• gut microbiota
• human health
• lactic acid bacteria
• metabolic disorders
• obesity

• American College students
• cardiometabolic risk markers
• diet quality
• fermentable carbohydrates
• gut microbiome

• Cost-effectiveness
• Gastric cancer
• Helicobacter pylori
• Intervention trial
• Precision prevention

• Apoe −/−  mice
• Lactiplantibacillus plantarum ATCC 14917
• Atherosclerosis
• Inflammation

• Animals
• Probiotics/administration & dosage
• Probiotics/pharmacology
• Plaque, Atherosclerotic
• Mice
• Atherosclerosis/microbiology
• Apolipoproteins E/genetics
• Male
• Disease Models, Animal
• Mice, Knockout
• Diet, High-Fat
• Lactobacillus plantarum
• Cytokines/metabolism
• Mice, Inbred C57BL
• Inflammation

• jfkyjf202203001 the Science and Technology Innovation Project of Jinfeng Laboratory, Chongqing, China
• jfkyjf202203001 the Science and Technology Innovation Project of Jinfeng Laboratory, Chongqing, China
• 31971242, 12032007 the National Natural Science Foundation of China

• obesity

• Humans
• Female
• Pregnancy
• Pregnancy in Obesity
• Dysbiosis
• Obesity/therapy
• Microbiota
• Cardiovascular Diseases

• Epistasis
• GWAS
• Interaction model
• Linear regression
• Partial correlation
• XOR

• R01 LM010098 NLM NIH HHS
• U01 AG066833 NIA NIH HHS
• R01 LM010098 NIH HHS
• National Institutes of Health

• antiobesity mechanism
• obesity
• polysaccharides
• structural-property
• traditional Chinese medicine

• BMI
• eating disorders
• mastocytosis
• microbiome

• 01-10022/0000679/01/231/231/0/2022 Medical University of Gdansk
• 01-10023/0004956/01/231/231/0/2023 Medical University of Gdansk

• Gut microbiota
• Panax ginseng
• ginseng glycosides
• ginseng metabolites
• immunity
• probiotics.

• Panax
• Humans
• Gastrointestinal Microbiome/drug effects
• Gastrointestinal Microbiome/physiology
• Animals
• Plant Extracts/pharmacology
• Ginsenosides/pharmacology
• Ginsenosides/isolation & purification
• Ginsenosides/metabolism

• C57BL/6 mice
• antiobesity
• catechin
• kimchi
• lactic acid bacteria (LAB)

• Animals
• Mice
• Catechin/pharmacology
• Catechin/metabolism
• Lactobacillales/metabolism
• Mice, Inbred C57BL
• Anti-Obesity Agents/pharmacology
• Liver/metabolism
• Diet, High-Fat/adverse effects
• Cholesterol
• Fermented Foods

• SCFAs
• butyrate
• gut microbiota
• metabolic disease
• obesity

• Humans
• Butyrates/pharmacology
• Obesity/metabolism
• Fatty Acids, Volatile/metabolism
• Risk Factors
• Weight Loss

• National Natural Science Foundation of China

• 16S rRNA sequencing
• Dairy cow
• Gut microbiome
• Hyperketonemia
• Metagenomics

Obesity in pregnancy induces metabolic syndrome, low-grade inflammation, altered endocrine factors, placental function, and the maternal gut microbiome. All these factors impact fetal growth and development, including brain development. The lipid metabolic transporters of the maternal-fetal-placental unit are dysregulated in obesity. Consequently, the transport of essential long-chain PUFAs for fetal brain development is disturbed. The mother’s gut microbiota is vital in maintaining postnatal energy homeostasis and maternal-fetal immune competence. Obesity during pregnancy changes the gut microbiota, affecting fetal brain development. Obesity in pregnancy can induce placental and intrauterine inflammation and thus influence the neurodevelopmental outcomes of the offspring. Several epidemiological studies observed an association between maternal obesity and adverse neurodevelopment. This review discusses the effects of maternal obesity and gut microbiota on fetal neurodevelopment outcomes. In addition, the possible mechanisms of the impacts of obesity and gut microbiota on fetal brain development are discussed.

• Africa
• amino acids
• fatty acids
• human milk
• human milk oligosaccharides (HMOs)

• Female
• Humans
• Infant
• Amino Acids/metabolism
• Breast Feeding
• Central African Republic
• Diet
• Fatty Acids/metabolism
• Food Insecurity
• Lactose/analysis
• Milk, Human/chemistry
• Oligosaccharides/analysis
• Vitamin A/metabolism

• 91-17 Institut Pasteur
• ANR-16-COV-005 Labex IBEID

Alterations in the oral or gut microbiotas have been reported in patients with subjective and mild cognitive impairment or AD dementia. However, whether these microbiotas change with the severity of the AD spectrum (mild, moderate, and severe AD) remains unknown. Thus, we compared alterations in the composition and gene functions of the oral and gut microbiota between different phases of AD.

We recruited 172 individuals and classified these into three groups: healthy controls (n = 40), a mild AD group (n = 43) and a moderate AD group (n = 89). Subgingival plaques and fecal samples were collected from all individuals. Then, we conducted 16S ribosomal RNA. sequencing to analyze the microbiotas.

In order of the severity of cognition impairment (from normal to mild and to moderate AD), the oral abundances of the phyla Firmicutes and Fusobacteria showed a gradual upwards trend, while the abundance of the Proteobacteria phylum gradually decreased. In contrast, the abundance of the Firmicutes and Bacteroidetes phyla in the gut decreased progressively, while that of the Proteobacteria, Verrucomicrobia and Actinobacteria phyla increased gradually. Key differences were identified in the microbiomes when compared between the mild AD and moderate AD groups when applying the linear discriminant analysis effect size (LEfSe) algorithm. LEfSe analysis revealed alterations that were similar to those described above; furthermore, different bacterial taxa were associated with MMSE scores and age. KEGG analysis showed that the functional pathways associated with the oral microbiota were mainly involved in membrane transport and carbohydrate metabolism, while the gene functions of the fecal microbiota related to metabolism of amino acids, energy, cofactors and vitamins; identified significant differences among the three groups. Venn diagram analysis revealed that the number of genera that were present in both the oral and gut microbiota increased progressively from NC to mild AD and then to moderate AD.

This study is the first to report a comparative analysis of the oral and fecal microbiota of patients with mild and moderate AD. The compositions and functions of the oral and gut microbiotas differed when compared between different stages of AD.

• Alzheimer Disease
• Feces/microbiology
• Firmicutes/genetics
• Gastrointestinal Microbiome/genetics
• Humans
• Proteobacteria/genetics
• RNA, Ribosomal, 16S/genetics
• Verrucomicrobia/genetics

• Adiposity
• Epigenetics
• Infant feeding
• Microbiome
• Programming

• fat–gut axis
• gut microbiota
• gut–brain axis
• intestinal permeability
• leaky gut
• low-grade inflammation
• microbial metabolites
• obesity

• Gastrointestinal Microbiome
• Humans
• Inflammation/etiology
• Microbiota
• Obesity/etiology

• PRIN2020NCKXBR Ministry of University and Research

• DHA
• apoptosis
• gut microbiota
• lipopolysaccharide
• liver

• National Natural Science Foundation of China

Overweight and obesity are growing health problems in domestic cats, increasing the risks of insulin resistance, lipid dyscrasias, neoplasia, cardiovascular disease, and decreasing longevity. The signature of obesity in the feline gut microbiota has not been studied at the whole-genome metagenomic level. We performed whole-genome shotgun metagenomic sequencing in the fecal samples of eight overweight/obese and eight normal cats housed in the same research environment. We obtained 271 Gbp of sequences and generated a 961-Mbp de novo reference contig assembly, with 1.14 million annotated microbial genes. In the obese cat microbiome, we discovered a significant reduction in microbial diversity (P < 0.01) and Firmicutes abundance (P = 0.005), as well as decreased Firmicutes/Bacteroidetes ratios (P = 0.02), which is the inverse of obese human/mouse microbiota. Linear discriminant analysis and quantitative PCR (qPCR) validation revealed significant increases of Bifidobacterium sp., Olsenella provencensis, Dialister sp.CAG:486, and Campylobacter upsaliensis as the hallmark of obese microbiota among 400 enriched species, whereas 1,525 bacterial species have decreased abundance in the obese microbiome. Phascolarctobacterium succinatutens and an uncharacterized Erysipelotrichaceae bacterium are highly abundant (>0.05%) in the normal gut with over 400-fold depletion in the obese microbiome. Fatty acid synthesis-related pathways are significantly overrepresented in the obese compared with the normal cat microbiome. In conclusion, we discovered dramatically decreased microbial diversity in obese cat gut microbiota, suggesting potential dysbiosis. A panel of seven significantly altered, highly abundant species can serve as a microbiome indicator of obesity. Our findings in the obese cat microbiome composition, abundance, and functional capacities provide new insights into feline obesity.

IMPORTANCE Obesity affects around 45% of domestic cats, and licensed drugs for treating feline obesity are lacking. Physical exercise and calorie restrictions are commonly used for weight loss but with limited efficacy. Through comprehensive analyses of normal and obese cat gut bacteria flora, we identified dramatic shifts in the obese gut microbiome, including four bacterial species significantly enriched and two species depleted in the obese cats. The key bacterial community and functional capacity alterations discovered from this study will inform new weight management strategies for obese cats, such as evaluations of specific diet formulas that alter the microbiome composition, and the development of prebiotics and probiotics that promote the increase of beneficial species and the depletion of obesity-associated species. Interestingly, these bacteria identified in our study were also reported to affect the weight loss success in human patients, suggesting translational potential in human obesity.

• Bifidobacterium
• Campylobacter
• Dialister
• Erysipelotrichaceae
• Firmicutes-to-Bacteroidetes ratio
• Olsenella
• feline obesity
• gut microbiota

Obesity has reached pandemic proportions in the last few decades. The global increase in obesity has contributed to an increase in the number of pregnant women with pre-pregnancy obesity or with excessive gestational weight gain. Obesity during pregnancy is associated with higher incidence of maternal co-morbidities such as gestational diabetes and hypertension. Both obesity during pregnancy and its associated complications are not only associated with immediate adverse outcomes for the mother and their newborns during the perinatal period but, more importantly, are linked with long-term morbidities in the offsprings. Neonates born to women with obesity are at higher risk for cardiac complications including cardiac malformations, and non-structural cardiac issues such as changes in the microvasculature, e.g., elevated systolic blood pressure, and overt systemic hypertension. Pulmonary diseases associated with maternal obesity include respiratory distress syndrome, asthma during childhood and adolescence, and adulthood diseases, such as chronic obstructive pulmonary disease. Sequelae of short-term complications compound long-term outcomes such as long-term obesity, hypertension later in life, and metabolic complications including insulin resistance and dyslipidemia. Multiple mechanisms have been proposed to explain these adverse outcomes and are related to the emerging knowledge of pathophysiology of obesity in adults. The best investigated ones include the role of obesity-mediated metabolic alterations and systemic inflammation. There is emerging evidence linking metabolic and immune derangements to altered biome, and alteration in epigenetics as one of the intermediary mechanisms underlying the adverse outcomes. These are initiated as part of fetal adaptation to obesity during pregnancy which are compounded by rapid weight gain during infancy and early childhood, a known complication of obesity during pregnancy. This newer evidence points toward the role of specific nutrients and changes in biome that may potentially modify the adverse outcomes observed in the offsprings of women with obesity.

• cardiac outcomes
• gestational weight gain (GWG)
• obesity
• pregnancy
• pulmonary outcomes

• gut microbiota
• metabolic syndrome
• osteoarthritis
• systemic inflammation

• Animals
• Dysbiosis/immunology
• Dysbiosis/microbiology
• Gastrointestinal Microbiome/immunology
• Humans
• Intestinal Mucosa/immunology
• Intestinal Mucosa/microbiology
• Osteoarthritis/etiology
• Osteoarthritis/immunology
• Osteoarthritis/microbiology

• adipose tissues
• energy metabolism
• gut microbiota
• inflammation
• obesity

• Adipose Tissue/metabolism
• Energy Metabolism/physiology
• Gastrointestinal Microbiome/physiology
• Humans
• Insulin Resistance
• Obesity/metabolism

• Adults
• Bariatric surgery
• Malnutrition
• Microbiota
• Obesity

• Bariatric Surgery
• Humans
• Malnutrition/complications
• Micronutrients
• Obesity, Morbid/surgery
• Quality of Life

