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The aim of this study was to examine the effect of free or immobilized Lacticaseibacillus rhamnosus OLXAL-1 cells on oat flakes on the gut microbiota and metabolic and inflammatory markers in a streptozotocin (STZ)-induced Type-1 Diabetes Mellitus (T1DM) animal model. Forty-eight male Wistar rats were assigned into eight groups (n = 6): healthy or diabetic animals that received either a control diet (CD and DCD), an oat-supplemented diet (OD and DOD), a diet supplemented with free L. rhamnosus OLXAL-1 cells (CFC and DFC), or a diet supplemented with immobilized L. rhamnosus OLXAL-1 cells on oat flakes (CIC and DIC). Neither L. rhamnosus OLXAL-1 nor oat supplementation led to any significant positive effects on body weight, insulin levels, plasma glucose concentrations, or lipid profile parameters. L. rhamnosus OLXAL-1 administration resulted in a rise in the relative abundances of Lactobacillus and Bifidobacterium, as well as increased levels of lactic, acetic, and butyric acids in the feces of the diabetic animals. Additionally, supplementation with oat flakes significantly reduced the microbial populations of E. coli, Enterobacteriaceae, coliforms, staphylococci, and enterococci and lowered IL-1β levels in the blood plasma of diabetic animals. These findings suggested that probiotic food-based strategies could have a potential therapeutic role in managing dysbiosis and inflammation associated with T1DM. [ABSTRACT FROM AUTHOR]

Background/Objectives: The gut microbiota is linked to the pathogenesis of type 1 diabetes mellitus (T1DM), while supplementation with probiotics may result in positive alterations in the composition of the gut microbiome. This research aimed to map the changes in the gut microbiome and blood markers of streptozotocin-induced diabetic rats after a dietary intervention with free or immobilized cells of the presumptive probiotic Pediococcus acidilactici SK on pistachio nuts. Methods: Twenty-four male Wistar rats were studied and divided into four groups (healthy or diabetic) which received the free or the immobilized P. acidilactici SK cells on pistachio nuts for 4 weeks. Blood, fecal, and intestinal tissue samples were examined. Results: The diabetic rats exhibited an elevated concentration of HDL-c, while the inflammatory IL-1β levels were significantly lower in the diabetic animals that received the immobilized cells compared to the group that received the free cells. The dietary intervention with immobilized cells led to decreased counts of fecal staphylococci and enterococci in the diabetic animals, while the diet with both free and immobilized P. acidilactici SK cells rendered levels of these populations in normal values in the feces and intestinal tissue of the diabetic animals. Noticeably, the Lactobacillus and Bifidobacterium genera were elevated after the supplementation with immobilized P. acidilactici SK cells on pistachio nuts. Conclusions: Dietary supplementation with P. acidilactici SK cells (in free or in immobilized form) beneficially affected the gut microbiota/microbiome of streptozotocin-induced diabetic rats, leading to the alleviation of dysbiosis and inflammation and control over their lipid levels. [ABSTRACT FROM AUTHOR]

Aims: Our study, employing a multi-omics approach, aimed to delineate the distinct gut microbiota and metabolic characteristics in individuals under 30 with unclassified diabetes, thus shedding light on the underlying pathophysiological mechanisms Methods: This age- and sex-matched case-control study involved 18 patients with unclassified diabetes, 18 patients with classic type 1 diabetes, 13 patients with type 2 diabetes, and 18 healthy individuals. Metagenomics facilitated the profiling of the gut microbiota, while untargeted liquid chromatography-mass spectrometry was used to quantify the serum lipids and metabolites. Results: Our findings revealed a unique gut microbiota composition in unclassified diabetes patients, marked by a depletion of Butyrivibrio proteoclasticus and Clostridium and an increase in Ruminococcus torques and Lachnospiraceae bacterium 8_1_57FAA. Comparative analysis identified the combined marker panel of five bacterial species, seven serum biomarkers, and three clinical parameters could differentiate patients with UDM from HCs with an AUC of 0.94 (95% CI 0.85–1). Notably, the gut microbiota structure of patients with unclassified diabetes resembled that of type 2 diabetes patients, especially regarding disrupted lipid and branched-chain amino acid metabolism. Conclusions: Despite sharing certain metabolic features with type 2 diabetes, unclassified diabetes presents unique features. The distinct microbiota and metabolites in unclassified diabetes patients suggest a significant role in modulating glucose, lipid, and amino acid metabolism, potentially influencing disease progression. Further longitudinal studies are essential to explore therapeutic strategies targeting the gut microbiota and metabolites to modify the disease trajectory. [ABSTRACT FROM AUTHOR]

The human gut is a complex ecosystem that supports billions of living species, including bacteria, viruses, archaea, phages, fungi, and unicellular eukaryotes. Bacteria give genes and enzymes for microbial and host-produced compounds, establishing a symbiotic link between the external environment and the host at both the gut and systemic levels. The gut microbiome, which is primarily made up of commensal bacteria, is critical for maintaining the healthy host's immune system, aiding digestion, synthesizing essential nutrients, and protecting against pathogenic bacteria, as well as influencing endocrine, neural, humoral, and immunological functions and metabolic pathways. Qualitative, quantitative, and/or topographic shifts can alter the gut microbiome, resulting in dysbiosis and microbial dysfunction, which can contribute to a variety of noncommunicable illnesses, including hypertension, cardiovascular disease, obesity, diabetes, inflammatory bowel disease, cancer, and irritable bowel syndrome. While most evidence to date is observational and does not establish direct causation, ongoing clinical trials and advanced genomic techniques are steadily enhancing our understanding of these intricate interactions. This review will explore key aspects of the relationship between gut microbiota, eubiosis, and dysbiosis in human health and disease, highlighting emerging strategies for microbiome engineering as potential therapeutic approaches for various conditions. [ABSTRACT FROM AUTHOR]

Background: Obesity is a growing health concern in China, closely linked to metabolic disorders such as type 2 diabetes. Laparoscopic Sleeve Gastrectomy (LSG) is effective in promoting weight loss and improving metabolic outcomes. Emerging evidence highlights the role of gut microbiota in metabolic regulation, yet the specific alterations in gut microbiota and their association with metabolic changes post-surgery in Chinese patients remain unclear. Understanding these shifts could provide key insights into optimizing treatment strategies for metabolic improvement following bariatric surgery. Methods: Stool samples and clinical data were collected from 30 obese patients before and 6 months after surgery. The composition of the gut microbiota was analyzed through 16S rRNA sequencing, and Spearman correlation analysis was used to determine the association between gut microbiota and clinical indicators. Results: The analysis of 30 patients showed a significant decrease in Body Mass Index (BMI) (36.75 ± 4.09 kg/m2 vs 26.37 ± 3.47 kg/m2, p < 0.0001). Glucose metabolism, including Hemoglobin A1C levels, improved significantly (6.05 ± 0.96 vs 5.05 ± 0.25, p < 0.0001), and liver function as well as serum lipid levels were also notably improved. LSG increased the richness and composition of gut microbiota in obese patients post-surgery. These changes in gut microbiota were closely associated with improved clinical metabolic parameters. Conclusion: LSG not only significantly reduces body weight while also alleviating metabolic syndrome and comorbidities by altering gut microbiota. [ABSTRACT FROM AUTHOR]

Type 1 Diabetes Mellitus (T1DM) is a chronic autoimmune disease that results in the destruction of pancreatic β cells, leading to hyperglycaemia and the need for lifelong insulin therapy. Although genetic predisposition and environmental factors are considered key contributors to T1DM, the exact causes of the disease remain partially unclear. Recent evidence has focused on the relationship between the gut, the oral cavity, immune regulation, and systemic inflammation. In individuals with T1DM, changes in the gut and oral microbial composition are commonly observed, indicating that dysbiosis may contribute to immune dysregulation. Gut dysbiosis can influence the immune system through increased intestinal permeability, altered production of short chain fatty acids (SCFAs), and interactions with the mucosal immune system, potentially triggering the autoimmune response. Similarly, oral dysbiosis may contribute to the development of systemic inflammation and thus influence the progression of T1DM. A comprehensive understanding of these relationships is essential for the identification of biomarkers for early diagnosis and monitoring, as well as for the development of therapies aimed at restoring microbial balance. This review presents a synthesis of current research on the connection between T1DM and microbiome dysbiosis, with a focus on the gut and oral microbiomes in pediatric populations. It explores potential mechanisms by which microbial dysbiosis contributes to the pathogenesis of T1DM and examines the potential of microbiome-based therapies, including probiotics, prebiotics, synbiotics, and faecal microbiota transplantation (FMT). This complex relationship highlights the need for longitudinal studies to monitor microbiome changes over time, investigate causal relationships between specific microbial species and T1DM, and develop personalised medicine approaches. [ABSTRACT FROM AUTHOR]

Background: The gut microbiome plays a crucial role in human health, and recent research has highlighted its potential impact on ocular health through the gut–eye axis. Dysbiosis, or an imbalance in the gut microbiota, has been implicated in various ocular diseases. Methods: A comprehensive literature search was conducted using relevant keywords in major electronic databases, prioritizing recent peer-reviewed articles published in English. Results: The gut microbiota influences ocular health through immune modulation, maintenance of the blood–retinal barrier, and production of beneficial metabolites. Dysbiosis can disrupt these mechanisms, contributing to ocular inflammation, tissue damage, and disease progression in conditions such as uveitis, age-related macular degeneration, diabetic retinopathy, dry eye disease, and glaucoma. Therapeutic modulation of the gut microbiome through probiotics, prebiotics, synbiotics, and fecal microbiota transplantation shows promise in preclinical and preliminary human studies. Conclusions: The gut–eye axis represents a dynamic and complex interplay between the gut microbiome and ocular health. Targeting the gut microbiome through innovative therapeutic strategies holds potential for improving the prevention and management of various ocular diseases. [ABSTRACT FROM AUTHOR]

The progression of chronic obstructive pulmonary disease (COPD) is characterized by functional changes in the airways. The lung–gut axis and gut microbiota (GM) have been linked to the pathophysiology of airway diseases. Regarding COPD, studies have shown that GM alterations could be related the stages of this disease. However, the relationship between GM and clinical, biochemical and immunological parameters in patients with COPD are not well understood. The aim of this study was to compare the relative abundance of specific groups of beneficial gut bacteria between COPD patients and healthy controls (CTLs) in order to evaluate relationships with metabolic and inflammatory markers in COPD. Methods: We included 16 stable COPD patients and 16 healthy volunteer CTLs. The relative abundances of Bifidobacterium spp. (Bf) and Akkermansia muciniphila (Akk) bacteria and the Bacteroidetes and Firmicutes phyla were assessed by qPCR. Pulmonary function was evaluated by spirometry, biochemical parameters by colorimetric methods and plasma cytokine levels by cytometric bead array analysis. Results: The Firmicutes/Bacteroides ratio was related to emergency hospital visits and six-minute walk test (6MWT) results. Furthermore, the relative abundance of Bf was associated with plasma concentrations of glucose, triglycerides, HDL-C and IL-10. In addition, Firmicutes levels and the Firmicutes/Bacteroidetes ratio were associated with the IL-12/IL-10 ratio, while Akk abundance was linked to IL-12 levels. Conclusions: The present findings suggest that the abundance of beneficial bacteria in the GM could influence clinical presentation and immunoregulation in COPD. [ABSTRACT FROM AUTHOR]

Monosodium glutamate (MSG) is used as a common food additive in some foods. However, based on our search and knowledge, no comprehensive study discussed the effect of MSG on the human gut microbiome. In this study, the effects of MSG on the gut microbiome, liver, and kidney were performed. Data were collected from databases including PubMed, Scopus, Web of Science, and ScienceDirect using the search strategy and keywords. Finally, 14 eligible studies were selected for systematic review. This study provides a new perspective on the effects of MSG on the gut flora, shedding light on the potential relationship between MSG intake and human health. [ABSTRACT FROM AUTHOR]

The burden of health issues surrounding the children and adolescents (ChAds) population is of great concern. From metabolic disorders such as obesity, non-alcoholic fatty liver disease, diabetes, multiple sclerosis including mental and several other psychological disorders like attention deficit hyperactivity, internet addiction, autism spectrum, subthreshold mood symptoms and depression, and stress disorders, is a nexus of the gut microbiota (GM) profile and physical activity (PA), as they both play a crucial role in ameliorating these disorders. The aim of this review is to explore the disorders with regard to their association with ChAds' GM and its health. We started with brief descriptions of PA and its connections with GM profile cum health in ChAds. In addition, the disorders in ChAds were broadly classified into metabolic and psychological. Observations from the discussed sections show that exercise and physical activity are efficient methods for enhancing physical, metabolic, and mental health, which are often GM-mediated, and thus might require certain levels of personalization. Furthermore, age, gender, genetics, baseline BMI, baseline exercise level, and diet are key parameters to be explored when proffering intervention of combative mechanisms against these disorders. [ABSTRACT FROM AUTHOR]

The role of Bifidobacterium species and microbial metabolites such as short-chain fatty acids (SCFAs) and human milk oligosaccharides in controlling intestinal inflammation and the pathogenesis of obesity and type 1 diabetes (T1D) has been largely studied in recent years. This paper discusses the discovery of signature biomarkers for obesity and T1D based on data from a novel test for profiling several Bifidobacterium species, combined with metabolomic analysis. Through the NUTRISHIELD clinical study, a total of 98 children were recruited: 40 healthy controls, 40 type 1 diabetics, and 18 obese children. Bifidobacterium profiles were assessed in stool samples through an innovative test allowing high taxonomic resolution and precise quantification, while SCFAs and branched amino acids were measured in urine samples through gas chromatography–mass spectrometry (GC-MS). KIDMED questionnaires were used to evaluate the children's dietary habits and correlate them with the Bifidobacterium and metabolomic profiles. We found that B. longum subs. infantis and B. breve were higher in individuals with obesity, while B. bifidum and B. longum subs. longum were lower compared to healthy individuals. In individuals with T1D, alterations were found at the metabolic level, with an overall increase in the level of the most measured metabolites. The high taxonomic resolution of the Bifidobacterium test used meant strong correlations between the concentrations of valine and isoleucine, and the relative abundance of some Bifidobacterium species such as B. longum subs. infantis, B. breve, and B. bifidum could be observed. [ABSTRACT FROM AUTHOR]

Metabolic syndrome (MetS) is a combination of metabolic disorders that concurrently act as factors promoting systemic pathologies such as atherosclerosis or diabetes mellitus. It is now believed to encompass six main interacting conditions: visceral fat, imbalance of lipids (dyslipidemia), hypertension, insulin resistance (with or without impairing both glucose tolerance and fasting blood sugar), and inflammation. In the last 10 years, there has been a progressive interest through scientific research investigations conducted in the field of metabolomics, confirming a trend to evaluate the role of the metabolome, particularly the intestinal one. The intestinal microbiota (IM) is crucial due to the diversity of microorganisms and their abundance. Consequently, IM dysbiosis and its derivate toxic metabolites have been correlated with MetS. By intervening in these two factors (dysbiosis and consequently the metabolome), we can potentially prevent or slow down the clinical effects of the MetS process. This, in turn, may mitigate dysregulations of intestinal microbiota axes, such as the lung axis, thereby potentially alleviating the negative impact on respiratory pathology, such as the chronic obstructive pulmonary disease. However, the biomolecular mechanisms through which the IM influences the host's metabolism via a dysbiosis metabolome in both normal and pathological conditions are still unclear. In this study, we seek to provide a description of the knowledge to date of the IM and its metabolome and the factors that influence it. Furthermore, we analyze the interactions between the functions of the IM and the pathophysiology of major metabolic diseases via local and systemic metabolome's relate endotoxemia. [ABSTRACT FROM AUTHOR]

(1) Background: Human fascioliasis is considered an endemic and hyper-endemic disease in the Peruvian Andean valleys. Our objective was to determine variations in the composition of the gut microbiota among children with Fasciola hepatica and children who do not have this parasitosis. (2) Method: A secondary analysis was performed using fecal samples stored in our biobank. The samples were collected as part of an epidemiological Fasciola hepatica cross-sectional study in children from 4 through 14 years old from a community in Cajamarca, Peru. (3) Results: In a comparison of the bacterial genera that make up the intestinal microbiota between the F. hepatica positive and negative groups, it was found that there are significant differences in the determination of Lactobacillus (p = 0.010, CI: 8.5–61.4), Bacteroides (p = 0.020, CI: 18.5–61.4), Clostridium (p < 0.001, CI: 3.5–36.0), and Bifidobacterium (p = 0.018, CI: 1.1–28.3), with each of these genera being less frequent in children parasitized with F. hepatica. (4) Conclusions: These results show that F. hepatica may be associated with direct or indirect changes in the bacterial population of the intestinal microbiota, particularly affecting three bacterial genera. [ABSTRACT FROM AUTHOR]

Cystic fibrosis-related diabetes (CFRD) affects 40%–50% of adults with CF and is associated with a decline in respiratory health. The microbial flora of the lung is known to change with the development of CF disease, but how CFRD affects the microbiome has not been described. We analyzed the microbiome in sputa from 14 people with CF, 14 with CFRD, and two who were classed as pre-CFRD by extracting DNA and amplifying the variable V3-V4 region of the microbial 16S ribosomal RNA gene by PCR. Sequences were analyzed and sources were identified to genus level. We found that the α-diversity of the microbiome using Shannon’s diversity index was increased in CFRD compared with CF. Bray Curtis dissimilarity analysis showed that there was separation of the microbiomes in CF and CFRD sputa. The most abundant phyla identified in the sputum samples were Firmicutes and Proteobacteria, Actinobacteriota and Bacteroidota, and the ratio of Firmicutes/Bacteroidota was reduced in CFRD compared with CF. Pseudomonas, Azhorizophilus, Porphyromonas, and Actinobacillus were more abundant in CFRD compared with CF, whereas Staphylococcus was less abundant. The relative abundance of these genera did not correlate with age; some correlated with a decline in FEV1/FVC but all correlated with hemoglobin A1C (HbA1c) indicating that development of CFRD mediates further changes to the respiratory microbiome in CF. NEW & NOTEWORTHY Cystic fibrosis-related diabetes (CFRD) is associated with a decline in respiratory health. We show for the first time that there was a change in the sputum microbiome of people with CFRD compared with CF that correlated with markers of raised blood glucose. [ABSTRACT FROM AUTHOR]

To support personalized diets targeting the gut microbiota, we employed an in vitro digestion-fermentation model and 16S rRNA gene sequencing to analyze the microbiota growing on representative foods of the Mediterranean and Western diets, as well as the influence of cooking methods. Plant- and animal-derived foods had significantly different impacts on the abundances of bacterial taxa. Animal and vegetable fats, fish and dairy products led to increases in many taxa, mainly within the Lachnospiraceae. In particular, fats favored increases in the beneficial bacteria Faecalibacterium, Blautia, and Roseburia. However, butter, as well as gouda cheese and fish, also resulted in the increase of Lachnoclostridium, associated to several diseases. Frying and boiling produced the most distinct effects on the microbiota, with members of the Lachnospiraceae and Ruminococcaceae responding the most to the cooking method employed. Nevertheless, cooking effects were highly individualized and food-dependent, challenging the investigation of their role in personalized diets. [ABSTRACT FROM AUTHOR]

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Background: Some observational studies have shown that immune thrombocytopenia (ITP) is highly associated with the alteration-composition of gut microbiota. However, the causality of gut microbiota on ITP has not yet been determined. Methods: Based on accessible summary statistics of the genome-wide union, the latent connection between ITP and gut microbiota was estimated using bidirectional Mendelian randomization (MR) and multivariable MR (MVMR) analyses. Inverse variance weighted (IVW), weighted median analyses, and MR-Egger regression methods were performed to examine the causal correlation between ITP and the gut microbiota. Several sensitivity analyses verified the MR results. The strength of causal relationships was evaluated using the MR-Steiger test. MVMR analysis was undertaken to test the independent causal effect. MR analyses of reverse direction were made to exclude the potential of reverse correlations. Finally, GO enrichment analyses were carried out to explore the biological functions. Results: After FDR adjustment, two microbial taxa were identified to be causally associated with ITP (PFDR < 0.10), namely Alcaligenaceae (PFDR = 7.31 × 10−2 ) and Methanobacteriaceae (PFDR = 7.31 × 10−2 ). In addition, eight microbial taxa were considered as potentially causal features under the nominal significance (P < 0.05): Actinobacteria, Lachnospiraceae, Methanobacteria, Bacillales, Methanobacteriales, Coprococcus2, Gordonibacter, and Veillonella. According to the reverse-direction MR study findings, the gut microbiota was not significantly affected by ITP. There was no discernible horizontal pleiotropy or instrument heterogeneity. Finally, GO enrichment analyses showed how the identified microbial taxa participate in ITP through their underlying biological mechanisms. Conclusion: Several microbial taxa were discovered to be causally linked to ITP in this MR investigation. The findings improve our understanding of the gut microbiome in the risk of ITP. [ABSTRACT FROM AUTHOR]

Purpose of review: This review comprehensively discusses the role of the gut microbiome and its metabolites in health and disease and sheds light on the importance of a holistic approach in assessing the gut. Recent findings: The gut microbiome consisting of the bacteriome, mycobiome, archaeome, and virome has a profound effect on human health. Gut dysbiosis which is characterized by perturbations in the microbial population not only results in gastrointestinal (GI) symptoms or conditions but can also give rise to extra-GI manifestations. Gut microorganisms also produce metabolites (shortchain fatty acids, trimethylamine, hydrogen sulfide, methane, and so on) that are important for several interkingdom microbial interactions and functions. They also participate in various host metabolic processes. An alteration in the microbial species can affect their respective metabolite concentrations which can have serious health implications. Effective assessment of the gut microbiome and its metabolites is crucial as it can provide insights into one's overall health. Summary: Emerging evidence highlights the role of the gut microbiome and its metabolites in health and disease. As it is implicated in GI as well as extra-GI symptoms, the gut microbiome plays a crucial role in the overall well-being of the host. Effective assessment of the gut microbiome may provide insights into one's health status leading to more holistic care. [ABSTRACT FROM AUTHOR]

Human leukocyte antigen (HLA) genes are associated with more diseases than any other region of the genome. Highly polymorphic HLA genes produce variable haplotypes that are specifically correlated with pathogenically different autoimmunities. Despite differing etiologies, however, many autoimmune disorders share the same risk-associated HLA haplotypes often resulting in comorbidity. This shared risk remains an unanswered question in the field. Yet, several groups have revealed links between gut microbial community composition and autoimmune diseases. Autoimmunity is frequently associated with dysbiosis, resulting in loss of barrier function and permeability of tight junctions, which increases HLA class II expression levels and thus further influences the composition of the gut microbiome. However, autoimmunerisk-associated HLA haplotypes are connected to gut dysbiosis long before autoimmunity even begins. This review evaluates current research on the HLAmicrobiome-autoimmunity triplex and proposes that pre-autoimmune bacterial dysbiosis in the gut is an important determinant between autoimmune comorbidities with systemic inflammation as a common denominator. [ABSTRACT FROM AUTHOR]

Human leukocyte antigen (HLA) genes are associated with more diseases than any other region of the genome. Highly polymorphic HLA genes produce variable haplotypes that are specifically correlated with pathogenically different autoimmunities. Despite differing etiologies, however, many autoimmune disorders share the same risk-associated HLA haplotypes often resulting in comorbidity. This shared risk remains an unanswered question in the field. Yet, several groups have revealed links between gut microbial community composition and autoimmune diseases. Autoimmunity is frequently associated with dysbiosis, resulting in loss of barrier function and permeability of tight junctions, which increases HLA class II expression levels and thus further influences the composition of the gut microbiome. However, autoimmunerisk-associated HLA haplotypes are connected to gut dysbiosis long before autoimmunity even begins. This review evaluates current research on the HLAmicrobiome-autoimmunity triplex and proposes that pre-autoimmune bacterial dysbiosis in the gut is an important determinant between autoimmune comorbidities with systemic inflammation as a common denominator. [ABSTRACT FROM AUTHOR]

Introduction: The human gut microbiota plays a crucial role in mental health through the gut-brain axis, impacting central nervous system functions, behavior, mood, and anxiety. Consequently, it is implicated in the development of neuropsychiatric disorders. This study aimed to assess and compare the gut microbiota profiles and populations of individuals with bipolar disorder and healthy individuals in Iran. Methods: Fecal samples were collected from 60 participants, including 30 bipolar patients (BPs) and 30 healthy controls (HCs), following rigorous entry criteria. Real-time quantitative PCR was utilized to evaluate the abundance of 10 bacterial genera/species and five bacterial phyla. Results: Notably, Actinobacteria and Lactobacillus exhibited the greatest fold change in BPs compared to HCs at the phylum and genus level, respectively, among the bacteria with significant population differences. Ruminococcus emerged as themost abundant genus in both groups,while Proteobacteria and Bacteroidetes showed the highest abundance in BPs and HCs, respectively, at the phylum level. Importantly, our investigation revealed a lower Firmicutes/Bacteroidetes ratio, potentially serving as a health indicator, in HCs compared to BPs. Conclusion: This study marks the first examination of an Iranian population and provides compelling evidence of significant differences in gut microbiota composition between BPs and HCs, suggesting a potential link between brain functions and the gut microbial profile and population. [ABSTRACT FROM AUTHOR]

