Lactobacillus gasseri LG-G12 Restores Gut Microbiota and Intestinal Health in Obesity Mice on Ceftriaxone Therapy.

Gut microbiota imbalance is associated with the occurrence of metabolic diseases such as obesity. Thus, its modulation is a promising strategy to restore gut microbiota and improve intestinal health in the obese. This paper examines the role of probiotics, antimicrobials, and diet in modulating gut microbiota and improving intestinal health. Accordingly, obesity was induced in C57BL/6J mice, after which they were redistributed and fed with an obesogenic diet (intervention A) or standard AIN-93 diet (intervention B). Concomitantly, all the groups underwent a treatment phase with Lactobacillus gasseri LG-G12, ceftriaxone, or ceftriaxone followed by L. gasseri LG-G12. At the end of the experimental period, the following analysis was conducted: metataxonomic analysis, functional profiling of gut microbiota, intestinal permeability, and caecal concentration of short-chain fatty acids. High-fat diet impaired bacterial diversity/richness, which was counteracted in association with L. gasseri LG-G12 and the AIN-93 diet. Additionally, SCFA-producing bacteria were negatively correlated with high intestinal permeability parameters, which was further confirmed via functional profile prediction of the gut microbiota. A novel perspective on anti-obesity probiotics is presented by these findings based on the improvement of intestinal health irrespective of undergoing antimicrobial therapy or not.

Antibiotic Followed by a Potential Probiotic Increases Brown Adipose Tissue, Reduces Biometric Measurements, and Changes Intestinal Microbiota Phyla in Obesity.

The development of adjuvant therapies for obesity treatment is justified by the high prevalence of this disease worldwide, and the relationship between obesity and intestinal microbiota is a promising target for obesity treatment. Therefore, this study aimed at investigating the adjuvant treatment of obesity through the use of potential probiotics and antibiotics, either separately or sequentially. In the first phase of the experiment, animals had diet-induced obesity with consumption of a high saturated fat diet and a fructose solution. After this period, there was a reduction in caloric supply, that is the conventional treatment of obesity, and the animals were divided into 5 experimental groups: control group (G1), obese group (G2), potential probiotic group (G3), antibiotic group (G4), and antibiotic followed by potential probiotic group (G5). The adjuvant treatments lasted 4 weeks and were administered daily, via gavage: Animals in G1 and G2 received distilled water, the G3 obtained Lactobacillus gasseri LG-G12, and the G4 received ceftriaxone. The G5 received ceftriaxone for 2 weeks, followed by the offer of Lactobacillus gasseri LG-G12 for another 2 weeks. Parameters related to obesity, such as biometric measurements, food consumption, biochemical tests, histological assessments, short-chain fatty acids concentration, and composition of the intestinal microbiota, were analyzed. The treatment with caloric restriction and sequential supply of antibiotics and potential probiotics was able to reduce biometric measures, increase brown adipose tissue, and alter the intestinal microbiota phyla, standing out as a promising treatment for obesity.

Diet-induced obesity in animal models: points to consider and influence on metabolic markers.

Overweight and obesity are a worldwide public health problem. Obesity prevalence has increased considerably, which indicates the need for more studies to better understand these diseases and related complications. Diet induced-obesity (DIO) animal models can reproduce human overweight and obesity, and there are many protocols used to lead to excess fat deposition. So, the purpose of this review was to identify the key points for the induction of obesity through diet, as well as identifying which are the necessary endpoints to be achieved when inducing fat gain. For this, we reviewed the literature in the last 6 years, looking for original articles that aimed to induce obesity through the diet. All articles evaluated should have a control group, in order to verify the results found, and had worked with Sprague-Dawley and Wistar rats, or with C57BL-/-6 mice strain. Articles that induced obesity by other methods, such as genetic manipulation, surgery, or drugs were excluded, since our main objective was to identify key points for the induction of obesity through diet. Articles in humans, in cell culture, in non-rodent animals, as well as review articles, articles that did not have obesity induction and book chapters were also excluded. Body weight and fat gain, as well as determinants related to inflammation, hormonal concentration, blood glycemia, lipid profile, and liver health, must be evaluated together to better determination of the development of obesity. In addition, to select the best model in each circumstance, it should be considered that each breed and sex respond differently to diet-induced obesity. The composition of the diet and calorie overconsumption are also relevant to the development of obesity. Finally, it is important that a non-obese control group is included in the experimental design.

Intestinal microbiota and colorectal cancer: changes in the intestinal microenvironment and their relation to the disease.

Tools that predict the risk of colorectal cancer are important for early diagnosis, given the high mortality rate for this cancer. The composition of the intestinal microbiota is now considered to be a risk factor for the development of colorectal cancer. This discovery has motivated a growing number of studies to identify the micro-organisms responsible for the onset and/or progression of colorectal cancer. With this in mind, this review discusses the relationship between the composition of the intestinal microbiota and colorectal cancer risk. Prospective and case-control studies indicate that the intestinal microbiota of individuals with colorectal cancer usually contains a greater proportion of bacteria responsible for gastrointestinal tract inflammatory diseases, as well as bacteria that produce toxins and carcinogenic metabolites. In contrast, there tends to be a reduced presence of butyric acid-producing bacteria, probiotic bacteria and potentially probiotic bacteria. Despite these differences, the onset and development of colorectal cancer cannot be attributed to a specific micro-organism. Thus, studies focused on the formation of the intestinal microbiota and factors that modulate its composition are important for the development of approaches for colorectal cancer prevention.