• Cognitive impairment
• Gut microbiota
• Mini-Mental State Examination (MMSE)
• Montreal Cognitive Assessment (MoCA)
• Stroke

• Clostridiales
• Cognitive Dysfunction/etiology
• Dysbiosis
• Gastrointestinal Microbiome
• Humans
• RNA, Ribosomal, 16S/genetics

Eosinophilic oesophagitis (EoE) is a chronic, allergic disease associated with a T-lymphocyte response inducing esophageal eosinophilic infiltration in the esophagus. Inflammation and tissue fibrosis are responsible for the main clinical symptoms such as food impaction and dysphagia. The etiopathogenesis is multifactorial in which genetic and environmental factors coexist. The most common trigger is a non-IgE-mediated food allergy to milk, wheat, egg, soybean, nuts, fish, and seafood. The second factor we focus on is the contribution of genetic variation to the risk of EoE, describing the expression profile of selected genes associated with eosinophilic oesophagitis. We raise the topic of treatment, aiming to eliminate inflammation through an elimination diet and/or use of pharmacologic therapy with the use of proton pump inhibitors or steroids and endoscopic procedures to dilate the esophagus. We demonstrate that early diagnosis and effective treatment prevent the development of food impaction and decreased quality of life. The increasing presence of EoE requires bigger awareness among medical specialists concerning clinical features, the course of EoE, diagnostic tools, and management strategies.

• diet therapy
• environmental factors
• eosinophilic esophagitis
• genetic factors
• microbiome
• molecular mechanism

• crosstalk
• dysbiosis
• human diseases
• metabolites
• microbiota

• Dysbiosis/metabolism
• Female
• Gastrointestinal Microbiome
• Health Status
• Humans
• Male
• Microbiota
• Mouth/microbiology
• Respiratory System/microbiology
• Skin/microbiology
• Urogenital System/microbiology
• Vagina/microbiology

• Atherosclerosis
• Human umbilical cords mesenchymal stem cells
• Inflammation
• Rabbit
• TMAO

• Animals
• Aorta
• Diet, High-Fat/adverse effects
• Disease Models, Animal
• Humans
• Mesenchymal Stem Cells
• Plaque, Atherosclerotic/therapy
• Rabbits
• Umbilical Cord

• Chinese Academy of Medical Sciences
• 2020 discipline construction project-special construction

• anti-bacterial agents
• cohort studies
• obesity
• republic of Korea

• gut microbiome
• ileal damage
• inflammation
• ramulus mori (sangzhi) alkaloids
• type 2 diabetes

• adiposity
• chronic diseases
• gut microbiota
• inflammation
• iron metabolism
• obesity

Intestinal epithelial cell tight junctions (TJs) contribute to the integrity of the intestinal barrier allowing for control of the physical barrier between external antigens or bacterial products and the internal environment. Zonula occludens-1 (ZO-1) is a protein that modulates intestinal TJs, and serum levels of ZO-1 has been suggested as a biomarker of disrupted barrier function in humans. Previous studies suggested that increased intestinal permeability was associated with evidence of TJ abnormalities. However, there is limited information on the serological measurement of ZO-1 and its relation to other tests of barrier function in healthy subjects. We investigated the correlation of serum ZO-1, with physiologic measures of intestinal permeability (as the ratio of the fractional excretion of lactulose-mannitol or LMR) in a cohort of 39 healthy FDRs of Crohn's disease (CD) patients. No significant correlation was found between LMR and ZO-1 levels (r2 = 0.004, P < 0.71), or intestinal fatty acid binding proteins (I-FABP) (r2 = 0.004, P < 0.71). In conclusion, our data show that ZO-1 and I-FABP are not a marker of gut permeability as defined by LMR.

