The Transplantation of ω3 PUFA-Altered Gut Microbiota of Fat-1 Mice to Wild-Type Littermates Prevents Obesity and Associated Metabolic Disorders.

Fiche publication

Date publication

mai 2018




Membres identifiés du Cancéropôle Est :
Dr LAGROST Laurent, Pr NARCE Michel

Tous les auteurs :
Bidu C, Escoula Q, Bellenger S, Spor A, Galan M, Geissler A, Bouchot A, Dardevet D, Morio-Liondor B, Cani PD, Lagrost L, Narce M, Bellenger J


Altering the gut microbiome may be beneficial to the host, and it recently arose as a promising strategy to manage obesity. Here, we investigated the relative contribution of ω3 polyunsaturated fatty acid (PUFA)-mediated alterations in the microbiota to metabolic parameter changes in mice. Four groups were compared: male fat-1 transgenic mice (with constitutive production of ω3 PUFAs) and male WT littermates fed either an obesogenic (high fat/high sucrose, HFHS) or a control diet. Unlike WT mice, HFHS-fed fat-1 mice were protected against obesity, glucose intolerance and hepatic steatosis. Unlike WT mice, fat-1 mice maintained a normal barrier function, resulting in a significantly lower metabolic endotoxemia. Fat-1 mice displayed greater phylogenic diversity in the cecum, and fecal microbiota transplantation from fat-1 to WT mice was able to reverse weight gain and to normalize glucose tolerance and intestinal permeability. We concluded that the ω3 fatty acid-mediated alteration of gut microbiota contributed to the prevention of metabolic syndrome in fat-1 mice. It occurred independently of changes in PUFA content of host tissues, and may represent a promising strategy to prevent metabolic disease and to preserve a lean phenotype.

Mots clés

Animals, Cadherins, genetics, Diet, Carbohydrate Loading, adverse effects, Diet, High-Fat, adverse effects, Dietary Sucrose, adverse effects, Dysbiosis, microbiology, Endotoxemia, etiology, Fatty Acids, Omega-3, metabolism, Fecal Microbiota Transplantation, adverse effects, Gastrointestinal Microbiome, Glucose Intolerance, microbiology, Insulin Resistance, Intestinal Mucosa, metabolism, Intestines, microbiology, Liver, metabolism, Male, Mice, Transgenic, Muscle, Skeletal, metabolism, Non-alcoholic Fatty Liver Disease, microbiology, Obesity, microbiology, Permeability, Phylogeny


Diabetes. 2018 May 23;: