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.

Relationship between Phase Angle and Objective and Subjective Indicators of Nutritional Status in Cancer Patients: A Systematic Review.

To investigate the relationship between phase angle (PA) and objective and subjective indicators of nutritional status in cancer patients, as well as to identify cutoff points for PA, to detect malnutrition in these patients. The study was a systematic review, carried out following the guidelines of the Preferred Reporting Items for Systematic Reviews and meta-analyses (PRISMA). Literature search was performed for two authors, in indexed databases, including the National Library of Medicine, Bethesda, MD (PubMed), Latin American and Caribbean Literature in Health Sciences (LILACS), and Scopus (Elsevier). We used the checklist from the Joanna Briggs Institute for assessing the risk of bias. The review was registered with the Systematic Review Registration (PROSPERO), number CRD42020134324. In total, nine papers were eligible. PA was correlated with several objective and subjective indicators of nutritional status in most cases. Cutoff point values for the PA, capable of detecting malnutrition, varied from 4.73° to 6°, despite the modest diagnostic accuracy. We assume that PA may be considered an indicator of nutritional status, when complementing additional data and assisting health practitioners in evaluating individuals with malignant neoplasms. However, a single cutoff point with fair and concomitant sensitivity and specificity was not identified.

Hand grip strength as predictor of undernutrition in hospitalized patients with cancer and a proposal of cut-off.

BACKGROUND & AIMS: Hand Grip Strength (HGS) has been proposed as an indicator of nutritional status, being an easy and non-invasive method and presenting high reliability among evaluators. However, there are no cut-off points. To compare HGS with objective methods of nutritional assessment and to propose a cut-off point for its use as a predictor of malnutrition in cancer patients. METHODS: This is a retrospective study with 76 patients (52.6% females, 56.8 ± 16.6 years old) admitted with a diagnosis of cancer in hospitals of Belo Horizonte (MG, Brazil). We evaluated the HGS of the dominant hand, Body Mass Index (BMI), calf circumference (CC), and arm circumference (AC), using the Receiver Operator Characteristic (ROC) curve analysis, being the Patient-Generated Subjective Global Assessment (PG-SGA) the reference method. Statistical tests were performed according to the distribution of the variables, verified by the Shapiro-Wilk test. The level of significance adopted was 5%. RESULTS: The HGS was higher in men (p = 0.001) and adults (p = 0.002). The HGS presented a better performance in the prediction of malnutrition (AUC = 0.766, 95% CI = 0.656-0.936) compared to the anthropometric indicators, with a cut-off point of 32.5 kg (sensitivity of 90.5% and specificity of 61.5%). The prevalence of malnutrition was 82.9% and 81.6% for PG-SGA and proposed cut-off point for HGS, respectively. CONCLUSIONS: The HGS was more sensitive to identify individuals at risk of malnutrition compared to other recognized indicators of nutritional status, indicating its application in a hospital setting with cancer patients.

Gluten-free diet reduces adiposity, inflammation and insulin resistance associated with the induction of PPAR-alpha and PPAR-gamma expression.

Gluten exclusion (protein complex present in many cereals) has been proposed as an option for the prevention of diseases other than coeliac disease. However, the effects of gluten-free diets on obesity and its mechanisms of action have not been studied. Thus, our objective was to assess whether gluten exclusion can prevent adipose tissue expansion and its consequences. C57BL/6 mice were fed a high-fat diet containing 4.5% gluten (Control) or no gluten (GF). Body weight and adiposity gains, leukocyte rolling and adhesion, macrophage infiltration and cytokine production in adipose tissue were assessed. Blood lipid profiles, glycaemia, insulin resistance and adipokines were measured. Expression of the PPAR-α and γ, lipoprotein lipase (LPL), hormone sensitive lipase (HSL), carnitine palmitoyl acyltransferase-1 (CPT-1), insulin receptor, GLUT-4 and adipokines were assessed in epidydimal fat. Gluten-free animals showed a reduction in body weight gain and adiposity, without changes in food intake or lipid excretion. These results were associated with up-regulation of PPAR-α, LPL, HSL and CPT-1, which are related to lipolysis and fatty acid oxidation. There was an improvement in glucose homeostasis and pro-inflammatory profile-related overexpression of PPAR-γ. Moreover, intravital microscopy showed a lower number of adhered cells in the adipose tissue microvasculature. The overexpression of PPAR-γ is related to the increase of adiponectin and GLUT-4. Our data support the beneficial effects of gluten-free diets in reducing adiposity gain, inflammation and insulin resistance. The data suggests that diet gluten exclusion should be tested as a new dietary approach to prevent the development of obesity and metabolic disorders.