Intestinal microbiota mediates the beneficial effects of n-3 polyunsaturated fatty acids during dietary obesity
Autor: | Pierre Weill, Quentin Escoula, Sandrine Bellenger, Jérôme Bellenger, Michel Narce, Amina Bourragat |
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Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
medicine.medical_specialty dietary obesity Saturated fat lcsh:TP670-699 fat-1 mice Biology Gut flora Biochemistry 03 medical and health sciences 0302 clinical medicine Insulin resistance Internal medicine microbiota medicine fecal transplantation chemistry.chemical_classification Intestinal permeability metabolic endotoxemia medicine.disease biology.organism_classification Obesity n-3 polyunsaturated fatty acids 030104 developmental biology Endocrinology chemistry 030220 oncology & carcinogenesis lcsh:Oils fats and waxes Metabolic syndrome Agronomy and Crop Science Dysbiosis Food Science Polyunsaturated fatty acid |
Zdroj: | Oilseeds and fats, crops and lipids, Vol 28, p 21 (2021) |
ISSN: | 2257-6614 2272-6977 |
DOI: | 10.1051/ocl/2021006 |
Popis: | Obesity, now considered as a real worldwide epidemic affecting more than 650 million people, is complex and mainly associated with excessive energy intake and changes in eating habits favoring the consumption of diets rich in saturated fat and sugar. This multifactorial pathology is linked to chronic low grade systemic inflammation. Indeed, a high fat diet (HFD) leads to intestinal microbiota dysbiosis increasing gut permeability (partly attributed to a downregulation of genes encoding tight junction proteins) leading to an increase in bacterial lipopolysaccharides (LPS) levels so-called metabolic endotoxemia. Studies have shown that n-3 polyunsaturated fatty acids (PUFAs) are involved in the prevention of obesity and insulin resistance partly through synthesis of lipid mediators. While studies suggest that n-3 PUFAs are able to modulate the gut microbiota, others show no effect of n-3 treatments on intestinal homeostasis. In the present work, we showed that when fed a hypercaloric and obsogenic diet, compared with wild-type (WT) mice, fat-1 mice (with constitutive production of n-3 PUFAs) resist to dietary obesity and associated metabolic disorders, maintain an effective gut barrier function and exhibit greater phylogenic diversity. Moreover, fecal microbiota transplantation from fat-1 to WT mice reversed body weight gain, normalized glucose tolerance and intestinal permeability in association with prevention of alteration of the colon mucus layer. We can conclude that the n-3 PUFA-mediated alterations of gut microbiota contribute to the prevention of metabolic syndrome in fat-1 mice and may represent a promising strategy to prevent metabolic disease and preserve a lean phenotype. |
Databáze: | OpenAIRE |
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