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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Interactions between gut microbiota, host genetics and diet modulate the predisposition to obesity and metabolic syndrome.
Cell Metab. 22, 516-530 (2015)
Obesity, diabetes, and metabolic syndrome result from complex interactions between genetic and environmental factors, including the gut microbiota. To dissect these interactions, we utilized three commonly used inbred strains of mice-obesity/diabetes-prone C57Bl/6J mice, obesity/diabetes-resistant 129S1/SvImJ from Jackson Laboratory, and obesity-prone but diabetes-resistant 129S6/SvEvTac from Taconic-plus three derivative lines generated by breeding these strains in a new, common environment. Analysis of metabolic parameters and gut microbiota in all strains and their environmentally normalized derivatives revealed strong interactions between microbiota, diet, breeding site, and metabolic phenotype. Strain-dependent and strain-independent correlations were found between specific microbiota and phenotypes, some of which could be transferred to germ-free recipient animals by fecal transplantation. Environmental reprogramming of microbiota resulted in 129S6/SvEvTac becoming obesity resistant. Thus, development of obesity/metabolic syndrome is the result of interactions between gut microbiota, host genetics, and diet. In permissive genetic backgrounds, environmental reprograming of microbiota can ameliorate development of metabolic syndrome.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Intestinal Microbiota; Insulin Sensitivity; Wide Association; Systems Biology; Mice; Disease; Individuals; Homeostasis; Metagenome; Resistance
ISSN (print) / ISBN
1550-4131
e-ISSN
1932-7420
Zeitschrift
Cell Metabolism
Quellenangaben
Band: 22,
Heft: 3,
Seiten: 516-530
Verlag
Elsevier
Verlagsort
Cambridge
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Diabetes and Obesity (IDO)