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      Fucoxanthin modulates cecal and fecal microbiota differently based on diet

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          Abstract

          Fucoxanthin supplementation to NCD or HFD significantly reduced the bodyweight gain in mice likely through its capability to differentially modulate cecal and fecal microbiota based on diet.

          Abstract

          Obesity is a major health concern worldwide and is considered to be associated with disruption of host-microbial homeostasis, especially microbiota composition in the gastrointestinal tract. Use of microbiota-directed foods or nutraceuticals therefore represents a promising approach for the control of obesity. Fucoxanthin, a marine carotenoid, has been proven to be one of the most effective anti-obesity natural products. However, its action mechanism is yet to be unraveled, especially with respect to its role in the modulation of gut microbiota composition. In the present study, profiles of microbiota in both the cecal and fecal samples from BALB/c mice given respectively the following treatments were examined: normal chow diet (NCD), NCD + fucoxanthin (NCDF), high-fat-diet (HFD), and HFD + fucoxanthin (HFDF). The results showed that fucoxanthin supplementation for 4 weeks significantly changed the composition of both cecal and fecal microbiota. In addition, a differential effect was observed between the supplementation to NCD and to HFD. The changes in the Firmicutes/ Bacteroidetes ratio and the abundance of S24-7 and Akkermansia were identified to be among the major gut microbiota modulating events associated with the anti-obesity bioactivity of fucoxanthin. Hence, our results suggested that fucoxanthin could be a promising microbiota-targeted functional-food ingredient.

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          Most cited references34

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          Diet rapidly and reproducibly alters the human gut microbiome

          Long-term diet influences the structure and activity of the trillions of microorganisms residing in the human gut 1–5 , but it remains unclear how rapidly and reproducibly the human gut microbiome responds to short-term macronutrient change. Here, we show that the short-term consumption of diets composed entirely of animal or plant products alters microbial community structure and overwhelms inter-individual differences in microbial gene expression. The animal-based diet increased the abundance of bile-tolerant microorganisms (Alistipes, Bilophila, and Bacteroides) and decreased the levels of Firmicutes that metabolize dietary plant polysaccharides (Roseburia, Eubacterium rectale, and Ruminococcus bromii). Microbial activity mirrored differences between herbivorous and carnivorous mammals 2 , reflecting trade-offs between carbohydrate and protein fermentation. Foodborne microbes from both diets transiently colonized the gut, including bacteria, fungi, and even viruses. Finally, increases in the abundance and activity of Bilophila wadsworthia on the animal-based diet support a link between dietary fat, bile acids, and the outgrowth of microorganisms capable of triggering inflammatory bowel disease 6 . In concert, these results demonstrate that the gut microbiome can rapidly respond to altered diet, potentially facilitating the diversity of human dietary lifestyles.
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            Microbial ecology: human gut microbes associated with obesity.

            Two groups of beneficial bacteria are dominant in the human gut, the Bacteroidetes and the Firmicutes. Here we show that the relative proportion of Bacteroidetes is decreased in obese people by comparison with lean people, and that this proportion increases with weight loss on two types of low-calorie diet. Our findings indicate that obesity has a microbial component, which might have potential therapeutic implications.
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              Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity.

              Obesity and type 2 diabetes are characterized by altered gut microbiota, inflammation, and gut barrier disruption. Microbial composition and the mechanisms of interaction with the host that affect gut barrier function during obesity and type 2 diabetes have not been elucidated. We recently isolated Akkermansia muciniphila, which is a mucin-degrading bacterium that resides in the mucus layer. The presence of this bacterium inversely correlates with body weight in rodents and humans. However, the precise physiological roles played by this bacterium during obesity and metabolic disorders are unknown. This study demonstrated that the abundance of A. muciniphila decreased in obese and type 2 diabetic mice. We also observed that prebiotic feeding normalized A. muciniphila abundance, which correlated with an improved metabolic profile. In addition, we demonstrated that A. muciniphila treatment reversed high-fat diet-induced metabolic disorders, including fat-mass gain, metabolic endotoxemia, adipose tissue inflammation, and insulin resistance. A. muciniphila administration increased the intestinal levels of endocannabinoids that control inflammation, the gut barrier, and gut peptide secretion. Finally, we demonstrated that all these effects required viable A. muciniphila because treatment with heat-killed cells did not improve the metabolic profile or the mucus layer thickness. In summary, this study provides substantial insight into the intricate mechanisms of bacterial (i.e., A. muciniphila) regulation of the cross-talk between the host and gut microbiota. These results also provide a rationale for the development of a treatment that uses this human mucus colonizer for the prevention or treatment of obesity and its associated metabolic disorders.
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                Author and article information

                Contributors
                Journal
                FFOUAI
                Food & Function
                Food Funct.
                Royal Society of Chemistry (RSC)
                2042-6496
                2042-650X
                September 18 2019
                2019
                : 10
                : 9
                : 5644-5655
                Affiliations
                [1 ]Institute for Advanced Study
                [2 ]Shenzhen University
                [3 ]Shenzhen
                [4 ]China
                [5 ]College of Life Science and Bioengineering
                [6 ]College of Bioscience and Biotechnology
                [7 ]Hunan Agricultural University
                [8 ]Changsha 410128
                [9 ]Institute of Agro-Food Science and Technology
                [10 ]Chinese Academy of Agricultural Science
                [11 ]Beijing
                [12 ]Institute for Food and Bioresource Engineering
                [13 ]College of Engineering
                [14 ]Peking University
                [15 ]Beijing 100871
                Article
                10.1039/C9FO01018A
                31433413
                3fde999a-23dd-4346-b35a-2229a458b2ad
                © 2019

                http://rsc.li/journals-terms-of-use

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