Introduction: Yu--Ye Tang (YYT) is a classical formula widely used in treatment of type 2 diabetes mellitus (T2DM). However, the specific mechanism of YYT in treating T2DM is not clear. Methods: The aim of this study was to investigate the therapeutic effect of YYT on T2DM by establishing a rat model of T2DM. The mechanism of action of YYT was also explored through investigating gut microbiota and serum metabolites. Results: The results indicated YYT had significant therapeutic effects on T2DM. Moreover, YYT could increase the abundance of Lactobacillus, Candidatus_ Saccharimonas, UCG-005, Bacteroides and Blautia while decrease the abundance of and Allobaculum and Desulfovibrio in gut microbiota of T2DM rats. Nontargeted metabolomics analysis showed YYT treatment could regulate arachidonic acid metabolism, alanine, aspartate and glutamate metabolism, arginine and proline metabolism, glycerophospholipid metabolism, pentose and glucuronate interconversions, phenylalanine metabolism, steroid hormone biosynthesis, terpenoid backbone biosynthesis, tryptophan metabolism, and tyrosine metabolism in T2DM rats. Discussion: In conclusion, our research showed that YYT has a wide range of therapeutic effects on T2DM rats, including antioxidative and anti-inflammatory effects. Furthermore, YYT corrected the altered gut microbiota and serum metabolites in T2DM rats. This study suggests that YYT may have a therapeutic impact on T2DM by regulating gut microbiota and modulating tryptophan and glycerophospholipid metabolism, which are potential key pathways in treating T2DM. [ABSTRACT FROM AUTHOR]

Introduction: Data show that disturbances in the gut microbiota play a role in glucose homeostasis, type 1 diabetes (T1D) risk and progression. The prebiotic high amylose maize starch (HAMS) alters the gut microbiome profile and metabolites favorably with an increase in bacteria producing short chain fatty acids (SCFAs) that have significant anti-inflammatory effects. HAMS also improves glycemia, insulin sensitivity, and secretion in healthy non-diabetic adults. Additionally, a recent study testing an acetylated and butyrylated form of HAMS (HAMS-AB) that further increases SCFA production prevented T1D in a rodent model without adverse safety effects. The overall objective of this human study will be to assess how daily HAMS-AB consumption impacts the gut microbiome profile, SCFA production, β cell heath, function, and glycemia as well as immune responses in newly diagnosed T1D youth. Methods and analysis: We hypothesize that HAMS-AB intake will improve the gut microbiome profile, increase SCFA production, improve β cell health, function and glycemia as well as modulate the immune system. We describe here a pilot, randomized crossover trial of HAMS-AB in 12 newly diagnosed T1D youth, ages 11–17 years old, with residual β cell function. In Aim 1, we will determine the effect of HAMS-AB on the gut microbiome profile and SCFA production; in Aim 2, we will determine the effect of HAMS-AB on β cell health, function and glycemia; and in Aim 3, we will determine the peripheral blood effect of HAMS-AB on frequency, phenotype and function of specific T cell markers. Results will be used to determine the effect-size estimate of using HAMS-AB. We anticipate beneficial effects from a simple, inexpensive, and safe dietary approach. Ethics and dissemination: The Institutional Review Board at Indiana University approved the study protocol. The findings of this trial will be submitted to a peer-reviewed pediatric journal. Abstracts will be submitted to relevant national and international conferences. Trial registration: NCT04114357; Pre-results. [ABSTRACT FROM AUTHOR]

Heart failure is a risk factor for adverse events such as sudden cardiac arrest, liver and kidney failure and death. The gut microbiota and its metabolites are directly linked to the pathogenesis of heart failure. As emerging studies have increased in the literature on the role of specific gut microbiota metabolites in heart failure development, this review highlights and summarizes the current evidence and underlying mechanisms associated with the pathogenesis of heart failure. We found that gut microbiota-derived metabolites such as short chain fatty acids, bile acids, branched-chain amino acids, tryptophan and indole derivatives as well as trimethylamine-derived metabolite, trimethylamine N-oxide, play critical roles in promoting heart failure through various mechanisms. Mainly, they modulate complex signaling pathways such as nuclear factor kappa-light-chain-enhancer of activated B cells, Bcl-2 interacting protein 3, NLR Family Pyrin Domain Containing inflammasome, and Protein kinase RNA-like endoplasmic reticulum kinase. We have also highlighted the beneficial role of other gut metabolites in heart failure and other cardiovascular and metabolic diseases. [ABSTRACT FROM AUTHOR]

Thyroid disorders are clinically characterized by alterations of L-3,5,3’,5’- tetraiodothyronine (T4), L-3,5,3’-triiodothyronine (T3), and/or thyroidstimulating hormone (TSH) levels in the blood. The most frequent thyroid disorders are hypothyroidism, hyperthyroidism, and hypothyroxinemia. These conditions affect cell differentiation, function, and metabolism. It has been reported that 40% of the world’s population suffers from some type of thyroid disorder and that several factors increase susceptibility to these diseases. Among them are iodine intake, environmental contamination, smoking, certain drugs, and genetic factors. Recently, the intestinal microbiota, composed of more than trillions of microbes, has emerged as a critical player in human health, and dysbiosis has been linked to thyroid diseases. The intestinal microbiota can affect host physiology by producing metabolites derived from dietary fiber, such as short-chain fatty acids (SCFAs). SCFAs have local actions in the intestine and can affect the central nervous system and immune system. Modulation of SCFAsproducing bacteria has also been connected to metabolic diseases, such as obesity and diabetes. In this review, we discuss how alterations in the production of SCFAs due to dysbiosis in patients could be related to thyroid disorders. The studies reviewed here may be of significant interest to endocrinology researchers and medical practitioners. [ABSTRACT FROM AUTHOR]

Objective: The real causal relationship between human gut microbiota and T1D remains unclear and difficult to establish. Herein, we adopted a two-sample bidirectional mendelian randomization (MR) study to evaluate the causality between gut microbiota and T1D. Methods: We leveraged publicly available genome-wide association study (GWAS) summary data to perform MR analysis. The gut microbiota-related GWAS data from 18,340 individuals from the international consortium MiBioGen were used. The summary statistic data for T1D (n = 264,137) were obtained from the latest release from the FinnGen consortium as the outcome of interest. The selection of instrumental variables conformed strictly to a series of preset inclusion and exclusion criteria. MR-Egger, weighted median, inverse variance weighted (IVW), and weighted mode methods were used to assess the causal association. The Cochran's Q test, MR-Egger intercept test, and leaveone-out analysis were conducted to identify heterogeneity and pleiotropy. Results: At the phylumlevel, only Bacteroidetes was indicated to have causality on T1D (OR = 1.24, 95% CI = 1.01-1.53, P = 0.044) in the IVW analysis. When it comes to their subcategories, Bacteroidia class (OR = 1.28, 95% CI = 1.06-1.53, P = 0.009, PFDR = 0.085), Bacteroidales order (OR = 1.28, 95% CI = 1.06-1.53, P = 0.009, PFDR = 0.085), and Eubacterium eligens group genus (OR = 0.64, 95% CI = 0.50-0.81, P= 2.84×10-4, PFDR = 0.031) were observed to have a causal relationship with T1D in the IVW analysis. No heterogeneity and pleiotropy were detected. Conclusions: The present study reports that Bacteroidetes phylum, Bacteroidia class, and Bacteroidales order causally increase T1D risk, whereas Eubacterium eligens group genus, which belongs to the Firmicutes phylum, causally decreases T1D risk. Nevertheless, future studies are warranted to dissect the underlying mechanisms of specific bacterial taxa's role in the pathophysiology of T1D. [ABSTRACT FROM AUTHOR]

Early life gut microbiota-influencing factors may play an important role in programming individuals long-term health and substantial efforts have been devoted into studying the development of the gut microbiota in relation to early life events. This study aimed to examine in a single study, the persistence of associations between 20 factors occurring in the early life and the gut microbiota at 3.5 years of 798 children from two French nationwide birth cohorts, EPIPAGE 2 (very preterm children) and ELFE (late preterm and full-term children). Gut microbiota profiling was assessed using 16S rRNA gene sequencing-based method. Upon thorough adjustment of confounding factors, we demonstrated that gestational age was one of the factors most associated with gut microbiota differences with a noticeable imprint of prematurity at 3.5 years of age. Children born by cesarean section harbored lower richness and diversity and a different overall gut microbiota composition independently of preterm status. Children who had ever received human milk were associated with a Prevotella-driven enterotype (P_type) compared to those who had never received human milk. Living with a sibling was associated with higher diversity. Children with siblings and those attending daycare centers were associated with a P_type enterotype. Maternal factors including the country of birth and preconception maternal body mass index were associated with some microbiota characteristics: children born to overweight or obese mothers showed increased gut microbiota richness. This study reveals that multiple exposures operating from early life imprint the gut microbiota at 3.5 years that is a pivotal age when the gut microbiota acquires many of its adult characteristics. [ABSTRACT FROM AUTHOR]