• gut barrier
• inflammatory bowel disease
• intestinal fatty acid binding proteins
• lactulose-mannitol ratio test
• zonulin

Cooked common beans (Phaseolus vulgaris) improve intestinal health in lean mice and attenuate intestinal dysbiosis and inflammation when consumed concurrent with obesity development. We determined the effects of a high-fat (HF) bean supplemented diet in mice with established obesity (induced by 12 weeks of HF diet (60% fat as kcal)) compared to obese mice consuming a HF or low-fat (LF) weight loss control diet. Obese C57BL/6 male mice remained consuming HF for eight weeks or were randomly switched from HF to an isocaloric HF with 15.7% cooked navy bean powder diet (HF→HFB) or LF (11% fat as kcal; HF→LF) (n = 12/group). HF→HFB improved the obese phenotype, including (i) fecal microbiome (increased Prevotella, Akkermansia muciniphila, and short-chain fatty acid levels), (ii) intestinal health (increased ZO-1, claudin-2, Muc2, Relmβ, and Reg3γ expression), and (iii) reduced adipose tissue (AT) inflammatory proteins (NFκBp65, STAT3, IL-6, MCP-1, and MIP-1α), versus HF (p < 0.05). Conversely, HF→LF reduced body weight and circulating hormones (leptin, resistin, and PAI-1) versus HF and HF→HFB (p < 0.05); however, AT inflammation and intestinal health markers were not improved to the same degree as HF→HFB (p < 0.05). Despite remaining on a HF obesogenic diet, introducing beans in established obesity improved the obese phenotype (intestinal health and adipose inflammation) more substantially than weight loss alone.

• adipose tissue inflammation
• caloric restriction
• epithelial barrier
• intestinal health
• navy beans
• obesity

• SCFAs
• TMAO
• atherosclerosis
• cardiovascular diseases
• gut microbiota
• hypertension

• CVD
• GPIIb-IIIa
• TMA
• TMAO
• atherosclerosis
• hypertension
• microbiota
• platelet
• platelet hyperactivity
• polyphenols
• short-chain fatty acids

Obesity is a major risk factor for developing gallstone disease (GSD). Previous studies have shown that obesity is associated with an elevated Firmicutes/Bacteroidetes ratio in the gut microbiota. These findings suggest that the development of GSD may be related to gut dysbiosis. This review presents and summarizes the recent findings of studies on the gut microbiota in patients with GSD. Most of the studies on the gut microbiota in patients with GSD have shown a significant increase in the phyla Firmicutes (Lactobacillaceae family, genera Clostridium, Ruminococcus, Veillonella, Blautia, Dorea, Anaerostipes, and Oscillospira), Actinobacteria (Bifidobacterium genus), Proteobacteria, Bacteroidetes (genera Bacteroides, Prevotella, and Fusobacterium) and a significant decrease in the phyla Bacteroidetes (family Muribaculaceae, and genera Bacteroides, Prevotella, Alistipes, Paludibacter, Barnesiella), Firmicutes (genera Faecalibacterium, Eubacterium, Lachnospira, and Roseburia), Actinobacteria (Bifidobacterium genus), and Proteobacteria (Desulfovibrio genus). The influence of GSD on microbial diversity is not clear. Some studies report that GSD reduces microbial diversity in the bile, whereas others suggest the increase in microbial diversity in the bile of patients with GSD. The phyla Proteobacteria (especially family Enterobacteriaceae) and Firmicutes (Enterococcus genus) are most commonly detected in the bile of patients with GSD. On the other hand, the composition of bile microbiota in patients with GSD shows considerable inter-individual variability. The impact of GSD on the Firmicutes/Bacteroidetes ratio is unclear and reports are contradictory. For this reason, it should be stated that the results of reviewed studies do not allow for drawing unequivocal conclusions regarding the relationship between GSD and the Firmicutes/Bacteroidetes ratio in the microbiota.

• Bacteroidetes
• Firmicutes
• bilemicrobiota
• gallstone patients
• gutmicrobiota

• chronic diseases
• diabetes
• diet
• gut microbiota
• obesity

• atherosclerosis
• dyslipidemia
• gut microbiota
• lipid metabolism
• metabolism
• microbiome
• probiotic

