The administration of Enterococcus faecium SF68 counteracts compositional shifts in the gut microbiota of diet-induced obese mice

Abstract

Microorganisms with probiotic properties are eliciting an increasing interest as coadjuvants in the prevention and treatment of obesity through modulation of the gut microbiota. In this study, a probiotic formulation based on Enterococcus faecium SF68 was administered to mice fed with a high-fat diet (HFD) to evaluate its efficacy in reducing body mass gain and in modulating the intestinal bacterial composition. Both stool and ileum samples were collected from untreated and treated mice and absolute abundances of specific taxa constituting the gut microbial consortium were evaluated. SF68 administration significantly reduced the HFD-induced weight gain. In these animals, the microbial gut composition shifted toward an enrichment in microbes positively correlated with mucus thickness, lower inflammation, lower glycemia levels, and SCFA production (i.e., Bifidobacterium, Akkermansia, and Faecalibacterium), as well as a depletion in bacterial phyla having a key role in obesity (i.e., Firmicutes, Proteobacteria). Our results demonstrate the efficacy of E. faecium SF68 in adjusting the composition of the dysbiotic microbiota of HFD-fed animals, thus ameliorating clinical conditions and exerting anti-obesity effects.

Supplementation of a high-fat diet with pentadecylresorcinol increases the representation of Akkermansia muciniphila in the mouse small and large intestines and may protect against complications caused by imbalanced nutrition

“…Administration of E. faecium to HFD-fed mice was shown to result in markedly decreased weight gain and led to an increase in the abundance of Bifidobacterium and A. muciniphila in the mouse intestine 37 . Bifidobacterium sp.…”

Investigation of the therapeutic effect of Hedan tablets on high‐fat diet‐induced obesity in rats by GC–MS technology and 16S ribosomal RNA gene sequencing

“…Ruminococcus is the most common bacterium in the gut, capable of producing SCFAs, stabilizing the intestinal barrier (Lakshmanan et al, 2022;Salas-Perez et al, 2023;Zhang et al, 2022), and playing a "cornerstone" role in degrading dietaryresistant starch. Some members of Enterococcus are used as probiotics and participate in the production of acetic acid and propionic acid (Celiberto et al, 2017;Panattoni et al, 2022). The significant increase of beneficial bacteria causes a structural change in the gut microbiota, subsequently leading to changes in the metabolic products of the gut microbiota, namely SCFAs.…”

Dietary Supplement, Containing the Dry Extract of Curcumin, Emblica and Cassia, Counteracts Intestinal Inflammation and Enteric Dysmotility Associated with Obesity

“…To pursue these aims, we employed a murine model of HFD-induced obesity, which closely mimics a human obesity condition [ 10 , 11 , 17 , 18 , 28 ]. In our study, consistent with previous reports [ 10 , 11 , 17 , 18 , 28 ], obese mice displayed a marked increase in body weight, BMI and plasmatic MPO levels, along with significant alterations of systemic metabolic indices, such as blood total cholesterol, triglycerides and glycated hemoglobin levels (regarded as an indirect index of insulin resistance [ 29 , 30 , 31 , 32 ]), thus further confirming the suitability of HFD murine model.…”

“…To pursue these aims, we employed a murine model of HFD-induced obesity, which closely mimics a human obesity condition [ 10 , 11 , 17 , 18 , 28 ]. In our study, consistent with previous reports [ 10 , 11 , 17 , 18 , 28 ], obese mice displayed a marked increase in body weight, BMI and plasmatic MPO levels, along with significant alterations of systemic metabolic indices, such as blood total cholesterol, triglycerides and glycated hemoglobin levels (regarded as an indirect index of insulin resistance [ 29 , 30 , 31 , 32 ]), thus further confirming the suitability of HFD murine model. Moreover, HFD mice showed signs of enteric inflammation and neutrophil infiltration, along with an increase in spleen weight (index of chronic systemic inflammation and immune system activation [ 33 ]) and liver weight, which represent the prodromal steps leading to the development of hepatic steatosis [ 5 , 34 , 35 ].…”

“…In particular, pre-clinical studies on high-fat diet (HFD)-fed mice showed that alterations in intestinal microbiota composition and the presence of an increased intestinal permeability represent among the main factors influencing early inflammatory events associated with obesity and metabolic dysfunction [ 6 , 7 , 8 ]. Indeed, the presence of an imbalanced gut microbiota composition has been reported to elicit fluctuations in the intestinal epithelial barrier (IEB) integrity, thus facilitating the translocation of immunogenic products (i.e., lipopolysaccharide (LPS), whole bacteria and other toxins) into the mucosa and the bloodstream, triggering the onset and maintenance of a meta-inflammation that is typically observed in obese patients [ 9 , 10 , 11 ]. Of note, the chronicization of such inflammatory conditions has an impact on the physiological functions of different organs, thus contributing to the development of several comorbidities associated with obesity [ 5 ].…”