Background: During the course of history, various important lifestyle changes have caused profound transitions of the gut microbiome. These include the introduction of agriculture and animal husbandry, a shift from a nomadic to a more sedentary lifestyle, and recently increased levels of urbanization and a transition towards a more Western lifestyle. The latter is linked with shifts in the gut microbiome that have a reduced fermentative capability and which are commonly associated with diseases of affluence. In this study, in which 5193 subjects are included, we investigated the direction of microbiome shifts that occur in various ethnicities living in Amsterdam by comparing 1st and 2nd generation participants. We furthermore validated part of these findings with a cohort of subjects that moved from rural Thailand to the USA. Results: The abundance of the Prevotella cluster, which includes P. copri and the P. stercorea trophic network, diminished in the 2nd generation Moroccans and Turks but also in younger Dutch, whilst the Western-associated Bacteroides/Blautia/Bifidobacterium (BBB) cluster, which has an inverse correlation with α-diversity, increased. At the same time, the Christensenellaceae/Methanobrevibacter/Oscillibacter trophic network, which is positively associated with α-diversity and a healthy BMI, decreased in younger Turks and Dutch. Large compositional shifts were not observed in South-Asian and African Surinamese, in whom the BBB cluster is already dominant in the 1st generation, but ASV-level shifts towards certain species, associated amongst others with obesity, were observed. Conclusion: The Moroccan and Turkish populations, but also the Dutch population are transitioning towards a less complex and fermentative less capable configuration of the gut microbiota, which includes a higher abundance of the Western-associated BBB cluster. The Surinamese, whom have the highest prevalence of diabetes and other diseases of affluence, are already dominated by the BBB cluster. Given the continuous increase in diseases of affluence, this devolution towards low-diversity and fermentatively less capable gut microbiome compositions in urban environments is a worrying development. 9koSLJh1fDbsjUtu7rD1NM Video Abstract [ABSTRACT FROM AUTHOR]

Metabolic diseases, such as obesity, metabolic syndrome (MetS) and type 2 diabetes (T2D), are now a widespread pandemic in the developed world. These pathologies show sex differences in their development and prevalence, and sex steroids, mainly estrogen and testosterone, are thought to play a prominent role in this sexual dimorphism. The influence of sex hormones on these pathologies is not only reflected in differences between men and women, but also between women themselves, depending on the hormonal changes associated with the menopause. The observed sex differences in gut microbiota composition have led to multiple studies highlighting the interaction between steroid hormones and the gut microbiota and its influence on metabolic diseases, ultimately pointing to a new therapy for these diseases based on the manipulation of the gut microbiota. This review aims to shed light on the role of sexual hormones in sex differences in the development and prevalence of metabolic diseases, focusing on obesity, MetS and T2D. We focus also the interaction between sex hormones and the gut microbiota, and in particular the role of microbiota in aspects such as gut barrier integrity, inflammatory status, and the gut–brain axis, given the relevance of these factors in the development of metabolic diseases. Highlights: Accumulating evidences show that the alterations in the gut microbiota associated to metabolic diseases are different in men and women, and these differences may influence sex differences in the development and prevalence of metabolic diseases. The key aspects involved in these pathologies include lipopolysaccharide-inflammation, gut barrier integrity, gut microbiota-derived metabolites and gut–brain axis. Sex steroids, mainly estrogen and testosterone, are thought to play a prominent role in the sexual dimorphism of gut microbiota. The influence of sex hormones is reflected both in men and women, and among women themselves due to hormonal changes associated with the menopause. The interaction between sex steroids and the gut microbiota plays a prominent role in the development of metabolic diseases. [ABSTRACT FROM AUTHOR]

Type 1 diabetes (T1D) is a chronic autoimmune metabolic disorder with onset in pediatric/adolescent age, characterized by insufficient insulin production, due to a progressive destruction of pancreatic β-cells. Evidence on the correlation between the human gut microbiota (GM) composition and T1D insurgence has been recently reported. In particular, 16S rRNA-based metagenomics has been intensively employed in the last decade in a number of investigations focused on GM representation in relation to a pre-disease state or to a response to clinical treatments. On the other hand, few works have been published using alternative functional omics, which is more suitable to provide a different interpretation of such a relationship. In this work, we pursued a comprehensive metaproteomic investigation on T1D children compared with a group of siblings (SIBL) and a reference control group (CTRL) composed of aged matched healthy subjects, with the aim of finding features in the T1D patients' GM to be related with the onset of the disease. Modulated metaproteins were found either by comparing T1D with CTRL and SIBL or by stratifying T1D by insulin need (IN), as a proxy of β-cells damage, showing some functional and taxonomic traits of the GM, possibly related to the disease onset at different stages of severity. [ABSTRACT FROM AUTHOR]

Background: Diabetic retinopathy (DR) is a common microvascular complication of diabetes. Luo Tong formula (LTF), a classical traditional Chinese medicine (TCM) prescription, consists of four plants that have been widely and effectively used to treat DR. Previous work in our laboratory has confirmed that LTF can effectively ameliorate DR. However, the potential mechanism underlying the therapeutic effect of LTF on DR has not been fully elucidated. To explore the potential mechanism of action through which LTF prevents and alleviates DR from an inflammation and gut microbiota perspective. Materials and methods: Metabolite profiling of LTF was performed using liquid chromatography–mass spectrometry (LC–MS) and gas chromatography–mass spectrometry (GC–MS). Type 1 diabetes was induced in male Sprague Dawley (SD) rats via tail vein injection of 45 mg/kg streptozotocin. Next, 100 SD rats were randomly divided into four groups, normal control; diabetic control; diabetic + insulin + calcium dobesilate; and diabetic + insulin + LTF. After 12 weeks of treatment, glucose metabolism, fundus oculi, blood-retinal barrier permeability, retinal thickness, microvascular damage, as well as cell junction expression in retinas were measured and the changes observed in different groups were compared. Finally, the alteration in gut microbiota and inflammatory cytokine expression in serum and tissues were monitored, and their correlation was analyzed. Results: A total of 1024 valid peaks were obtained for LTF using GC–MS. The HbA1c and fasting blood glucose (FBG) levels in the LTF group were slightly decreased. LTF exerted protective effects on fundus oculi and the retina structure to different degrees. LTF attenuated systemic and local retinal inflammation by significantly decreasing the levels of seven pro-inflammatory cytokines, including ICAM-1, IL-6, IL-8, MCP-1, VCAM-1, VEGF, and IL-1β. LTF restored the intestinal microbiota of diabetic rats to levels that were similar to those of normal rats. Further analysis revealed that Enterobacteriales, Prevotellaceae, Enterobacteriaceae, Bacteroides, and Klebsiella were significantly and positively correlated with the inflammatory factors in DR after LTF treatment. Conclusions: Our results revealed the mechanisms underlying the preventive effects of LTF on DR development and progression. LTF inhibited pathological changes in retinal histopathology, cell composition, and cell junction proteins while effectively ameliorating systemic and local retinal inflammation via regulating pivotal gut microbiota. [ABSTRACT FROM AUTHOR]

Ursolic acid (UA), a natural pentacyclic triterpenoid obtained from fruit and several traditional Chinese medicinal plants, exhibits anti-inflammatory and hypoglycemic properties. However, its protective effects against type 1 diabetes mellitus (T1DM) have not been explored. In this study, streptozotocin-induced T1DM rat models were established and treated with UA for six weeks. T1DM rats treated with UA were used to observe the effects of UA on body weight and fasting blood glucose (FBG) levels. Pathological changes in the pancreas were observed using immunohistochemical staining. The gut microbiota distribution was measured using 16S rDNA high-throughput sequencing. The proportions of Th17 and Treg cells were examined using flow cytometry. Protein and mRNA expression of molecules involved in Th17/Treg cell differentiation were assessed by quantitative real-time PCR and western blotting. The correlation between gut microbiota and Th17/Treg cell differentiation in T1DM was analyzed using redundancy analysis (RDA) analysis. Compared with the model group, FBG levels declined, and the progressive destruction of pancreatic β cells was alleviated. The diversity and uniformity of gut microbiota in T1DM rats treated with UA increased significantly. Interestingly, the Th17/Treg cell differentiation imbalance was corrected and positively correlated with the expression of Foxp3 and IL-10, and negatively correlated with the expression of RORγt, IL-17A, and TNF-α. These findings suggest that UA can lower FBG levels in T1DM rats, delay the progressive destruction of pancreatic β-cells, and modulate gut microbiota homeostasis and immune function in streptozotocin-induced T1DM rats. [ABSTRACT FROM AUTHOR]

