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Gualou-Xiebai-Banxia-Tang regulates liver-gut axis to ameliorate Metabolic Syndrome in HFD-fed mice.
BACKGROUND: Metabolic syndrome (MetS), characterized by obesity, hyperglycemia, and abnormal blood lipid levels, is the pathological basis of many cardiovascular diseases. Gualou-Xiebai-Banxia-Tang decoction (GT) was first described in the Synopsis of the Golden Chamber, the earliest traditional Chinese medicine (TCM) monograph on diagnosis and treatment of miscellaneous diseases in China. According to TCM precepts, based on its ability to activate yang to release stagnation, activate qi to reduce depression, remove phlegm, and broaden the chest, GT has been used for more than 2,000 years to treat cardiovascular ailments. However, the molecular bases of its therapeutic mechanisms remain unclear. PURPOSE: The aim of this study was to identify lipid- and glucose-related hepatic genes differentially regulated by GT, and to assess GT impact on gut microbiota composition, in mice with high-fat diet (HFD)-induced MetS. STUDY DESIGN AND METHODS: ApoE-/- mice were fed with an HFD for 24 weeks, with or without concurrent GT supplementation, to induce MetS. At the study's end, body weight, visceral fat weight, blood lipid levels, and insulin sensitivity were measured, and histopathological staining was used to evaluate hepatosteatosis and intestinal barrier integrity. Liver transcriptomics was used for analysis of differentially expressed genes in liver and prediction of relevant regulatory pathways. Hepatic lipid/glucose metabolism-related genes and proteins were detected by RT-qPCR and western blotting. Gut microbial composition was determined by 16S rRNA gene sequencing. RESULTS: GT administration reduced MetS-related liver steatosis and weight gain, promoted insulin sensitivity and lipid metabolism, and beneficially modulated gut microbiota composition by decreasing the relative abundance of g_Lachnospiraceae_NK4A136_group and increasing the relative abundance of g_Alistipes. Liver transcriptomics revealed that GT regulated the expression of genes related to lipid and glucose metabolism (Pparγ, Igf1, Gpnmb, and Trem2) and of genes encoding chemokines/chemokine receptors (e.g. Cxcl9 and Cx3cr1). Significant, positive correlations were found for Ccr2, Ccl4, Ccr1, and Cx3cr1 and the g_Lachnospiraceae_NK4A136_group, and between Cxcl9, Ccr2, Ccl4, and Cx3cr1 and g_Desulfovibrio. GT treatment downregulated the protein expressions of SCD1 and CX3CR1 and upregulated the expression of PCK1 protein. CONCLUSION: GT supplementation alleviates HFD-induced MetS in mice by improving hepatic lipid and glucose metabolism. The anti-metabolic syndrome effects of GT may be related to the regulation of the gut-liver axis.
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Jianchang No. 1 (1) formula alleviates irritable bowel syndrome with diarrhea improving gut microbiota and regulating toll-like receptors/nuclear factor-kappa B signaling pathway in bowel syndrome with diarrhea rats.
OBJECTIVE: To evaluate the therapeutic efficacy of Jianchang No. 1 (1) in treating irritable bowel syndrome with diarrhea (IBS-D) and to explore its underlying mechanisms of action. METHODS: IBS-D rat models were established through a combination of chronic restraint stress, water avoidance stress, and the administration of senna decoction. Body weight, fecal water content (FWC), and intestinal capacity threshold in IBS-D rats were monitored before and after treatment. Pathological alterations in colon tissue were examined using hematoxylin and eosin staining. Serum levels of lipopolysaccharide (LPS), along with LPS content in colon tissue were measured using the enzyme-linked immunosorbent assay. 16S rRNA sequencing technology was employed to assess the abundance and compositional shifts within the gut microbiota. Quantitative real-time polymerase chain reaction, Western blot, and immunofluorescence were employed to determine gene and protein expression in colonic samples. RESULTS: Jianchang No. 1 treatment restored body weight, lowered FWC, and raised the intestinal capacity threshold in IBS-D rats. Meanwhile, Jianchang No. 1 enhanced both the richness and composition of the gut microbiota. Moreover, Jianchang No. 1 markedly upregulated the tight-junction proteins zonula occludens-1 and occludin together with the anti-inflammatory cytokine interleukin-10, while simultaneously downregulating the LPS-toll-like receptor (TLR) 2/4- myeloid differentiation factor 88- nuclear factor kappa B (NF-κB) axis and the downstream pro-inflammatory mediators interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha, together with interleukin-4 and interferon-gamma. CONCLUSIONS: Jianchang No. 1 maintains intestinal barrier integrity by reshaping gut-microbial diversity and composition, dampening the TLR/NF-κB signaling cascade, and thereby alleviating low-grade colonic inflammation and its attendant clinical symptoms in IBS-D rats.
