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2015 ; 22
(3
): 516-530
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Interactions between Gut Microbiota, Host Genetics and Diet Modulate the
Predisposition to Obesity and Metabolic Syndrome
#MMPMID26299453
Ussar S
; Griffin NW
; Bezy O
; Fujisaka S
; Vienberg S
; Softic S
; Deng L
; Bry L
; Gordon JI
; Kahn CR
Cell Metab
2015[Sep]; 22
(3
): 516-530
PMID26299453
show ga
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.