The human gut microbiome interacts with each other and the host, which has significant effects on health and disease development. Intestinal homeostasis and inflammation are maintained by the dynamic interactions between gut microbiota and the innate and adaptive immune systems. Numerous metabolic products produced by the gut microbiota play a role in mediating cross‐talk between gut epithelial and immune cells. In the event of an imbalance between the immune system and microbiota, the body becomes susceptible to infections and homeostasis is compromised. This review mainly focuses on the interplay between microbes and the immune system, such as T‐cell‐ and B‐cell‐mediated adaptive responses to microbiota and signalling pathways for effective communication between the two. We have also highlighted the role of microbes in the activation of the immune response, the development of memory cells and how the immune system determines the diversity of human gut microbiota. The review also explains the relationship of commensal microbiota and their relation to the production of immunoglobulins. [ABSTRACT FROM AUTHOR]

The human gut possesses millions of microbes that define a complex microbial community. The gut microbiota has been characterized as a vital organ forming its multidirectional connecting axis with other organs. This gut microbiota axis is responsible for host-microbe interactions and works by communicating with the neural, endocrinal, humoral, immunological, and metabolic pathways. The human gut microorganisms (mostly nonpathogenic) have symbiotic host relationships and are usually associated with the host’s immunity to defend against pathogenic invasion. The dysbiosis of the gut microbiota is therefore linked to various human diseases, such as anxiety, depression, hypertension, cardiovascular diseases, obesity, diabetes, inflammatory bowel disease, and cancer. The mechanism leading to the disease development has a crucial correlation with gut microbiota, metabolic products, and host immune response in humans. The understanding of mechanisms over gut microbiota exerts its positive or harmful impacts remains largely undefined. However, many recent clinical studies conducted worldwide are demonstrating the relation of specific microbial species and eubiosis in health and disease. A comprehensive understanding of gut microbiota interactions, its role in health and disease, and recent updates on the subject are the striking topics of the current review. We have also addressed the daunting challenges that must be brought under control to maintain health and treat diseases. [ABSTRACT FROM AUTHOR]

Type-1 Diabetes Mellitus (T1DM) is regarded as a multifunctional, immune-related disease which causes massive destruction of islet β-cells in pancreas resulting in hyperglycemic, hypoinsulinemia and hyperlipidimic conditions. The aim of the present study, was to investigate the hypothesis that streptozotocin (STZ)-induced T1DM in Balb/c mice when treated with crude polysaccharide from seaweed, Dictyopteris divaricata (CDDP) depicts improvement in diabetes-related symptoms. Treatment with CDDP resulted in decreased body weight loss, improved food consumption and water intake disbalances. The CDDP effectively improved fasting blood glucose, oral glucose tolerance (OGTT), serum insulin, insulin secretion, rejuvenation of β-cells mass, serum lipid profile and pro-inflammatory cytokines levels. Additionally, treatment with CDDP increased the population of beneficial bacteria such as Firmicutes, Bacteroidetes and Lactobacillus at phylum, family and genus levels by 16S rRNA sequencing. Furthermore, immunohistological examination confirmed that CDDP reduces the inflammation and restored the structural morphology of colon and upraised the levels of insulin receptor substrate-1 (IRS-1), Mucin-2 (MUC-2) and tight-junction proteins (TJs) whereby maintaining the gut structures and barrier permeability. Thus, the above presented data, highlights the safe and therapeutic effects of crude polysaccharide (CDDP) from D. divaricata in the treatment and restoration of T1DM disorders and can be used as a food supplement alternative to diabetes medicine. [ABSTRACT FROM AUTHOR]

Alterations of gut microbiota have been identified before clinical manifestation of type 1 diabetes (T1D). To identify the associations amongst gut microbiome profile, metabolism and disease markers, the 16S rRNA-based microbiota profiling and 1H-NMR metabolomic analysis were performed on stool samples of 52 T1D patients at onset, 17 T1D siblings and 57 healthy subjects (CTRL). Univariate, multivariate analyses and classification models were applied to clinical and -omic integrated datasets. In T1D patients and their siblings, Clostridiales and Dorea were increased and Dialister and Akkermansia were decreased compared to CTRL, while in T1D, Lachnospiraceae were higher and Collinsella was lower, compared to siblings and CTRL. Higher levels of isobutyrate, malonate, Clostridium, Enterobacteriaceae, Clostridiales, Bacteroidales, were associated to T1D compared to CTRL. Patients with higher anti-GAD levels showed low abundances of Roseburia, Faecalibacterium and Alistipes and those with normal blood pH and low serum HbA1c levels showed high levels of purine and pyrimidine intermediates. We detected specific gut microbiota profiles linked to both T1D at the onset and to diabetes familiarity. The presence of specific microbial and metabolic profiles in gut linked to anti-GAD levels and to blood acidosis can be considered as predictive biomarker associated progression and severity of T1D. [ABSTRACT FROM AUTHOR]

(1) Background: Consumption of barley has been known to exert beneficial effects on glucose tolerance; however, it has also been reported that there are inter-individual differences in these responses. Recent evidence has suggested that these individual differences are mediated by the gut microbiota. (2) Methods: In the present study, we aimed to understand the relationship between the intestinal environment, including intestinal microbiome and their metabolome, and glucose tolerance. A randomized controlled trial with a 4-week consumption of barley or control food was conducted. We conducted an integrated analysis of the intestinal microbiome and metabolome and analyzed the relationship with improvement of glucose tolerance. (3) Results: We found that metabolites such as azelate were significantly increased after barley consumption. Furthermore, the subjects whose glucose tolerance was slightly impaired showed improvement in their glucose tolerance index following the barley consumption. Additionally, the analysis showed that the increase in the abundance of the Anaerostipes was correlated with the improvement in the glucose tolerance index. (4) Conclusions: Our findings indicate that the effects of barley consumption for glucose tolerance are partly defined by the intestinal environment of consumers, providing a quantitative measurement of the dietary effect based on the intestinal environment. [ABSTRACT FROM AUTHOR]

BACKGROUND Sacha inchi (Plukenetia volubilis L.) tea has been used as an adjuvant treatment for diabetes in Pu'er, in the Yunnan province of China. The effects of sacha inchi tea on diabetes and the underlying mechanisms remain unknown. This study was conducted to investigate the influence of a water extract of sacha inchi (P. volubilis L.) leaves (PWE) on hypoglycemic activity and gut microbiota composition in mice with streptozotocin (STZ)‐induced type 1 diabetes mellitus (T1DM). During the 6 weeks of the study, T1DM mice were administered PWE intragastrically at 400 mg kg−1 body weight (BW) per day. RESULTS: Treatment with PWE reduced excessive loss of BW and excessive intake of food. It significantly decreased blood glucose levels and improved oral glucose tolerance. The treatment caused protective histopathological transformations in sections of the pancreas, leading to decreased insulin resistance and improved insulin sensitivity. Treatment with PWE also significantly ameliorated disorders of the gut microbiota structure and increased the richness and diversity of intestinal microbial species in T1DM mice. At the genus level, the populations of several crucial bacteria, such as Akkermansia, Parabacteroides, and Muribaculum increased in the PWE treatment group but the abundance of Ruminiclostridium and Oscillibacter decreased. CONCLUSIONS: Treatment with PWE can ameliorate hyperglycemic symptoms in STZ‐induced T1DM mice, and the anti‐diabetic effect of PWE was related to the amelioration of gut microbial structural disorder and the enrichment of functional bacteria. © 2022 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Background: Individuals with type 1 diabetes and those with depression show differences in the composition of the gut microbiome from that of healthy people. However, these differences have not yet been studied in patients with both diseases. Therefore, we compared the gut microbiome of people with type 1 diabetes with or without depression with matched healthy controls. Methods: A case-control study was conducted in 20 adults with type 1 diabetes (group A), 20 adults with type 1 diabetes and depression (group B), and 20 healthy adults (group C). Gut microbiota composition was determined by sequencing of the V3-V4 region of the bacterial 16S rDNA and alpha and beta diversity was compared between the groups. Results: Groups A and B both showed higher alpha diversity than the healthy control group (P < 0.001) but alpha diversity did not differ significantly between groups A and B. Participants having type 1 diabetes with (P < 0.05) or without comorbid depression (P < 0.001) differed regarding beta diversity from healthy controls but not between each other. Group B (diabetes with depression) had significantly higher abundance of Megaspaera than groups A and C. Both diabetes groups had a higher abundance of Christensenellaceae, Succinivibrionaceae, and Rhodospirillaceae than the healthy group but similar between-group abundances. Conclusions: While differences in alpha and beta diversity and in some bacterial taxa occurred only between participants with diabetes and healthy controls, specific characteristics regarding the abundance of Megasphaera were observed in people with diabetes and comorbid depression. In summary, the study findings indicate a possible involvement of bacterial groups in depression in people with diabetes. The results suggest replication studies in larger samples to verify these findings. [ABSTRACT FROM AUTHOR]

