLoS Biology
DOI 10.1371/journal.pbio.1001212
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Abstract

Environmental factors and host genetics interact to control the gut microbiota, which may have a role in the development of obesity and insulin resistance. TLR2-deficient mice, under germ-free conditions, are protected from diet-induced insulin resistance. It is possible that the presence of gut microbiota could reverse the phenotype of an animal, inducing insulin resistance in an animal genetically determined to have increased insulin sensitivity, such as the TLR2 KO mice. In the present study, we investigated the influence of gut microbiota on metabolic parameters, glucose tolerance, insulin sensitivity, and signaling of TLR2-deficient mice. We investigated the gut microbiota (by metagenomics), the metabolic characteristics, and insulin signaling in TLR2 knockout (KO) mice in a non-germ free facility. Results showed that the loss of TLR2 in conventionalized mice results in a phenotype reminiscent of metabolic syndrome, characterized by differences in the gut microbiota, with a 3-fold increase in Firmicutes and a slight increase in Bacteroidetes compared with controls. These changes in gut microbiota were accompanied by an increase in LPS absorption, subclinical inflammation, insulin resistance, glucose intolerance, and later, obesity. In addition, this sequence of events was reproduced in WT mice by microbiota transplantation and was also reversed by antibiotics. At the molecular level the mechanism was unique, with activation of TLR4 associated with ER stress and JNK activation, but no activation of the IKKβ-IκB-NFκB pathway. Our data also showed that in TLR2 KO mice there was a reduction in regulatory T cell in visceral fat, suggesting that this modulation may also contribute to the insulin resistance of these animals. Our results emphasize the role of microbiota in the complex network of molecular and cellular interactions that link genotype to phenotype and have potential implications for common human disorders involving obesity, diabetes, and even other immunological disorders.

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Crossref · 10.1371/journal.pbio.1001212This paper is marked retracted.

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Metadata

Authors
Caricilli, A. M., Picardi, P. K., de Abreu, L. L., Ueno, M., Prada, P. O., Ropelle, E. R., Hirabara, S. M., Castoldi, Â., Vieira, P., Camara, N. O. S., Curi, R., Carvalheira, J. B., & Saad, M. J. A.
Venue
PLoS Biology
Publisher
Public Library of Science (PLoS)
Published
2011-12-06
Volume
9
Issue
12
Pages
e1001212
ISSN
  • 1544-9173 (ISSN-L)
  • 1545-7885
DOI
10.1371/journal.pbio.1001212
OpenAlex
W1990908543
Cited by
282
References
75
FWCI
12.11
Type
journal article
Language
en
Status
Retracted
Open access
gold

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

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