The gut microbiota is disrupted in schizophrenia (SZ) patients and is associated with cognitive function. This study aimed to investigate the gut microbiota composition in SZ patients with different body mass index (BMI) levels and their associations with cognitive function.

We analyzed 16S rRNA sequencing data from 156 SZ patients, including 88 with overweight/obesity (OW) and 68 with normal weight (NW), and 156 normal control (NC), including 48 with OW and 108 with NW. We analyzed differences in microbial diversity and gut microbiota composition between SZ patients and NC at different BMI levels. Additionally, we explored the correlations between microbial communities, and symptom severity, as well as cognitive function. Furthermore, we examined between-group differences in metabolic pathways.

The abundance of Turicibacter was higher in the SZ_OW group but lower in the SZ_NW group compared to the NC groups at the same BMI level, respectively. In the SZ_OW group, increased Collinsella was significantly negatively associated with cognitive function, whereas decreased Clostridium and Butyricicoccus were significantly positively associated with cognitive function. Additionally, the functional analysis revealed enrichment of "metabolism of other amino acids" and "neurodegenerative disease" pathways, associated with non-standard amino acid metabolism and oxidative stress in the SZ_OW group compared to the NC_OW group.

Our findings revealed significant differences in the gut microbiota between SZ patients and NC with different BMI levels and identified microbial associations with clinical characteristics, providing new insights into the mechanism of how the gut microbiota could impact cognitive deficits in SZ patients with obesity.

To examine gut microbiota diversity, composition and metabolites in relation to overall mass (OM), fat mass (FM) and lean soft tissue mass (LSTM) measured by dual x-ray absorptiometry (DXA) in 5-year-old children.

Mothers of the Gen3G cohort were enrolled prenatally in 2010-2013 in Quebec, Canada; 153 children from the cohort had data on gut microbiota and DXA scans at 5-6.4 years of age, and 140 also had plasma metabolite data. We characterized gut microbiota by 16S rRNA Illumina sequencing and metabolites by untargeted multiplatform mass spectrometry. We examined associations of microbial alpha diversity, beta diversity, composition (amplicon sequence variants; ASVs) and metabolites (microbial metabolites) with DXA measures, adjusting for age, sex, diet and drinking water.

Of the 153 children, 43.1% were female, and 96.1% self-identified as white. The median BMI was the 52nd percentile. Microbial richness (alpha diversity) was positively associated with OM, FM and LSTM. Of the 542 ASVs tested, 7 were associated with OM, 5 with FM and 4 with LSTM. One Veillonella ASV and two Blautia ASVs were significantly associated with all outcomes. Among 278 microbial metabolites, no metabolites were associated with FM, while glycoursodeoxycholate was associated with OM, and glycoursodeoxycholate, 3-hydroxybutyrate and gamma-glutamylalanine were associated with LSTM.

In 5-year-old children, gut microbiota alpha diversity, richness and specific gut microbes were associated with OM, FM and LSTM. Many of the associations followed a similar pattern for FM and LSTM, suggesting they may not be specific to adiposity but rather reflect overall growth.

Secondary bile acids, lithocholic acid and deoxycholic acid (LCA and DCA), are dehydroxylated derivatives of primary bile acids. However, in addition to LCA and DCA the intestinal microbiota produced a variety of poorly characterized metabolites. Allo-LCA, a LCA metabolite, acts as a dual GPBAR1 agonist and RORγt inverse agonist and modulates intestinal immunity, although is not yet known whether allo-LCA exerts regulatory functions outside the intestine. In the present study we have therefore investigated whether administration of allo-LCA, 10 mg/kg/day, to mice administered a high fat/high fructose diet (HFD-F) and carbon tetrachloride (Ccl4), a model for metabolic dysfunction-associated steatohepatitis (MASH), protects from development of liver damage. In vitro allo-LCA functions as GPBAR1 agonist and RORγt inverse agonist and prevents macrophages M1 polarization and Th17 polarization of CD4 cells. In vivo studies, while exposure to a HFD-F/Ccl4 promoted insulin resistance and development of a pro-atherogenic lipid profile and liver steatosis and fibrosis, allo-LCA reversed this pattern by improving insulin sensitivity and liver lipid accumulation. The liver transcriptomic profile demonstrated that allo-LCA reversed the dysregulation of multiple pathways associated with immunological, inflammatory and metabolic signaling. Allo-LCA also restored bile acid homeostasis, reversing HFD/Ccl4-induced shifts in bile acid pool composition and restored adipose tissue histopathology and function by reducing the expression of leptin and resistin, two pro-inflammatory adipokines, and restored a healthier composition of the intestinal microbiota. In conclusion, present results expand on the characterization of entero-hepatic signaling and suggest that allo-LCA, a microbial metabolite, might have therapeutic potential in liver diseases.

Evidence is insufficient to establish a longitudinal association between combined trajectories of body mass index (BMI) and waist circumference (WC) and dyslipidemia. This study investigated the associations between multi-trajectories of BMI and WC over 24 years and the subsequent risk of dyslipidemia in a large cohort of 10,678 Chinese adults from the China Health and Nutrition Survey. Utilizing a group-based trajectory model, we identified four distinct trajectories: normal, normal-increasing, overweight-increasing, and obesity-increasing. Our results indicated that ascending trajectories of BMI and WC are significantly associated with increased odds of dyslipidemia, particularly in males, with odds ratios (OR) of 2.10, 2.69, and 3.56 for the normal-increasing, overweight-increasing, and obesity-increasing groups, respectively. Among females, the normal-increasing group exhibited a significant increased risk (OR: 1.54). Furthermore, we explored the gut microbiota associated with these trajectories, identifying 3, 8, and 4 bacterial genera linked to increasing BMI and WC in males, alongside two genera in females with the normal-increasing trajectory. We identified a total of 23, 25, and 10 differential metabolites significantly associated with these genera, except for Group 2 in males. The inclusion of relevant microbiome and metabolite data improved the model's predictive capacity for the risk of dyslipidemia, with ROC values increasing from 0.655 to 0.875. Our findings underscore the critical implications of continuous weight gain on metabolic health and suggest that gut microbiota may play a pivotal role in understanding these associations.IMPORTANCEEmerging evidence suggests a close connection between the gut microbiome and both human obesity and dyslipidemia, suggesting that the gut microbiome may play an important role in the obesity-dyslipidemia relationship. In this study, we observed several characteristic genera, including Clostridium_sensu_stricto_1, Turicibacter, and CHKCI002 among males and Parabacteroides and [Eubacterium]_brachy_group among females, which were negatively associated with high-risk trajectories. They were also related to free fatty acids (FFAs) and oxidized lipid metabolites. These shared and unique gut microbial and metabolic signatures among combined trajectories of BMI and WC with a higher risk of dyslipidemia could provide important evidence for the omics mechanism pathway of long-term obesity trend leading to dyslipidemia.

Amyotrophic lateral sclerosis (ALS) is a neurological disease marked by the degeneration of motor neurons, leading to muscle weakness and paralysis. While the cause of ALS is uncertain, research indicates that changes in the gut microbiome may influence the disease's progression. This chapter explores how alterations in gut microbiota affect the enteric neuromuscular system (ENS) in ALS. In ALS patients, disrupted gut microbiota are linked to the brain-gut axis, impacting both gastrointestinal function and neuronal health. Studies show that microbial changes are associated with inflammation, immune instability, and neurodegeneration, which exacerbate the disease. Gastrointestinal issues like constipation and dysphagia in ALS are tied to ENS dysregulation. Understanding the connections between the gut microbiome, ENS, and central nervous system (CNS) may lead to novel therapies targeting neurodegeneration and microbial dysbiosis in ALS.

This study examined the health benefits of 3-O-butanoylresveratrol (ED4), a monoester derivative of resveratrol butyrate esters. Using a high-calorie diet model simulation with Chinese sausage, ED4 was tested against changes in physiological indices like body weight (BW), body fat, blood pressure, and SCFA levels (stools and serum) in rats. This study found that the obesity-inducing model utilizing sausage as a high-calorie diet worked, and that supplementing rats with ED4 (20 mg/kg BW/day) for 5 weeks inhibited BW increase and body fat buildup. Blood lipid and SCFA dysregulation improved significantly. In addition, ED4 effectively increased PPAR-γ and decreased SREBP-1C mRNA expression, preventing fat accumulation and overproduction. A novel food-driven relationship between gut microbiota and adipose was found, promoting health. Our findings showed that ED4 supplementation exacerbated metabolic abnormalities caused by high-calorie diets and reduced body fat. Notably, these metabolic benefits were enhanced through the involvement of intestinal microbiota.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing global health challenge, characterized by significant variability in progression and clinical outcomes. While the gut microbiome is increasingly recognized as a key factor in liver disease development, its role in disease progression and associated mechanisms remains unclear. This study systematically investigated the gut microbiota's role in MASLD and liver cirrhosis progression, focusing on individual bacterial strains, microbial community dynamics, and functional characteristics across different enterotypes.

Publicly available next-generation sequencing(NGS) datasets from healthy individuals and patients with MASLD and cirrhosis were analyzed. Enterotype classification was performed using principal component analysis, with advanced bioinformatics tools, including Linear Discriminant Analysis Effect Size (LEfSe), eXtreme Gradient Boosting (XGBoost), and Deep Cross-Fusion Networks for Genome-Scale Identification of Pathogens (DCiPatho), to identify differentially abundant microbes and potential pathogens. Microbial co-occurrence networks and functional predictions via PICRUSt2 revealed distinct patterns across enterotypes.

The Prevotella-dominated(ET-P) group exhibited a 33% higher cirrhosis rate than the Bacteroides-dominated(ET-B) group. Unique microbial signatures were identified: Escherichia albertii and Veillonella nakazawae were associated with cirrhosis in ET-B, while Prevotella copri was linked to MASLD. In ET-P, Prevotella hominis and Clostridium saudiense were significantly associated with cirrhosis. Functional analysis revealed reduced biosynthesis of fatty acids, proteins, and short-chain fatty acids (SCFAs), coupled with increased lipopolysaccharide(LPS) production and altered secondary bile acid metabolism in MASLD and cirrhosis patients. There were significant microbial and functional differences across enterotypes in MASLD and cirrhosis progression, providing critical insights for developing personalized microbiome-targeted interventions to mitigate liver disease progression.

The APOE ε4 allele (APOE4) is a known risk factor for neurodegenerative and cardiovascular diseases, but its link to body composition and metabolism remains debated. The gut microbiota influences host metabolism and immunity, yet its relationship with APOE genotype in healthy individuals is not well understood. The objective of this work was to examine associations between APOE genotype and gut microbiota composition and function in healthy adults, focusing on microbial and metabolic differences related to the APOE4 allele. Seventy-seven healthy Spanish adults were genotyped for APOE. Fecal microbiota profiles were assessed by 16 S rRNA gene sequencing, and predicted functions were inferred using PICRUSt2. Body composition (DEXA) and physical activity (accelerometry) were also measured. APOE4 carriers exhibited subtle shifts in microbiota composition, including a five-fold reduction in Megamonas and lower abundance of the Eubacterium brachy group-both linked to energy harvest and adiposity-compared to APOE3 homozygotes. An uncharacterized Puniceicoccaceae genus was enriched in APOE4 carriers. Although E. brachy group abundance correlated with adiposity, no significant differences in body composition were observed. Functional predictions showed APOE4-associated microbiota enriched in pathways for carotenoid biosynthesis and trehalose metabolism, and depleted in tryptophan biosynthesis, propionate production, and multidrug resistance mechanisms. APOE4 carriers harbor gut microbiota with distinct taxonomic and functional features, potentially reflecting adaptations to metabolic and oxidative challenges. These findings underscore the relevance of the gut microbiome in shaping APOE4-associated phenotypes and warrant further investigation into its mechanistic contributions to health and disease.

The timing of dietary total fat intake influences glucose homeostasis, however, the impact of unsaturated fat (USFA) intake has yet to be explored. This 12-week, double-blind, randomized, controlled, 2 × 2 factorial-designed feeding trial investigated the effects of timing (lunch or dinner) and types of dietary USFA (high monounsaturated fat or polyunsaturated fat diet) intake on glucose metabolism in seventy prediabetes participants (mean age, 57 years). Sixty participants with completed fecal samples were included in the final analysis (n = 15 for each group). Postprandial serum glucose was first primary outcome, postprandial insulin levels and insulin sensitivity indices were co-primary outcomes Secondary outcomes were continuous glucose levels, serum fatty acid profile, gut microbiome (metagenomic sequencing) and fecal metabolites. Results showed no significant differences in postprandial glucose between groups. However, USFA intake at lunch (vs. dinner) improved insulin sensitivity and reduced postprandial insulin and serum free saturated fatty acid (Ptiming < 0.05, Ptype > 0.05, Pinteraction > 0.05), which was associated with alterations in gut microbiome and bile acid metabolism, regardless of USFA type. In summary, these results suggest that advancing timing of USFA intake improves insulin sensitivity through the gut microbiome and bile acid metabolism. Trial registration: ChiCTR2100045645.

The human gastrointestinal tract is estimated to be populated by 38 trillion bacteria from almost 1000 different species. The dominant phyla are Firmicutes, Bacteroidetes, Actinobacteria, and Proteobacteria. However, the diversity and amount of gut microbiota depends on various factors. The importance of gut microbiota is increasingly noticed due to the influence of bacteria on energy homeostasis, the immune system, general health, and metabolism. Bariatric surgery is the mainstay treatment for patients with obesity. Two of the most common mechanisms are reducing gastric volume and decreasing ghrelin secretion. This literature review aims to depict the diverse impact of different bariatric procedures on gut microbiota. The original research papers were collected from the PubMed, Cochrane, and Elsevier databases. This literature review is focused on human studies. However, several references include animal models, specifically rats and germ-free mice. The findings suggest that bariatric surgery causes changes in the diversity of gut microbiota. However, the specificity of the changes depends on the type of bariatric surgery. The Firmicutes/Bacteroidetes ratio is elevated in the groups of patients with obesity compared to lean individuals. Bariatric surgery lowers the ratios impact on metabolism and energy absorption. Gut microbiota produces short-chain fatty acids, of which butyrate is responsible for strengthening the gut barrier, and acetate is correlated with fat deposition and lipogenesis. Moreover, changes in short-chain fatty acids influence insulin resistance and inflammation. In conclusion, bariatric surgery impacts gut microbiota, resulting in metabolic changes in patients, and the need for further study regarding long-term microbiota alterations post-operation is notable.

The intestinal microbiota, in terms of both composition and functioning, exerts a significant influence on the human body. Disturbed microbiota is a common occurrence in the context of numerous diseases. The available evidence increasingly points to a correlation between this condition and the development of prostate diseases, including benign prostatic hyperplasia and prostate cancer. 16 S sequencing of the V3-V4 region was performed and then evaluated alpha and beta diversity of the faeces microbiota of healthy (control group, N = 81) and BPH patients (study group, N = 76). The exploration of enterotypes involved the application of the Dirichlet-Multinomial model, executed for selecting community types. The study revealed no statistically significant difference in alpha diversity between the control group and the group of patients diagnosed with BPH. However, a significant difference was observed in beta diversity (Permanova test: F-value = 5.56, p-value < 0.001). The identification of enterotypes revealed significant differences between the healthy male cohort and those diagnosed with BPH (p = 0.035). In the cohort of men with BPH, the most prevalent was enterotype 3, characterized by a predominance of Blautia, Bacteroides, and Streptococcus. The occurrence of enterotype 3 was associated with an increased likelihood of BPH, exceeding threefold that of enterotype 1 (OR = 3.24). These findings suggest that alterations in the gut microbiota, particularly the presence of enterotype 3, may serve as a microbiological pattern associated with BPH.

A strain of Streptococcus thermophilus 90301, characterized by robust growth and high exopolysaccharide (EPS) production, was selected. Following isolation and purification, two EPS components, EPS-1 and EPS-2, were obtained. The analysis revealed that EPS-1 was composed of mannose, rhamnose, glucosamine, glucose, and galactose with molar ratios of 0.94:0.09:0.11:1.00:0.16, whereas EPS-2 was composed of mannose, ribose, glucose, and galactose with molar ratios of 15.11:0.26:1.00:0.38; respectively. The average molecular weights were determined to be 2.31 × 105 Da for EPS-1 and 2.41 × 105 Da for EPS-2. Furthermore, the prebiotic potential of the two fractions (EPS-1 and EPS-2) was investigated through in vitro simulation of human fecal fermentation digestion. Both EPS-1 and EPS-2 were not digested by the digestive fluids and were able to significantly modulate the composition of the gut microbiota. Additionally, they enhanced the gut microbiota's ability to produce short-chain fatty acids. These findings provide some basis for the functional application of polysaccharide components extracted from S. thermophilus 90301 as a potential prebiotic.

Background and Aim: The human gut microbiome plays a crucial role in maintaining health. Artificial sweeteners, also known as non-nutritive sweeteners (NNS), have garnered attention for their potential to disrupt the balance of the gut microbiome. This review explores the complex relationship between NNS and the gut microbiome, highlighting their potential benefits and risks. By synthesizing current evidence, we aim to provide a balanced perspective on the role of AS in dietary practices and health outcomes, emphasizing the need for targeted research to guide their safe and effective use. Methods: A comprehensive literature review was conducted through searches in PubMed and Google Scholar, focusing on the effects of artificial sweeteners on gut microbiota. The search utilized key terms including "Gut Microbiome", "gut microbiota", "Eubiosis", "Dysbiosis", "Artificial Sweeteners", and "Nonnutritive Sweeteners". Results: NNS may alter the gut microbiome, but findings remain inconsistent. Animal studies often report a decrease in beneficial bacteria like Bifidobacterium and Lactobacillus, and an increase in harmful strains such as Clostridium difficile and E. coli, potentially leading to inflammation and gut imbalance. Disruptions in short-chain fatty acid (SCFA) production and gut hormone signaling have also been observed. However, human studies generally show milder or no significant changes, highlighting the limitations in translating animal model findings directly to humans. Differences in study design, dosage, exposure time, and sweetener type likely contribute to these varied outcomes. Conclusions: While NNS offer certain benefits, including reduced caloric intake and improved blood sugar regulation, their impact on gut microbiome health raises important concerns. The observed reduction in beneficial bacteria and the rise in pathogenic strains underscore the need for caution in NNS consumption. Furthermore, the disruption of SCFA production and metabolic pathways illustrates the intricate relationship between diet and gut health.

The gut microbiota has been implicated in adult obesity, but the causality is still unclear. It has been hypothesized that an obesity-prone gut microbiota can be established in infancy, but only few studies have examined the early-life gut microbiota in relation to obesity in childhood, and no consistent associations have been reported. Here, we examine the association between the early-life gut microbiota and body mass index (BMI) development and body composition throughout childhood.

Gut microbiota from stool were collected from 700 children in the Copenhagen Prospective Studies on Asthma in Childhood2010 (COPSAC2010) cohort at ages of 1 week, 1month, 1 year, 4 years, and 6 years and analyzed by 16S rRNA gene sequencing. Outcomes included BMI World Health Organization (WHO) Z scores (zBMI), overweight (zBMI > 1.04) and obesity (zBMI > 1.64) (0-10 years), and adiposity rebound and body composition from dual-energy X-ray absorptiometry at 6 years.

The early-life gut microbiota diversity, overall composition, and individual taxon abundances in unsupervised and supervised models were not consistently associated with either current or later BMI Z scores, overweight, obesity, adiposity rebound, or body composition in childhood.

In a deeply characterized longitudinal birth cohort, we did not observe any consistent associations between the early-life gut microbiota and BMI or risk of obesity in later childhood. While this does not conclusively rule out a relationship, it suggests that if such associations exist, they may be more complex and potentially influenced by factors emerging later in life, including lifestyle changes.

COPSAC is funded by private and public research funds (all listed on www.copsac.com).

The intricate relationship between human health and gut microecology has emerged as a central theme in contemporary medical research. Postmenopausal osteoporosis, primarily driven by estrogen deficiency, remains a major health concern. Traditional Chinese herbal medicines have attracted significant interest for their promising role in osteoporosis treatment.

The effects of Isaria felina, derived from Cordyceps sinensis, on postmenopausal osteoporosis in rats are the focus of this study. Adult female Sprague-Dawley rats were categorized into control, postmenopausal osteoporosis (OVX), and Isaria felina-treated (IF+OVX) groups. Following a 12-week treatment period, various analyses, including micro-CT, histological assessments, 16S rDNA sequencing, untargeted metabolomics, flow cytometry, and ELISA, were performed.

Micro-CT and histological assessments indicated significant improvements in bone loss and obesity control in OVX rats treated with Isaria felina. 16S rDNA sequencing revealed that Isaria felina corrected gut microbiota dysbiosis, particularly in the Bacteroides and Ruminococcus genera. Untargeted metabolomics highlighted alterations in nucleotide and lipid metabolism. Flow cytometry and ELISA analyses demonstrated that Isaria felina modulated the Th17/Treg immune balance, resulting in reduced levels of inflammatory cytokines IL-17 and TNF-α.

These findings indicate that Isaria felina mitigates bone loss in postmenopausal osteoporosis through modulation of gut microbiota and immune responses, underscoring its potential as a therapeutic agent for osteoporosis treatment.

Dyslipidemia is a major risk factor for cardiovascular diseases and is influenced by genetic and environmental factors, including diet. Emerging research suggests a link between the gut microbiome and metabolic disorders. While the connection between the gut microbiota and dyslipidemia is well documented, the specific relationship between oral bacteria and dyslipidemia has not been thoroughly investigated. This study aimed to identify oral bacterial species associated with dyslipidemia in a community-based Japanese population. We conducted a metagenomic analysis on tongue coating samples from 763 participants in the Iwaki Health Promotion Project, which were collected during health checkups in 2017 and 2019. Dyslipidemia was diagnosed using standard lipid level criteria. The oral microbiome was analyzed via 16S rDNA amplicon sequencing. Statistical analyses included multiple regression and β diversity assessments. Our analysis revealed that the abundances of several bacterial genera, including Veillonella, Atopobium, Stomatobaculum, Tanneralla, and Megasphaera, are significantly associated with dyslipidemia. A higher relative abundance of Megasphaera was specifically observed in individuals with dyslipidemia. Moreover, Megasphaera abundance was closely associated with the onset of dyslipidemia (P = 0.038, odds ratio: 1.005, 95% confidence interval: 1.000-1.009), suggesting its role in metabolic regulation. This study revealed a significant association between the abundance of specific oral bacteria and dyslipidemia, suggesting the potential of using the oral microbiota as a biomarker for the early detection and management of dyslipidemia. Future research should explore the mechanisms through which oral bacteria influence lipid metabolism and the potential for microbioma-based therapies.

The relationship between diet, micronutrient supplementation, and metabolic regulation emphasizes the potential of nutritional strategies to address obesity and related disorders. Certain vitamins have the potential to enhance thermogenesis and metabolic health. However, the impact of multivitamin supplementation on white adipose tissue (WAT) browning, the gut microbiome (GM), and metabolic function is not well understood. This study investigated the effects of multivitamin supplementation on obesity-related metabolic dysfunction in mice fed a high-fat diet (HFD) or a low-fat diet (LFD).

Male C57BL/6J mice were assigned to group 1: control chow diet (CHD); 2: control HFD; 3: multivitamin-supplemented HFD (Mv-HFD); 4: control LFD; or 5: multivitamin-supplemented LFD (Mv-LFD). Diets, either supplemented with multivitamins A, D, B1, B5, and C or non-supplemented, were administered for 12 weeks. Metabolic parameters, adipose tissue browning, and the GM composition were analyzed.

The Mv-HFD significantly reduced weight gain, adipose tissue mass, blood glucose levels, and insulin resistance induced by an HFD. Additionally, it increased energy expenditure and thermogenic gene expression in WAT. Both the Mv-HFD and Mv-LFD improved the GM composition by increasing beneficial bacteria.

Multivitamin supplementation improved metabolic health by potentially promoting WAT browning, enhancing energy expenditure, and modulating the GM composition. These findings suggest that multivitamins could offer a promising strategy for combating obesity and associated metabolic dysfunction.

Background/Objective: This study investigated the relationship between the composition of oral microbiota and metabolic dysfunction-associated steatotic liver disease (MASLD) in the general population. Methods: In total, 712 participants in a health check-up project were divided into four oral microbiota patterns by principal component analysis and cluster analysis; they were included in Neisseria, Streptococcus, Fusobacterium, and Veillonella groups. The Neisseria group had the largest number of patients and was used as a reference group to compare the incidence of MASLD and cardiometabolic criteria with the other groups. Results: In a multivariate analysis, the Veillonella group was a risk factor for MASLD independent of cardiometabolic criteria compared with the Neisseria group. The correlation between oral bacterial species and MASLD-related items showed that Neisseria was negatively correlated with controlled attenuation parameters, body mass index, waist circumference, hemoglobin A1c, alanine aminotransferase, and fatty liver index. Veillonella showed a positive correlation with controlled attenuation parameters, waist circumference, body mass index, blood pressure, triglycerides, alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transpeptidase, and fatty liver index, and a negative correlation with high-density lipoprotein cholesterol. In contrast, the Streptococcus and Fusobacterium groups were not clearly associated with MASLD. Conclusions: Maintaining oral hygiene and preventing periodontitis may contribute to preventing MASLD and extending a healthy lifespan.

Obesity is a major global concern and is generally attributed to a combination of genetic and environmental factors. Several hypotheses have been proposed to explain the evolutionary origins of obesity epidemic, including thrifty and drifty genotypes, and changes in thermogenesis. Here, we put forward the hypothesis of metaflammation, which proposes that due to intense selection pressures exerted by environmental pathogens, specific genes that help develop a robust defense mechanism against infectious diseases have had evolutionary advantages and that this may contribute to obesity in modern times due to connections between the immune and energy storage systems. Indeed, incorporating the genetic variations of gut microbiota into the complex genetic framework of obesity makes it more polygenic than previously believed. Thus, uncovering the evolutionary origins of obesity requires a multifaceted approach that considers the complexity of human history, the unique genetic makeup of different populations, and the influence of gut microbiome on host genetics.

Despite the widespread adoption of gluten-free diets for weight management, the relationship between gluten intake and obesity remains unclear because of the limited number of controlled studies available in the literature. Furthermore, there is ongoing debate regarding the impact of gluten-containing diets on the gut microbiota. This study aimed to investigate the effects of gluten consumption on the body weight and intestinal microbiota of mice fed a high-fat diet. Twenty-four Bagg albino laboratory-bred mice (BALB/c) were randomly divided into four groups for oral gavage feeding: standard diet control (SDC), standard diet + 5 mg/day gluten (SD + gluten), high-fat diet control (HFDC), and high-fat diet + 5 mg/day gluten (HFD + gluten). Each subject's body weight was measured and recorded weekly. For microbiota analysis, fecal samples were collected weekly from the cages after overnight cage changes. The microbiota was analyzed using via the 16 S ribosomal ribonucleic acid (rRNA) method. Compared with the control diet, both gluten consumption and a high fat diet significantly increased weight gain (p < 0.05). No significant difference was observed in the total mesophilic aerobic bacterial count among the groups (p > 0.05). However, the addition of gluten to the diet positively affected Lactobacillus bulgaricus (p < 0.05). Conversely, gluten-containing diets negatively impacted the total coliform bacteria and Escherichia coli counts in the gut (p < 0.05). These findings suggest that gluten, when combined with either a normal diet or a high-fat diet, contributes to weight gain while exerting positive effects on the intestinal microbiota.

Kratom (Mitragyna speciosa Korth.), rich in mitragynine and polyphenols, suppresses and affects the metabolism of macronutrients, making it a functional ingredient in medical food for obese patients. This research focuses on the formulation of a kratom-supplemented medical food (MKT) and its effects on the gut microbiota of obese patients using in vitro fecal fermentation, as well as the production of their metabolites in a simulated human colon system. The 16S rRNA gene sequencing and studies on α- and β-diversity revealed favorable outcomes for MKT, demonstrating the promotion of beneficial bacteria and the suppression of pathogens in obese patients. However, the commercial medical food (MC) resulted in the production of more short-chain fatty acids. In conclusion, the developed kratom-supplemented formula shows potential for use in the diets of obese patients. However, further investigation through animal and human trials is needed to confirm its safety and effectiveness.

In 2023, the World Obesity Atlas Federation concluded that more than 50% of the world's population would be overweight or obese within the next 12 years. At the heart of this epidemic lies the gut microbiota, a complex ecosystem that profoundly influences obesity-related metabolic health. Its multifaced role encompasses energy harvesting, inflammation, satiety signaling, gut barrier function, gut-brain communication, and adipose tissue homeostasis. Recognizing the complexities of the cross-talk between host physiology and gut microbiota is crucial for developing cutting-edge, microbiome-targeted therapies to address the global obesity crisis and its alarming health and economic repercussions. This narrative review analyzed the current state of knowledge, illuminating emerging research areas and their implications for leveraging gut microbial manipulations as therapeutic strategies to prevent and treat obesity and related disorders in humans. By elucidating the complex relationship between gut microflora and obesity, we aim to contribute to the growing body of knowledge underpinning this critical field, potentially paving the way for novel interventions to combat the worldwide obesity epidemic.

The human gut microbiome plays a crucial role in regulating intestinal and systemic health, impacting host immune response and metabolic function. Dysbiosis of the gut microbiome is linked to various diseases, including steatotic liver diseases. Metabolic dysfunction-associated steatotic liver disease (MASLD), a chronic liver disease characterized by excess hepatic lipid content and impaired metabolism, is the leading cause of liver disease worldwide. Among the gut microbes, Ruminococcus gnavus (R. gnavus) has garnered attention for its association with inflammatory and metabolic diseases. While R. gnavus abundance correlates to liver fat accumulation, further research is needed to identify a causal role or therapeutic intervention in steatotic liver disease. This review surveys our current understanding of R. gnavus in the development and progression of steatotic liver diseases, highlighting its potential mechanisms through metabolite secretion, and emphasizes the need for comprehensive microbiome analyses and longitudinal studies to better understand R. gnavus' impact on liver health. This knowledge could pave the way for targeted interventions aimed at modulating gut microbiota to treat and prevent MASLD and its comorbidities.

Eating disorders (EDs) are a heterogeneous class of increasing mental disorders that are characterized by disturbances in eating behaviors, body weight regulation, and associated psychological dysfunctions. These disorders create physiological imbalances that alter the diversity and composition of the gut microbiota. While evidence suggests that EDs can arise from epigenetic aberrations, alterations in gut microbial communities may also contribute to the development and/or persistence of EDs through epigenetic mechanisms. Understanding the interplay among gut microbial communities, epigenetic processes, and the risk of EDs provides opportunities for designing preventive and/or therapeutic interventions through gut microbiome modulation. This review highlights how microbiome-based therapeutics and specific dietary interventions can contribute to improving various subtypes of EDs by modulating gut microbial communities and mitigating epigenetic aberrations. First, we briefly review the literature on links between epigenetic aberrations and the pathophysiology of EDs. Second, we examine the potential role of the gut microbiome in the pathogenesis of EDs through epigenetic mechanisms. Next, we explore the associations between EDs and other psychiatric disorders, and examine the potential roles of the microbiome in their pathogenesis. Finally, we present evidence supporting the potential of microbiome-based therapeutics and specific dietary interventions to improve EDs through epigenetic modifications.

Obesity is associated with metabolic and immune perturbations (ie, insulin resistance, increased inflammation, and oxidative stress), circadian rhythm dysregulation, and gut microbial changes that can promote colorectal tumorigenesis. Colorectal cancer (CRC) is the third most incident cancer in the United States. This narrative review examines the effects of intermittend fasting on factors influencing colon tumorigenesis, such as body weight, metabolic and immune markers, circadian rythm, and the gut microbiota in humans. Findings suggest that intermittent fasting regimens can lead to weight loss and shifts in metabolic markers, which could be preventive for CRC but effects on the gut microbiota composition and functions still remains elusive.

Background: Rapid weight gain in early infancy increases the risk of childhood obesity, while exclusive breastfeeding can protect against it, depending on breastmilk composition, maternal diet, and infant gut microbiota. Objective: The objective of this study was to analyze the association between maternal diet, breastmilk components, infant gut microbiota, and weight gain in the first year of life of Mexican breastfed infants. Methods: This longitudinal study included 27 mothers with exclusively breastfed infants (≥5 months of age). We evaluated maternal diet and breastmilk composition at 5 months postpartum (pp), the infant fecal microbiota at 5 and 12 months pp using 16S rRNA gene sequencing, and weight gain as normal, rapid or slow weight gain (NWG, RWG or SWG) in periods 1 (0-5.5 months) and 2 (5.5-12 months). Results: Infants with NWG in periods 1 and 2 made up 51% and 56%, respectively. In period 1, ingested breastmilk protein content was higher for NWG infants than for infants with SWG (p = 0.01), and the protein content was negatively correlated with maternal BMI (r = -0.42, p = 0.02). The genera Veillonella (19.5%), Bifidobacterium (19.5%), and Escherichia-Shigella (16.8%) dominated the microbiota at 5 months. At 12 months, Bacteroides predominated, and the first two genera remained. Breastmilk fat correlated with Veillonella abundance (r = -0.50, p = 0.02) and oligosaccharides with Lachnospiraceae (r = 0.73, p = 0.03) at 5 months. There was a trend of a higher abundance of Bifidobacterium in NWG infants than in other infants in period 1, while infants with RWG and SWG had a higher abundance of Ruminococcus gnavus (p = 0.03) in period 1 and Alistipes in period 2 (p = 0.01), respectively. Conclusions: Breastfeeding shaped the gut microbiota of exclusively breastfed infants, and its structure was associated with infant weight gain trajectories.

Low relative muscle mass was identified to be related to ascending risk of pre-cancerous polyps (adenoma) in recent cohort study. Our study aimed to dig out the correlation between muscle mass and different pathological types of colorectal polyps in Chinese asymptomatic population.

In all, 5923 adults were included. The effects of low skeletal muscle mass index (SMI) on colorectal polyp occurrence, including different pathological types, and the effects modification of age and BMI were analyzed using univariate and multivariate logistic regression.

Lower SMI was connected with the lower occurrence of colorectal polyp (OR: 0.810, 95% CI: 0.683~0.960, p=0.015). Considering different pathological types of colorectal polyps, lower SMI was associated with lower occurrence of inflammatory polyp (OR: 0.633, 95% CI: 0.434~0.898, p=0.013), rather than conventional adenoma and serrated polyp (all p>0.05). Besides, SMI was positively related to the occurrence of 2 pathological types of colorectal polyp in males: inflammatory polyp (OR: 1.237, 95% CI: 1.058~1.444, p=0.007) and serrated polyp (OR: 1.288, 95% CI: 1.143~1.456, p<0.001). The interaction effect of BMI and SMI on occurrence of inflammatory polyp after adjusting age and smoking status was significant (p=0.015). For individuals with low SMI (compared with the normal SMI group), the incidence of inflammatory polyp was reduced from 8.95% to 3.50% in the low BMI quartile (Q1) in the adjusted model (OR of 0.332, 95% CI: 0.005-0.061, p<0.001). It was noticeable for males rather than females that individuals with colorectal polyps had higher levels of SMI (p=0.003). In addition, individuals with inflammatory polyps as well as serrated polyps possessed higher levels of SMI in males (all p<0.05).

Generally, especially in Chinese asymptomatic males, low SMI kept independent effect on the presence of inflammatory polyp and serrated polyp, rather than conventional adenoma.

Understanding the link between prepregnancy nutritional status and gut microbiota during pregnancy may lead to novel maternal and child health interventions.

To explore the association of prepregnancy body mass index (BMI) status with gut microbiota diversity and abundance during pregnancy.

A cross-sectional study was conducted on 90 pregnant women from primary health centers in Jakarta, Indonesia. Trained staff interviewed women on sociodemographic characteristics and nutrient intake, gathered data on prepregnancy BMI from antenatal records, and obtained fecal samples. Samples were analyzed for microbiota diversity indices [Shannon, Faith phylogenetic diversity (Faith PD), and Chao1] and abundance using 16S ribosome ribonucleic acid sequencing. Multivariate logistic regression was performed adjusting for carbohydrate and protein intake, ethnicity, and education to determine the relationship between prepregnancy BMI and the alpha diversity indices and the presence of the phylum Firmicutes and genera Prevotella and Blautia.

Pregnant women who were overweight or obese (BMI ≥23.0 kg/m2) before pregnancy had significantly lower odds of having gut microbiota diversity above the median of the Shannon index [adjusted odds ratio (aOR): 0.37, 95% confidence interval (CI): 0.14, 0.97, P = 0.042], Faith PD (aOR: 0.23, 95% CI: 0.07, 0.75, P = 0.015), and Chao1 (aOR: 0.25, 95% CI: 0.09, 0.67, P = 0.006) compared with those who were neither overweight nor obese. Prepregnant women who were overweight or obese also had significantly lower odds of having levels above the median of the phylum Firmicutes (aOR: 0.38, 95% CI: 0.15, 0.98, P = 0.045) and genus Blautia (aOR: 0.32, 95% CI: 0.12, 0.85, P = 0.022) compared with women who were neither overweight nor obese.

Prepregnancy overweight or obese status was associated with lower gut microbiota diversity and lower abundance of Firmicutes and Blautia among pregnant women in an urban community. These findings suggest that prepregnancy interventions to control BMI may improve gut flora and potentially benefit pregnant women.

Epilepsy causes a heavy disease burden, and the gut microbiota (GM) influences the progression of epilepsy, while plasma metabolites directly or indirectly associated with GM may play a mediating role. However, the causal relationships between epilepsy, GM, and potential metabolite mediators are lack of investigation.

Mendelian randomization (MR) analysis was applied to estimate the effects of GM and plasma metabolites on epilepsy. Genetic instruments were obtained from large-scale genome-wide meta-analysis of GM (n = 5959), plasma metabolites (n = 136,016), and epilepsy (Cases/controls = 12891/312803) of European ancestry. Epilepsy phenotypes included all epilepsy, generalized epilepsy and focal epilepsy from the Finn Gen R10 database. And two-step MR (TSMR) to discover the potential mediating metabolites.

In total, we found 19 gut microbial taxa to be causally associated with the risk of epilepsy, among which Omnitrophota phylum had the strongest association (OR, 2.3; P = 0.009) with promoting effect. We also identified 21 plasma metabolites associated with epilepsy, the strongest ones of which are eastotal fatty acids (OR, 1.12; P = 0.001) that exhibited a facilitating effect. We observed indirect effects of free cholesterol to total lipids ratio in large LDL in associations between Fournierella massiliensis species and epilepsy, with a mediated proportion of -3.64% (95%CI, -7.22%∼-0.06%; P = 0.046).

This study supports a causal link between Fournierella massiliensis species, free cholesterol to total lipids ratio in large LDL and epilepsy, as well as a mediating effect of free cholesterol to total lipids ratio in large LDL in epilepsy.

The association of sorbitol intake with maintaining healthy body weight through the gut microbiome during early life was investigated.

Sorbitol intake, body mass index (BMI), and fecal samples were collected in the total of 369 pregnant women with their infants (aged 4 months to 5 years) from the Taipei Mother-Infant Nutrition Cohort and 1946 children and adolescents (aged 6-18 years) from the Taiwan Puberty Longitudinal Study. The BMI-z score in sorbitol users was compared to that in sorbitol nonusers using generalized linear mixed model. The beta diversity of microbiome was investigated in both cohorts. The association between the richness of microbes and body composition was analyzed.

The children and adolescents with high sorbitol intake had lower BMI-z score at 6 to 10 and 11 to 18 years of age (P < 0.01) compared with those without sorbitol intake. The beta diversity of the microbiome differed significantly between the sorbitol users and nonusers. Bifidobacterium was higher in the gut of infants and children whose mothers were sorbitol users than that of infants and children whose mothers were sorbitol nonusers during pregnancy. Several microbes were involved in the regulation of obesity, such as Staphylococcus, Faecalibacterium, and Oscillospiraceae_UCG-005 negatively associated with anthropometric measures.

Sorbitol intake was associated with lower child and adolescent BMI. Sorbitol consumption could shape the composition and richness of beneficial microbiota, contributing to the maintenance of ideal body weight and metabolic homeostasis in early life.

The effect of luteoloside on the regulation of lipid metabolism imbalance in obese mice and its mechanism were investigated. After 12 weeks of luteoloside (25, 50 and 100 mg/kg), obesity-related indicators were analyzed, such as serum, liver and adipose tissue indexes as well as gut microbiota and liver tissue-related protein expression levels. The results suggested that luteoloside intervention could reduce body fat mass and fat storage, improve lipid levels, glucose tolerance, and alleviate inflammatory disorders, especially in medium-dose treated mice. The serum levels of TC, TG, LDL-C in the HFD + M group decreased by 25.74 %, 42.03 %, 29.61 %, respectively, while HDL-C levels increased by 27.45 %. The levels of ALT and AST decreased by 44.15 % and 33.00 %, respectively. The intervention of luteoloside improved the variegation of gut microbes, more specifically, it balanced homeostasis of gut microbiota in obese mice. Luteoloside could regulate the expression of PPARα protein and down-regulate the expression proteins related to lipid synthesis, thereby inhibiting lipid accumulation and regulating lipid metabolism. The purpose of this study was to elucidate the molecular mechanism of luteoloside regulating lipid metabolism imbalance in obese mice and to provide a rationale for it.

Childhood obesity continues to rise worldwide. Family gut microorganisms may be associated with childhood obesity. The aim of the study was to analyze bacterial similarities in fecal microbiota composition between parent-offspring pairs as linked to body weight.

A total of 146 father/mother and offspring pairs were categorized into four groups according to the weight status of the parent-child pair as follows: group 1, parent and child with normal weight; group 2, parent and child with overweight/obesity; group 3, parent with normal weight and child with overweight/obesity; group 4, parent with overweight/obesity and child with normal weight. Anthropometric measurements and lifestyle assessments were performed in all participants. Microbiota characteristics were determined by 16S ribosomal RNA gene sequencing. Logistic regression models were performed to determine whether the abundance of any bacteria was able to predict childhood obesity. Moreover, receiver operating characteristic curves were fitted to define the relative diagnostic strength of bacterial taxa for the correct identification of childhood obesity.

The absence/abundance of Catenibacterium mitsuokai, Prevotella stercorea, Desulfovibrio piger, Massiliprevotella massiliensis, and Phascolarctobacterium succinatutens was involved in body weight family associations. A positive relationship between P. succinatutens richness from parents and M. massiliensis from children was observed with regard to body weight status (odds ratio, 1.14, P = 0.013).

This study describes five potential gut bacteria that may be putatively involved in family weight status relationships and appear to be useful for predicting obesity.

The gut microbiota has emerged as a critical player in metabolic and liver health, with its influence extending to the pathogenesis and progression of steatotic liver diseases. This review delves into the gut-liver axis, a dynamic communication network linking the gut microbiome and liver through metabolic, immunological, and inflammatory pathways. Dysbiosis, characterized by altered microbial composition, contributes significantly to the development of hepatic steatosis, inflammation, and fibrosis via mechanisms such as gut barrier dysfunction, microbial metabolite production, and systemic inflammation. Dietary patterns, including the Mediterranean diet, are highlighted for their role in modulating the gut microbiota, improving gut-liver axis integrity, and attenuating liver injury. Additionally, emerging microbiota-based interventions, such as fecal microbiota transplantation and bacteriophage therapy, show promise as therapeutic strategies for steatotic liver disease. However, challenges such as population heterogeneity, methodological variability, and knowledge gaps hinder the translational application of current findings. Addressing these barriers through standardized approaches and integrative research will pave the way for microbiota-targeted therapies to mitigate the global burden of steatotic liver disease.

This study prepared enzymatic theabrownins (TBs-e), alkaline theabrownins (TBs-a), and Pu-erh tea theabrownins (TBs-f), and investigated whether different preparation processes affected the structures, nonvolatile metabolites, and biofunctional activities of TBs. Structural characterization revealed that TBs were polymeric phenolic compounds rich in hydroxyl and carboxyl groups. Nontargeted metabolomics revealed that amino acids were the primary nonvolatile metabolites in TBs-e and TBs-a, accounting for over 70 % of the total nonvolatile content. TBs-f contained more polyphenols, caffeine, and flavonoids, accounting for 14.2 %, 3.9 %, and 0.8 % of total nonvolatile content, respectively. In vivo, at 560 mg/kg body weight, TBs-f were associated with regulation of blood glucose and lipid concentrations in mice. Moreover, 16S rRNA indicated that at 1120 mg/kg body weight, TBs-a were associated with increased numbers of microbiota linked with hypolipidemic activity. This study explores the impacts of different preparation processes on TBs and provides a theoretical foundation for the understanding of TBs.

Modern treatment, a healthy diet, and physical activity routines lower the risk factors for metabolic syndrome; however, this condition is associated with all-cause and cardiovascular mortality worldwide. This investigation involved a randomized controlled trial, double-blind, parallel study. Fifty-eight participants with risk factors of metabolic syndrome according to the inclusion criteria were randomized into two groups and given probiotics (Lacticaseibacillus paracasei MSMC39-1 and Bifidobacterium animalis TA-1) (n = 31) or a placebo (n = 27). The participants had a mean age of 42.29 ± 7.39 and 43.89 ± 7.54 years in the probiotics and placebo groups, respectively. Stool samples, anthropometric data, and blood chemistries were taken at baseline and at 12 weeks. The primary outcome was achieved by the probiotics group as their low-density lipoprotein-cholesterol level dramatically lowered compared to the placebo group (the difference was 39.97 ± 26.83 mg/dl, p-value <0.001). Moreover, significant reductions in body weight, body mass index, waist circumference, systolic blood pressure, and total cholesterol were observed in the volunteers treated with probiotics compared to the placebo. In the gut microbiome analysis, the results showed statistically significant differences in the beta diversity in the post-intervention probiotics group. Blautia, Roseburia, Collinsella, and Ruminococcus were among the gut microbiomes that were more prevalent in the post-intervention probiotics group. In addition, this group exhibited increases in the predicted functional changes in ATP-binding cassette (ABC) transporters, as well as ribonucleic acid transport, the biosynthesis of unsaturated fatty acids, glycerophospholipid metabolism, and pyruvate metabolism. In conclusion, this research demonstrated that the probiotics L. paracasei MSMC39-1 and B. animalis TA-1 have the efficacy to lower risk factors associated with metabolic syndrome.