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FMT from IBS-D Rats Impairs Intestinal Barrier Function and is Associated with Increased Intestinal Benzoic Acid and Ruminococcus Abundance.
While the etiology of diarrhea-predominant irritable bowel syndrome (IBS-D) is multifactorial, current studies have converged to identify gut microbiota dysbiosis as a principal contributor. This study aimed to elucidate the role of the gut microbiota in IBS-D progression and to uncover the underlying mechanisms. In this study, a rat model of IBS-D was successfully established, characterized by prominent visceral hypersensitivity and diarrhea. To assess the impact of the gut microbiota, recipient rats pretreated with broad-spectrum antibiotics underwent fecal microbiota transplantation (FMT) from IBS-D model rats. The model-microbiota recipient rats (the MR group) developed IBS-D-like symptoms, such as abdominal pain, diarrhea, and depression-like behaviors. Both the IBS-D and MR groups exhibited elevated serum diamine oxidase (DAO) concentrations, reduced intestinal tight junction protein levels, increased serum TNF-α concentrations, upregulated TNF-α mRNA expression, and downregulated IL-10 mRNA expression in the intestine. These findings indicated that the transplanted microbiota disrupted intestinal barrier integrity and triggered low-grade inflammation. Moreover, an elevated abundance of Ruminococcaceae in the gut microbiota was a common feature of both the IBS-D and MR groups. Metabolomic analysis revealed an enrichment in the phenylalanine, tyrosine, and tryptophan biosynthesis pathway in both IBS-D and recipient groups, with benzoic acid being particularly prominent. Pearson correlation analysis demonstrated a strong positive correlation between the Ruminococcus abundance and benzoic acid levels. Together, these findings indicated that FMT robustly recapitulated core IBS-D pathophysiology in recipient rats, and the identified bacteria and metabolites provided novel insights into the pathogenesis of IBS-D.
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Bacillus licheniformis prevents and reduces anxiety-like and depression-like behaviours.
As common mental disorders, depression and anxiety impact people all around the world. Recent studies have found that the gut microbiome plays an important role in mental health. It is becoming possible to treat mental disorders by regulating the composition of the gut microbiota. Bacillus licheniformis is a probiotic used to treat gut diseases through balancing the gut microbiome during lasting years. Considering the role of gut microbiota in the gut-brain axis, this study used chronic unpredictable mild stress (CUMS) model rats to explore whether Bacillus licheniformis can prevent and treat depression and anxiety. We found that B. licheniformis reduced the depressive-like and anxiety-like behaviours of the rats during the CUMS process. Meanwhile, B. licheniformis changed the gut microbiota composition; increased the short chain fatty acids (SCFAs) in the colon, decreased kynurenine, norepinephrine, and glutamate levels; and increased the tryptophan, dopamine, epinephrine, and γ-aminobutyric acid (GABA) in the brain. After correlation analysis, we found Parabacteroides, Anaerostipes, Ruminococcus-2, and Blautia showed significant correlation with neurotransmitters and SCFAs, indicating the gut microbiome plays an important role in B. licheniformis reducing depressive-like behaviours. Therefore, this study suggested B. licheniformis may prevent depressive-like and anxiety-like behaviours while regulating the gut microbiota composition and increasing the SCFA levels in the colon to alter the levels of the neurotransmitters in the brain. KEY POINTS: • B. licheniformis reduced depressive-like and anxiety-like behaviours induced by the chronic unpredictable mild stress. • GABA levels in the brain are assonated with B. licheniformis regulating depressive-like and anxiety-like behaviours. • Gut microbiota composition alteration followed by metabolic changes may play a role in the GABA levels increase.
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Sex-based differences in fecal short-chain fatty acid and gut microbiota in irritable bowel syndrome patients.
OBJECTIVE: To explore alterations in fecal short-chain fatty acids (SCFA) and gut microbiota in patients with diarrhea-predominant irritable bowel disease (IBS-D) and their relationships with clinical manifestations. METHODS: We recruited 162 patients with IBS-D and 66 healthy controls (HC). Their manifestations and psychological status were evaluated using the IBS severity scoring system and the Hospital Anxiety and Depression Scale (HADS). Colorectal visceral sensitivity was evaluated using a barostat. Systemic inflammation was evaluated using plasma cytokine levels. Fecal SCFA were quantified using ultra-performance liquid chromatography-tandem mass spectrometry, and fecal microbiota communities were analyzed using 16S rRNA sequencing. RESULTS: More men presented with IBS-D than women in our patient cohort. Patients with IBS-D had more severe manifestations, higher HADS score, and a higher rate of previous infectious enteritis than HC. Notably, female patients had significantly higher HADS scores than male patients. Male patients had significantly higher levels of plasma interleukin (IL)-12, fecal propionate and colorectal visceral sensitivity than male HC, while no differences were observed between female patients and female HC. Fecal acetate, butyrate and valerate correlated with the initial visceral sensory threshold, stressors, and IL-10 and IL-12 levels. The propionate-producing Prevotella 9 genus was significantly increased in male patients and positively correlated with fecal propionate. CONCLUSION: Distinct sex-based differences in clinical manifestations, fecal SCFA and microbiota richness are found in Chinese patients with IBS-D, which may be used to diagnose dysbiosis in these patients.