Blautia is a genus of anaerobic bacteria that is widely distributed in the mammalian gut. Recently, an increasing body of research has demonstrated a link between this genus and human health, suggesting applications as a novel probiotic strain. Moreover, we have previously shown that 2′-fucosyllactose (2′-FL), a major component of human milk oligosaccharides, increases the relative abundance of Blautia sp., particularly Blautia wexlerae , in the cultured fecal microbiota of healthy adults using a pH-controlled single-batch fermenter. However, the effects of 2′-FL on Blautia proliferation vary among individuals. In this study, we assessed the impact of the intrinsic gut microbiota on the prebiotic effects of 2′-FL. Metagenomic analysis of feces collected from all donors showed that the homolog of the intracellular GH95 α-l-fucosidase gene was considerably enriched in two non-responders (individuals who showed no increase in Blautia proliferation), whereas the homologous genes encoding extracellular α-l-fucosidase were more abundant in responders, suggesting that lactose and fucose released into the environment could be substrates mediating the growth of Blautia. In vitro assays confirmed the ability of B. wexlerae to utilize the two carbohydrates but not 2′-FL. We also observed that B. wexlerae utilized fucose released from 2′-FL by Bifidobacterium bifidum , which possessed extracellular GH95 α-l-fucosidase, in co-cultures of these two organisms. Finally, increasing the proportion of extracellular GH95 by the addition of a B. bifidum strain led to Blautia proliferation by 2′-FL in fecal cultures of the two non-responders. These findings provided valuable perspectives on individualized nutritional approaches to properly control the gut microbiota. Future clinical trials are needed to obtain further insights into the characteristics of responders vs. non-responders. [ABSTRACT FROM AUTHOR]

Acute pancreatitis (AP) is followed by structural and functional changes in the intestine, resulting from microbiome dysbiosis. However, it remains unclear how gut microbiome changes within the initial 72h of onset. In this study, severe acute pancreatitis (SAP), mild acute pancreatitis (MAP), and sham operation (SO) were replicated in rat models. 16S ribosomal RNA gene sequencing was used to explore the gut bacteria community. The predicted Cluster of Orthologous Genes (COG) and Kyoto Encyclopedia of Genes and Genomes (KEGG) metabolic pathways were associated with the 16S rRNA profiles. Compared to the SO group, significant community succession was found during the initial 72h in AP group. At 72 h after AP induction, the Firmicutes/Bacteroidetes (F/B) ratios were significantly different, with the highest ratio in SAP group and the lowest in MAP group. Lactobacillus was the most abundant genus, but it nearly disappeared in SAP rats at 72 h. Clostridiaceae 1 and Clostridium sensu stricto 1 were significantly enriched in AP group. Bacteroidales S24-7 and Bacteroidales S24-7 group norank were enriched in MAP group, while Collinsella , Morganella , and Blautia were enriched in SAP group. Lactobacillus was significantly correlated with nine COGs. Nine COGs showed significant differences between AP group and SO group. Moreover, four COGs showed significant differences between the MAP and SAP groups. KEGG Level_3 pathways propanoate metabolism (Ko00640) in AP group was significantly higher than that in SO group. The aspartate‒ammonia ligase and four KEGG orthology terms of the AP group were lower than that in the SO group, respectively. All these results suggest that the intestinal bacterial community structure and function was changed during the initial 72h in AP rats. The intestinal F/B ratio and the relative abundance of Lactobacillus could be potential markers for early diagnosis of MAP and SAP. The genus Clostridium sensu stricto 1 was the most enriched genus in AP, and may be an important marker for AP. [ABSTRACT FROM AUTHOR]

Pharmaceutical interest in the human intestinal microbiota has increased considerably, because of the increasing number of studies linking the human intestinal microbial ecology to an increasing number of non-communicable diseases. Many efforts at modulating the gut microbiota have been made using probiotics, prebiotics and recently postbiotics. However, there are other, still little-explored opportunities from a pharmaceutical point of view, which appear promising to obtain modifications of the microbiota structure and functions. This review summarizes all in vitro, in vivo and clinical studies demonstrating the possibility to positively modulate the intestinal microbiota by using probiotics, prebiotics, postbiotics, essential oils, fungus and officinal plants. For the future, clinical studies investigating the ability to impact the intestinal microbiota especially by using fungus, officinal and aromatic plants or their extracts are required. This knowledge could lead to effective microbiome modulations that might support the pharmacological therapy of most non-communicable diseases in a near future. [ABSTRACT FROM AUTHOR]

Probiotics are known to regulate host metabolism. In randomized controlled trial we aimed to assess whether interventions with probiotic containing following strains: Bifidobacterium bifidum W23, Bifidobacterium lactis W51, Bifidobacterium lactis W52, Lactobacillus acidophilus W37, Levilactobacillus brevis W63, Lacticaseibacillus casei W56, Ligilactobacillus salivarius W24, Lactococcus lactis W19, and Lactococcus lactis W58 affect gut microbiota to promote metabolic effects. By 16S rRNA sequencing we analyzed the fecal microbiota of 56 obese, postmenopausal women randomized into three groups: (1) probiotic dose 2.5 × 109 CFU/day (n = 18), (2) 1 × 1010 CFU/day (n = 18), or (3) placebo (n = 20). In the set of linear mixed-effects models, the interaction between pre- or post-treatment bacterial abundance and time on cardiometabolic parameters was significantly (FDR-adjusted) modified by type of intervention (26 and 19 three-way interactions for the pre-treatment and post-treatment abundance, respectively), indicating the modification of the bio-physiological role of microbiota by probiotics. For example, the unfavorable effects of Erysipelotrichi , Erysipelotrichales , and Erysipelotrichaceae on BMI might be reversed, but the beneficial effect of Betaproteobacteria on BMI was diminished by probiotic treatment. Proinflammatory effect of Bacteroidaceae was alleviated by probiotic administration. However, probiotics did not affect the microbiota composition, and none of the baseline microbiota-related features could predict therapeutic response as defined by cluster analysis. Conclusions: Probiotic intervention alters the influence of microbiota on biochemical, physiological and immunological parameters, but it does not affect diversity and taxonomic composition. Baseline microbiota is not a predictor of therapeutic response to a multispecies probiotic. Further multi-omic and mechanistic studies performed on the bigger cohort of patients are needed to elucidate the cardiometabolic effect of investigated probiotics in postmenopausal obesity. [ABSTRACT FROM AUTHOR]

Background: Growing evidence has shown that alterations in gut microbiota composition are associated with multiple autoimmune diseases (ADs). However, it is unclear whether these associations reflect a causal relationship. Objective: To reveal the causal association between gut microbiota and AD, we conducted a two-sample Mendelian randomization (MR) analysis. Materials and Methods: We assessed genome-wide association study (GWAS) summary statistics for gut microbiota and six common ADs, namely, systemic lupus erythematosus, rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis, type 1 diabetes (T1D), and celiac disease (CeD), from published GWASs. Two-sample MR analyses were first performed to identify causal bacterial taxa for ADs in discovery samples. Significant bacterial taxa were further replicated in independent replication outcome samples. A series of sensitivity analyses was performed to validate the robustness of the results. Finally, a reverse MR analysis was performed to evaluate the possibility of reverse causation. Results: Combining the results from the discovery and replication stages, we identified one causal bacterial genus, Bifidobacterium. A higher relative abundance of the Bifidobacterium genus was associated with a higher risk of T1D [odds ratio (OR): 1.605; 95% CI, 1.339–1.922; PFDR = 4.19 × 10−7] and CeD (OR: 1.401; 95% CI, 1.139–1.722; PFDR = 2.03 × 10−3), respectively. Further sensitivity analyses validated the robustness of the above associations. The results of reverse MR analysis showed no evidence of reverse causality from T1D and CeD to the Bifidobacterium genus. Conclusion: This study implied a causal relationship between the Bifidobacterium genus and T1D and CeD, thus providing novel insights into the gut microbiota-mediated development mechanism of ADs. [ABSTRACT FROM AUTHOR]

The delivery mode is an important factor driving alteration in the gut microbiota during the neonatal period. Several studies prove that the alteration of gut microbiota induced by cesarean section could influence the activation of intestinal epithelial cells and the development of immune system. Further, some autoimmune and metabolic disorders may be related to the microbiota dysbiosis in infants caused by cesarean section. It is noteworthy that probiotics could promote the intestinal microecology, which may further prevent and treat cesarean section related diseases. This review summarized the great significance of delivery mode on microbiota and health, as well as provided clinically feasible methods for the prevention and treatment of cesarean section related gut diseases. [ABSTRACT FROM AUTHOR]

Purpose: This paper aims to evaluate hematological parameters, blood glutathione (GSH), serum glucose-6-phosphate dehydrogenase (G6-PD) and liver function in favism animals' models after oral intake with a mixture of pickled olives and Vicia faba (V. faba) seeds. Design/methodology/approach: Favism is a life-threatening hemolytic crisis. It results from the ingestion of V. faba by the individuals. The hemoglobin (Hb), hematocrit (Hct), red blood cells (RBCs), white blood cells (WBCs), serum glucose, blood GSH, serum G6-PD, serum thiobarbaturic acid reactive substances (TBARS), liver protein and liver function were evaluated after oral administration with a mixture of pickled olives with V. faba seeds in favism animals' models. Findings: The favism-, vicine- and convicine-treated animals showed a significant decrease (p < 0.01) in Hb (6.42, 7.23 and 5.96 g/dl), Hct (25.4, 26.4 and 25.1%), RBCs (2.56, 2.45 and 2.60 106 cells/mm3, WBCs (4.35, 4.25 and 4.30 103 cells/mm3), serum glucose (95.8, 97.1 and 96.5 mg/dl), blood GSH (24.7, 26.6 and 23.8 mg/dl), serum G6-PD (15.8, 15.9 and 15.7 U/L), serum aspartate aminotransferase (6.35, 6.59 and 5.97 U/L), alanine aminotransferase (4.49, 4.61 and 4.50 U/L), total protein (6.54, 6.59 and 6.40 g/dl), albumin (3.84, 3.91 and 3.75 g/dl), globulin (2.70, 2.48 and 2.65 g/dl) and liver protein (3.37, 3.10 and 3.42 g/g tissue) but a significant increase (p < 0.01) in serum TBARS (38.7, 38.9 and 39.4 nmol/dl), alkaline phosphatase (275, 271 and 281 U/L) and total bilirubin (0.93, 0.89 and 0.91 mg/dl) compared to Hb (16.3 g/dl), Hct (45.3%), RBCs (5.80 106 cells/mm3), WBCs (9.45 103 cells/mm3), serum glucose (96.5 mg/dl), blood GSH (39.7 mg/dl), serum G6-PD (36.1 U/L), serum TBARS (18.0 nmol/dl), serum aspartate aminotransferase (19.8 U/L), alanine aminotransferase (9.23 U/L), alkaline phosphatase (214 U/L), total bilirubin (0.57 mg/dl), total protein (8.76 g/dl), albumin (4.85 g/dl), globulin (3.91 g/dl) and liver protein (6.28 g/g tissue) in control group. The oral administration with pickled olives + V. faba, pickled olives + vicine and pickled olives + convicine into favism animals' models, vicine-treated animals and convicine-treated animals, respectively pushed all the above-mentioned parameters to near the control levels. Originality/value: V. faba contains vicine and convicine glycosides. Vicine and convicine glycosides in V. faba are hydrolyzed by intestinal microflora to aglycones divicine and isouramil, respectively. Divicine and isouramil are highly reactive compounds generating free radicals where divicine and isouramil are the main factors of favism. The ß-glucosidase in pickled olives converts both vicine and convicine glycosides into aglycones divicine and isouramil, respectively, in aerobic condition outside the human body (in inactive forms) and prevent these glycosides to cause favism. [ABSTRACT FROM AUTHOR]

BACKGROUND Lactulose was one of the earliest prebiotics to be identified. To assess the potential risk of large intakes of lactulose to the intestinal microbiota, mice were fed a diet containing lactulose (0%, 5% and 15%, w/w) for 2 weeks and the changes in the fecal microbiota were evaluated by 16S rRNA high‐throughput sequencing. RESULTS: Lactulose intervention decreased the α‐diversity of the fecal microbiota in both low‐dose and high‐dose groups. The relative abundance of Actinobacteria was significantly increased, while that of Bacteroidetes was significantly decreased after lactulose intervention. At the genus level, the relative abundance of Bifidobacterium belonging to Actinobacteria was significantly increased, and that of Alistipes belonging to Bacteroidetes was decreased in both low‐dose and high‐dose groups. The relative abundance of Blautia was significantly increased from 0.2% to 7.9% in the high‐dose group and one strain of Blautia producta was isolated from the mice feces. However, the strain could not utilize lactulose. CONCLUSION: Overall, the microbial diversity was decreased after lactulose treatment, with significant increases in the relative abundance of Bifidobacterium. We also provide a strategy to increase the relative abundance of Blautia in the intestine by lactulose feeding at high doses, although the mechanism is not revealed. This will help us understand the prebiotic effect of lactulose on the host health. © 2021 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

The intestinal microecology is an extremely complex ecosystem consisting of gut microbiota, intestinal mucosa and the intestinal immune system. The intestinal microecology performs several important functions and is considered to be an essential 'organ' because it plays an important role in regulating human metabolism. Fucoidan contains a large amount of fucose and galactose residues, as well as various other neutral and acidic monosaccharides. Fucoidan particularly effects tumors, inflammatory bowel disease, diabetes and obesity by repairing intestinal mucosal damage and improving the intestinal microecological environment. It has been proposed that fucoidan could be used as a prebiotic agent for pharmaceutical and functional foods. In this review, we elucidate the potential mechanisms of the metabolic regulation of fucoidan with respect to the intestinal microecology of diseases. [ABSTRACT FROM AUTHOR]

The incidence and prevalence rate of chronic inflammatory disorders is on the rise in the pediatric population. Recent research indicates the crucial role of interactions between the altered intestinal microbiome and the immune system in the pathogenesis of several chronic inflammatory disorders in children, such as inflammatory bowel disease (IBD) and autoimmune diseases, such as type 1 diabetes mellitus (T1DM) and celiac disease (CeD). Here, we review recent knowledge concerning the pathogenic mechanisms underlying these disorders, and summarize the facts suggesting that the initiation and progression of IBD, T1DM, and CeD can be partially attributed to disturbances in the patterns of composition and abundance of the gut microbiota. The standard available therapies for chronic inflammatory disorders in children largely aim to treat symptoms. Although constant efforts are being made to maximize the quality of life for children in the long-term, sustained improvements are still difficult to achieve. Additional challenges are the changing physiology associated with growth and development of children, a population that is particularly susceptible to medication-related adverse effects. In this review, we explore new promising therapeutic approaches aimed at modulation of either gut microbiota or the activity of the immune system to induce a long-lasting remission of chronic inflammatory disorders. Recent preclinical studies and clinical trials have evaluated new approaches, for instance the adoptive transfer of immune cells, with genetically engineered regulatory T cells expressing antigen-specific chimeric antigen receptors. These approaches have revolutionized cancer treatments and have the potential for the protection of high-risk children from developing autoimmune diseases and effective management of inflammatory disorders. The review also focuses on the findings of studies that indicate that the responses to a variety of immunotherapies can be enhanced by strategic manipulation of gut microbiota, thus emphasizing on the importance of proper interaction between the gut microbiota and immune system for sustained health benefits and improvement of the quality of life of pediatric patients. [ABSTRACT FROM AUTHOR]

Background: Obesity and diabetes are public health problems that are leading causes of death in the world. Recent surveys suggest that there is a relationship between diabetes and bacterial residents of the gastrointestinal tract. Objective: This case-control study was designed to evaluate the composition of the gut microbiota in patients with type 2 diabetes (T2DM) and obesity compared to the healthy people. Methods: A total of 91 adult subjects (25 patients diagnosed with T2DM, 48 obese patients, and 18 healthy individuals) were included in the study. The gut microbiota composition was investigated by quantitative real-time polymerase chain reaction (qPCR) method using bacterial 16S rRNA gene. Results: The frequency of all bacterial species in the obese group compared to the control group have significantly changed (p < 0.05) except Bacteroides fragilis, whereas the level of bacterial composition was not changed significantly (p > 0.05) in the diabetic patients versus the control ones, except for Bacteroides phylum and Lactobacillus spp. Moreover, the mean body mass index (BMI) in control, T2DM, and obese groups were 24.28 ± 3.00, 26.83 ± 3.29, and 44.65 ± 3.73, respectively. Our analysis showed a positive correlation between diabetic patients plus obese ones and the number of bacteria (p < 0.05). Conclusions: To sum up, these findings show that specific changes in microbial community composition are associated with T2DM and obesity. More extensive, our survey suggests that modulation of the microbiome warrants further investigation as a potential therapeutic strategy for metabolic diseases. [ABSTRACT FROM AUTHOR]