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Toll-like receptor 5 in obesity: The role of gut microbiota and adipose tissue inflammation

Tutkimustuotosvertaisarvioitu

Standard

Toll-like receptor 5 in obesity: The role of gut microbiota and adipose tissue inflammation. / Pekkala, S.; Munukka, E.; Kong, L.; Pöllänen, E.; Autio, R.; Roos, C.; Wiklund, P.; Fischer-Posovszky, P.; Wabitsch, M.; Alen, M.; Huovinen, P.; Cheng, S.

julkaisussa: Obesity, Vuosikerta 23, Nro 3, 2015, s. 581-590.

Tutkimustuotosvertaisarvioitu

Harvard

Pekkala, S, Munukka, E, Kong, L, Pöllänen, E, Autio, R, Roos, C, Wiklund, P, Fischer-Posovszky, P, Wabitsch, M, Alen, M, Huovinen, P & Cheng, S 2015, 'Toll-like receptor 5 in obesity: The role of gut microbiota and adipose tissue inflammation', Obesity, Vuosikerta. 23, Nro 3, Sivut 581-590. https://doi.org/10.1002/oby.20993

APA

Pekkala, S., Munukka, E., Kong, L., Pöllänen, E., Autio, R., Roos, C., ... Cheng, S. (2015). Toll-like receptor 5 in obesity: The role of gut microbiota and adipose tissue inflammation. Obesity, 23(3), 581-590. https://doi.org/10.1002/oby.20993

Vancouver

Pekkala S, Munukka E, Kong L, Pöllänen E, Autio R, Roos C et al. Toll-like receptor 5 in obesity: The role of gut microbiota and adipose tissue inflammation. Obesity. 2015;23(3):581-590. https://doi.org/10.1002/oby.20993

Author

Pekkala, S. ; Munukka, E. ; Kong, L. ; Pöllänen, E. ; Autio, R. ; Roos, C. ; Wiklund, P. ; Fischer-Posovszky, P. ; Wabitsch, M. ; Alen, M. ; Huovinen, P. ; Cheng, S. / Toll-like receptor 5 in obesity: The role of gut microbiota and adipose tissue inflammation. Julkaisussa: Obesity. 2015 ; Vuosikerta 23, Nro 3. Sivut 581-590.

Bibtex - Lataa

@article{5be7f3d1ea6e4cbfabf66c88d6963515,
title = "Toll-like receptor 5 in obesity: The role of gut microbiota and adipose tissue inflammation",
abstract = "Objective This study aimed at establishing bacterial flagellin-recognizing toll-like receptor 5 (TLR5) as a novel link between gut microbiota composition, adipose tissue inflammation, and obesity. Methods An adipose tissue microarray database was used to compare women having the highest (n = 4, H-TLR) and lowest (n = 4, L-TLR) expression levels of TLR5-signaling pathway genes. Gut microbiota composition was profiled using flow cytometry and FISH. Standard laboratory techniques were used to determine anthropometric and clinical variables. In vivo results were verified using cultured human adipocytes. Results The H-TLR group had higher flagellated Clostridium cluster XIV abundance and Firmicutes-to-Bacteroides ratio. H-TLR subjects had obese phenotype characterized by greater waist circumference, fat {\%}, and blood pressure (P < 0.05 for all). They also had higher leptin and lower adiponectin levels (P < 0.05 for both). Six hundred and sixty-eight metabolism-and inflammation-related adipose tissue genes were differentially expressed between the groups. In vitro studies confirmed that flagellin activated TLR5 inflammatory pathways, decreased insulin signaling, and increased glycerol secretion. Conclusions The in vivo findings suggest that flagellated Clostridium cluster XIV bacteria contribute to the development of obesity through distorted adipose tissue metabolism and inflammation. The in vitro studies in adipocytes show that the underlying mechanisms of the human findings may be due to flagellin-activated TLR5 signaling.",
author = "S. Pekkala and E. Munukka and L. Kong and E. P{\"o}ll{\"a}nen and R. Autio and C. Roos and P. Wiklund and P. Fischer-Posovszky and M. Wabitsch and M. Alen and P. Huovinen and S. Cheng",
note = "siirret{\"a}{\"a}n 2015<br/>Contribution: organisation=sgn,FACT1=1<br/>Portfolio EDEND: 2015-01-14<br/>Publisher name: Wiley-Blackwell Publishing",
year = "2015",
doi = "10.1002/oby.20993",
language = "English",
volume = "23",
pages = "581--590",
journal = "Obesity",
issn = "1930-7381",
publisher = "Wiley",
number = "3",

}

RIS (suitable for import to EndNote) - Lataa

TY - JOUR

T1 - Toll-like receptor 5 in obesity: The role of gut microbiota and adipose tissue inflammation

AU - Pekkala, S.