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Gut microbiota profiling reflects the renal dysfunction and psychological distress in patients with diabetic kidney disease.
BACKGROUND: The gut microbiota plays a pivotal role in the development of diabetes and kidney disease. However, it is not clear how the intestinal microecological imbalance is involved in the context of diabetic kidney disease (DKD), the leading cause of renal failure. OBJECTIVES: To elucidate the gut microbial signatures associated with DKD progression towards end-stage renal disease (ESRD) and explore whether they could reflect renal dysfunction and psychological distress. METHODS: A cross-sectional study was conducted to explore the gut microbial signatures of 29 DKD non-ESRD patients and 19 DKD ESRD patients compared to 20 healthy controls. Differential analysis was performed to detect distinct gut microbial alterations in diversities and taxon abundance of DKD with and without ESRD. Renal dysfunction was estimated by urea, creatinine, and estimated glomerular filtration rate. Psychological distress was assessed using the Self-Rating Anxiety Scale, Self-Rating Depression Scale, Hamilton Anxiety Rating Scale, and Hamilton Depression Rating Scale. RESULTS: Alpha diversity indexes were reduced in DKD patients, particularly those with ESRD. Beta diversity analysis revealed that the gut microbial compositions of DKD patients were different with healthy individuals whereas similar compositions were observed in DKD patients. Taxon differential analysis showed that when compared with the controls, DKD patients exhibit distinct microbial profiles including reduced abundances of butyrate-produced, anti-inflammatory bacteria Faecalibacterium, Lachnospira, Roseburia Lachnoclostridium, and increased abundances of pro-inflammatory bacteria Collinsella, Streptococcus etc. These distinctive genera presented consistent associations with renal dysfunction, as well as psychological distress, especially in DKD patients. CONCLUSIONS: DKD patients, especially those who have progressed to ESRD, exhibit unique characteristics in their gut microbiota that are associated with both renal dysfunction and psychological distress. The gut microbiota may be a significant factor in the deterioration of DKD and its eventual progression to ESRD.
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ESRRA (estrogen related receptor alpha) is a critical regulator of intestinal homeostasis through activation of autophagic flux via gut microbiota.
The orphan nuclear receptor ESRRA (estrogen related receptor alpha) is critical in mitochondrial biogenesis and macroautophagy/autophagy function; however, the roles of ESRRA in intestinal function remain uncharacterized. Herein we identified that ESRRA acts as a key regulator of intestinal homeostasis by amelioration of colonic inflammation through activation of autophagic flux and control of host gut microbiota. Esrra-deficient mice presented with increased susceptibility to dextran sodium sulfate (DSS)-induced colitis with upregulation of intestinal inflammation. In addition, esrra-null mice had depressed AMP-activated protein kinase phosphorylation (AMPK), lower levels of TFEB (transcription factor EB), and accumulation of SQSTM1/p62 (sequestosome 1) with defective mitochondria in intestinal tissues. Esrra-deficient mice showed distinct gut microbiota composition and significantly higher microbial diversity than wild-type (WT) mice. Cohousing or fecal microbiota transplantation from WT mice to Esrra-deficient mice ameliorated DSS-induced colitis severity. Importantly, patients with ulcerative colitis (UC) had significantly decreased ESRRA expression in intestinal mucosal tissues that correlated with disease activity, suggesting clinical relevance of ESRRA in UC. Taken together, our results show that ESRRA contributes to intestinal homeostasis through autophagy activation and gut microbiota control to protect the host from detrimental inflammation and dysfunctional mitochondria.Abbreviations: ABX, antibotics; AMPK, AMP-activated protein kinase; ATP5A1, ATP synthase, H+ transporting, mitochondrial F1 complex, alpha subunit 1; BECN1, beclin1, autophagy related, CCL, C-C motif chemokine ligand; CD, Crohn disease; CLDN, claudin; COX4I1, cytochrome c oxidase subunit 4I1; cKO, conditional knockout; cWT, conditional wild-type; CXCL, C-X-C motif chemokine ligand; DAI, disease activity index; DSS, dextran sodium sulfate; EGFP, enhanced green fluorescent protein; ESRR, estrogen related receptor; ESRRA, estrogen related receptor alpha; Esrra+/+, Esrra wild type; esrra-/-, esrra homozygous knockout; FMT, fecal microbiota transplantation; GABARAP, gamma-aminobutyric acid receptor associated protein; GSEA, gene set enrichment analysis; IBD, inflammatory bowel disease; IL, interleukin; KO, knockout; LAMP1, lysosomal-associated