Abstract
The aim of this study was to characterize the effects of Maresin 1 (MaR1), a DHA-derived pro-resolving lipid mediator, on obesity-related colonic inflammation and gut dysbiosis in diet-induced obese (DIO) mice. In colonic mucosa of DIO mice, the MaR1 treatment decreased the expression of inflammatory genes, such as Tnf-α and Il-1β. As expected, the DIO mice exhibited significant changes in gut microbiota composition at the phylum, genus, and species levels, with a trend to a higher Firmicutes/Bacteroidetes ratio. Deferribacteres and Synergistetes also increased in the DIO animals. In contrast, these animals exhibited a significant decrease in the content of Cyanobacteria and Actinobacteria. Treatment with MaR1 was not able to reverse the dysbiosis caused by obesity on the most abundant phyla. However, the MaR1 treatment increased the content of P. xylanivorans, which have been considered to be a promising probiotic with healthy effects on gut inflammation. Finally, a positive association was found between the Deferribacteres and Il-1β expression, suggesting that the increase in Deferribacteres observed in obesity could contribute to the overexpression of inflammatory cytokines in the colonic mucosa. In conclusion, MaR1 administration ameliorates the inflammatory state in the colonic mucosa and partially compensates changes on gut microbiota caused by obesity.
Highlights
Gut microbiota is a complex and dynamic entity which works as a metabolic organ, constituted by 109 to 1013 bacteria, including approximately 500–1000 different bacteria species, which are mainly classified into two bacteria phyla: Firmicutes and Bacteroidetes [1]
It is known that gut microbiota plays an important role in the harvesting, storage, and expenditure of energy obtained from the diet, becoming a critical factor which contributes to the development of obesity [2,3]
Preclinical studies using different mice models have shown that both obesity and high fat diet (HFD), containing a higher percentage of energy in the form of saturated lipids, led to gut microbiota dysbiosis characterized by an overgrowth of some bacteria phyla and a reduction of other phyla, which caused undesired consequences, such as intestinal inflammation or epithelial barrier disruption [6]
Summary
Gut microbiota is a complex and dynamic entity which works as a metabolic organ, constituted by 109 to 1013 bacteria, including approximately 500–1000 different bacteria species, which are mainly classified into two bacteria phyla: Firmicutes and Bacteroidetes [1]. Preclinical studies using different mice models have shown that both obesity and high fat diet (HFD), containing a higher percentage of energy in the form of saturated lipids, led to gut microbiota dysbiosis characterized by an overgrowth of some bacteria phyla and a reduction of other phyla, which caused undesired consequences, such as intestinal inflammation or epithelial barrier disruption [6]. In some HFD models, it has been suggested that gastrointestinal microbiome alterations can affect the pathogenesis of cardiometabolic diseases by enhancing its development through different pathways, including an increase of energy harvesting, a rise in metabolism harvesting, and a higher level of some proinflammatory cytokines expression [15]. These cytokines include tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) [16]
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