AU - Munukka, E.

AU - Kong, L.

AU - Pöllänen, E.

AU - Autio, R.

AU - Roos, C.

AU - Wiklund, P.

AU - Fischer-Posovszky, P.

AU - Wabitsch, M.

AU - Alen, M.

AU - Huovinen, P.

AU - Cheng, S.

N1 - siirretään 2015<br/>Contribution: organisation=sgn,FACT1=1<br/>Portfolio EDEND: 2015-01-14<br/>Publisher name: Wiley-Blackwell Publishing

PY - 2015

Y1 - 2015

N2 - Objective This study aimed at establishing bacterial flagellin-recognizing toll-like receptor 5 (TLR5) as a novel link between gut microbiota composition, adipose tissue inflammation, and obesity. Methods An adipose tissue microarray database was used to compare women having the highest (n = 4, H-TLR) and lowest (n = 4, L-TLR) expression levels of TLR5-signaling pathway genes. Gut microbiota composition was profiled using flow cytometry and FISH. Standard laboratory techniques were used to determine anthropometric and clinical variables. In vivo results were verified using cultured human adipocytes. Results The H-TLR group had higher flagellated Clostridium cluster XIV abundance and Firmicutes-to-Bacteroides ratio. H-TLR subjects had obese phenotype characterized by greater waist circumference, fat %, and blood pressure (P < 0.05 for all). They also had higher leptin and lower adiponectin levels (P < 0.05 for both). Six hundred and sixty-eight metabolism-and inflammation-related adipose tissue genes were differentially expressed between the groups. In vitro studies confirmed that flagellin activated TLR5 inflammatory pathways, decreased insulin signaling, and increased glycerol secretion. Conclusions The in vivo findings suggest that flagellated Clostridium cluster XIV bacteria contribute to the development of obesity through distorted adipose tissue metabolism and inflammation. The in vitro studies in adipocytes show that the underlying mechanisms of the human findings may be due to flagellin-activated TLR5 signaling.

AB - Objective This study aimed at establishing bacterial flagellin-recognizing toll-like receptor 5 (TLR5) as a novel link between gut microbiota composition, adipose tissue inflammation, and obesity. Methods An adipose tissue microarray database was used to compare women having the highest (n = 4, H-TLR) and lowest (n = 4, L-TLR) expression levels of TLR5-signaling pathway genes. Gut microbiota composition was profiled using flow cytometry and FISH. Standard laboratory techniques were used to determine anthropometric and clinical variables. In vivo results were verified using cultured human adipocytes. Results The H-TLR group had higher flagellated Clostridium cluster XIV abundance and Firmicutes-to-Bacteroides ratio. H-TLR subjects had obese phenotype characterized by greater waist circumference, fat %, and blood pressure (P < 0.05 for all). They also had higher leptin and lower adiponectin levels (P < 0.05 for both). Six hundred and sixty-eight metabolism-and inflammation-related adipose tissue genes were differentially expressed between the groups. In vitro studies confirmed that flagellin activated TLR5 inflammatory pathways, decreased insulin signaling, and increased glycerol secretion. Conclusions The in vivo findings suggest that flagellated Clostridium cluster XIV bacteria contribute to the development of obesity through distorted adipose tissue metabolism and inflammation. The in vitro studies in adipocytes show that the underlying mechanisms of the human findings may be due to flagellin-activated TLR5 signaling.

U2 - 10.1002/oby.20993

DO - 10.1002/oby.20993

M3 - Article

VL - 23

SP - 581

EP - 590

JO - Obesity

JF - Obesity

SN - 1930-7381

IS - 3

ER -