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Helicobacter pylori Colonization Ameliorates Glucose Homeostasis in Mice through a PPAR γ-Dependent Mechanism

Overview of attention for article published in PLOS ONE, November 2012
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Title
Helicobacter pylori Colonization Ameliorates Glucose Homeostasis in Mice through a PPAR γ-Dependent Mechanism
Published in
PLOS ONE, November 2012
DOI 10.1371/journal.pone.0050069
Pubmed ID
Authors

Josep Bassaganya-Riera, Maria Gloria Dominguez-Bello, Barbara Kronsteiner, Adria Carbo, Pinyi Lu, Monica Viladomiu, Mireia Pedragosa, Xiaoying Zhang, Bruno W. Sobral, Shrinivasrao P. Mane, Saroj K. Mohapatra, William T. Horne, Amir J. Guri, Michael Groeschl, Gabriela Lopez-Velasco, Raquel Hontecillas

Abstract

There is an inverse secular trend between the incidence of obesity and gastric colonization with Helicobacter pylori, a bacterium that can affect the secretion of gastric hormones that relate to energy homeostasis. H. pylori strains that carry the cag pathogenicity island (PAI) interact more intimately with gastric epithelial cells and trigger more extensive host responses than cag(-) strains. We hypothesized that gastric colonization with H. pylori strains differing in cag PAI status exert distinct effects on metabolic and inflammatory phenotypes.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 50 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 2 4%
France 1 2%
Unknown 47 94%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 11 22%
Researcher 7 14%
Student > Bachelor 7 14%
Student > Master 6 12%
Student > Doctoral Student 3 6%
Other 11 22%
Unknown 5 10%
Readers by discipline Count As %
Agricultural and Biological Sciences 13 26%
Medicine and Dentistry 13 26%
Biochemistry, Genetics and Molecular Biology 7 14%
Immunology and Microbiology 7 14%
Computer Science 1 2%
Other 2 4%
Unknown 7 14%