Abstract
Recent evidence indicates that the gut microbiota plays a key role in the pathophysiology of obesity. Indeed, diet-induced obesity (DIO) has been associated to substantial changes in gut microbiota composition in rodent models. In the context of obesity, enhanced adiposity is accompanied by low-grade inflammation of this tissue but the exact link with gut microbial community remains unknown. In this report, we studied the consequences of high-fat diet (HFD) administration on metabolic parameters and gut microbiota composition over different periods of time. We found that Akkermansia muciniphila abundance was strongly and negatively affected by age and HFD feeding and to a lower extend Bilophila wadsworthia was the only taxa following an opposite trend. Different approaches, including multifactorial analysis, showed that these changes in Akkermansia muciniphila were robustly correlated with the expression of lipid metabolism and inflammation markers in adipose tissue, as well as several circulating parameters (i.e., glucose, insulin, triglycerides, leptin) from DIO mice. Thus, our data shows the existence of a link between gut Akkermansia muciniphila abundance and adipose tissue homeostasis on the onset of obesity, thus reinforcing the beneficial role of this bacterium on metabolism.
Highlights
Recent evidence indicates that the gut microbiota plays a key role in the pathophysiology of obesity
In the current study we explored the potential interconnection between adipose tissue inflammation/ function and changes in specific microbes during obesity and type 2 diabetes (T2D) development following chronic high-fat diet (HFD) feeding in mice
These results indicate that the greatest impact on body weight gain and adiposity in mice occurs after 6 consecutive weeks of HFD administration
Summary
Recent evidence indicates that the gut microbiota plays a key role in the pathophysiology of obesity. The pathological massive expansion of adipose tissue in obesity states is associated with the development of low-grade inflammation, which is reflected by enhanced production of cytokines, chemokines and pro-inflammatory fatty acids. Despite the well-established link between DIO and gut microbiota alterations, it is currently unknown whether changes in the abundance of specific bacteria precedes or remains present during the development of obesity and related adipose tissue metabolic alterations. In the current study we explored the potential interconnection between adipose tissue inflammation/ function and changes in specific microbes during obesity and T2D development following chronic HFD feeding in mice. Our results demonstrate specific changes in gut bacteria over the progress of obesity, together with a robust negative association between Akkermansia muciniphila and inflammation and a positive association with adipose tissue browning process markers. This work demonstrates that this bacterium declines before the onset of metabolic alterations, thereby suggesting a putative causative implication in the disease progression
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