A high fat Western-style diet leads to hepatic steatosis that can progress to steatohepatitis and ultimately cirrhosis or liver cancer. The mechanism that leads to the development of steatosis upon nutritional overload is complex and only partially understood. Using click chemistry-based metabolic tracing and microscopy, we study the interaction between Kupffer cells and hepatocytes ex vivo. In the early phase of steatosis, hepatocytes alone do not display significant deviations in fatty acid metabolism. However, in co-cultures or supernatant transfer experiments, we show that tumor necrosis factor (TNF) secretion by Kupffer cells is necessary and sufficient to induce steatosis in hepatocytes, independent of the challenge of hepatocytes with elevated fatty acid levels. We further show that free fatty acid (FFA) or lipopolysaccharide are both able to trigger release of TNF from Kupffer cells. We conclude that Kupffer cells act as the primary sensor for both FFA overload and bacterial lipopolysaccharide, integrate these signals and transmit the information to the hepatocyte via TNF secretion. Hepatocytes react by alteration in lipid metabolism prominently leading to the accumulation of triacylglycerols (TAGs) in lipid droplets, a hallmark of steatosis.

• lipids/chemistry
• metabolic disease
• non-alcoholic fatty liver disease
• nutrition/lipids

• Animals
• Click Chemistry/methods
• Diet, High-Fat/adverse effects
• Disease Models, Animal
• Fatty Acids, Nonesterified/metabolism
• Fatty Acids, Nonesterified/physiology
• Fatty Liver/etiology
• Fatty Liver/metabolism
• Hepatocytes/metabolism
• Hepatocytes/physiology
• Inflammation/metabolism
• Kupffer Cells/metabolism
• Kupffer Cells/physiology
• Lipid Metabolism/physiology
• Lipids/physiology
• Liver/metabolism
• Liver/pathology
• Male
• Mice
• Mice, Inbred C57BL
• Non-alcoholic Fatty Liver Disease/etiology
• Non-alcoholic Fatty Liver Disease/metabolism
• Tumor Necrosis Factor-alpha

The proper communication between gut and brain is pivotal for the maintenance of health and, dysregulation of the gut-brain axis can lead to several clinical disorders. In Parkinson’s disease (PD) 85% of all patients experienced constipation many years before showing any signs of motor phenotypes. For differential diagnosis and preventive treatment, there is an urgent need for the identification of biomarkers indicating early disease stages long before the disease phenotype manifests. DJ-1 is a chaperone protein involved in the protection against PD and genetic mutations in this protein have been shown to cause familial PD. However, how the deficiency of DJ-1 influences the risk of PD remains incompletely understood. In the present study, we provide evidence that DJ-1 is implicated in shaping the gut microbiome including; their metabolite production, inflammation and innate immune cells (ILCs) development. We revealed that deficiency of DJ-1 leads to a significant increase in two specific genera/species, namely Alistipes and Rikenella. In DJ-1 knock-out (DJ-1^-/-) mice the production of fecal calprotectin and MCP-1 inflammatory proteins were elevated. Fecal and serum metabolic profile showed that malonate which influences the immune system was significantly more abundant in DJ-1^−/− mice. DJ-1 appeared also to be involved in ILCs development. Further, inflammatory genes related to PD were augmented in the midbrain of DJ-1^−/− mice. Our data suggest that metabolites and inflammation produced in the gut could be used as biomarkers for PD detection. Perhaps, these metabolites and inflammatory mediators could be involved in triggering inflammation resulting in PD pathology.

Atherosclerosis is the leading cause of cardiovascular mortality and morbidity worldwide and is described as a complex disease involving several different cell types and their molecular products. Recent studies have revealed that atherosclerosis arises from a systemic inflammatory process, including the accumulation and activities of various immune cells. However, the immune system is a complicated network made up of many cell types, hundreds of bioactive cytokines, and millions of different antigens, making it challenging to readily define the associated mechanism of atherosclerosis. Nevertheless, we previously reported a potential persistent inflammatory process underlying atherosclerosis development, centered on a pathological humoral immune response between commensal microbes and activated subpopulations of substantial B cells in the vicinity of the arterial adventitia. Accumulating evidence has indicated the importance of gut microbiota in atherosclerosis development. Commensal microbiota are considered important regulators of immunity and metabolism and also to be possible antigenic sources for atherosclerosis development. However, the interplay between gut microbiota and metabolism with regard to the modulation of atherosclerosis-associated immune responses remains poorly understood. Here, we review the mechanisms by which the gut microbiota may influence atherogenesis, with particular focus on humoral immunity and B cells, especially the gut-immune-B2 cell axis.

Graphical abstract