membrane protein 1; LCN2, lipocalin 2; LEfSe, linear discriminant analysis (LDA) effect size; LPS, lipopolysachharide; MAP1LC3/LC3, microtubule associated protein 1 light chain 3; NDUFAB1, NADH: ubiquinone oxidoreductase subunit AB1; OCLN, occludin; OUT, operational taxonomic unit; OXPHOS, oxidative phosphorylation; PCoA, principal coordinate analysis; PPARGC1A, PPARG coactiva- tor 1 alpha; PRKAA, 5'-AMP-activated protein kinase catalytic subunit alpha; PTGS2/COX2, prostaglandin-endoperoxide synthase 2; RAB7, member RAS oncogene family; SDHB, succinate dehydrogenase complex, subunit B, iron sulfur (Ip); SQSTM1/p62, sequestosome 1; S100A9, S100 calcium binding protein A9 (calgranulin B); TCA, tricarboxylic acid; TFEB, transcription factor EB; TNF, tumor necrosis factor; UC, ulcerative colitis; UCP2, uncoupling protein 2 (mitochondrial, proton carrier); UQCRC1, ubiquinol-cytochrome c reductase core protein 1; UVRAG, UV radiation resistance associated gene; Vil1, villin; VPS11, VPS11, CORVET/HOPS core sub-unit; WT, wild type.
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Fecal transplant prevents gut dysbiosis and anxiety-like behaviour after spinal cord injury in rats.
Secondary manifestations of spinal cord injury beyond motor and sensory dysfunction can negatively affect a person's quality of life. Spinal cord injury is associated with an increased incidence of depression and anxiety; however, the mechanisms of this relationship are currently not well understood. Human and animal studies suggest that changes in the composition of the intestinal microbiota (dysbiosis) are associated with mood disorders. The objective of the current study is to establish a model of anxiety following a cervical contusion spinal cord injury in rats and to determine whether the microbiota play a role in the observed behavioural changes. We found that spinal cord injury caused dysbiosis and increased symptoms of anxiety-like behaviour. Treatment with a fecal transplant prevented both spinal cord injury-induced dysbiosis as well as the development of anxiety-like behaviour. These results indicate that an incomplete unilateral cervical spinal cord injury can cause affective disorders and intestinal dysbiosis, and that both can be prevented by treatment with fecal transplant therapy.
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The impact of DASH diet and concurrent training on cardiometabolic risk factors and gut microbiota in individuals with ischemic heart disease: a study protocol for a randomized controlled trial.
BACKGROUND: Ischemic heart disease (IHD) has a substantial burden on individuals and health system infrastructure worldwide. Meanwhile, mounting evidence has declared remarkable contrasts in gut microbiota between individuals with IHD and healthy counterparts. The Dietary Approaches to Stop Hypertension (DASH) might be one of the most reliable strategies to manage cardiometabolic risk factors. Nonetheless, no experiment has tested the impact of a DASH diet and exercise on gut microbiota composition in IHD individuals. Hence, we aim to explore the effects of a DASH diet and concurrent exercise on gut microbiota, oxidized LDL, and cardiometabolic risk factors among men. METHODS: In total, 48 men aged 40-70 years with IHD will be recruited in this parallel randomized, controlled, 2 × 2 factorial clinical trial. These patients will be randomly assigned to the following four intervention groups: DASH diet (D), concurrent exercise (E), concurrent DASH diet and exercise (DE), and control (usual care) (C) for 8 weeks. At baseline and the end of the study, stool samples and serum levels will be gathered to detect gut microbiota (Firmicutes, Bacteroidetes, Bifidobacteria, clostridium, Faecalibacterium prausnitzi, Bacteroidetes, and Akkermansia muciniphila) and cardiometabolic risk factors, as well as anthropometric measures, blood pressure, quality of life, 6-min walking test, and Beck Depression Inventory (BDI). DISCUSSION: Based on our information, the present study is the primary randomized controlled trial testing the impacts of short-term concurrent training and DASH diet on intestinal bacteria diversity and several cardiometabolic risk factors in men with IHD. TRIAL REGISTRATION: Iranian Registry of Clinical Trials (www.irct.ir, IRCT20181205041859N1). Registered on 29 September 2024.
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Low fermentable, oligo-, di-, mono-saccharides and polyol diet in the treatment of irritable bowel syndrome: A systematic review and meta-analysis.
OBJECTIVES: The aim of this review was to systematically assess and meta-analyze the effects of a low fermentable, oligo-, di-, mono-saccharides and polyol (FODMAP) diet (LFD) on the severity of symptoms, quality of life, and safety in patients with irritable bowel syndrome (IBS). METHODS: The MEDLINE/PubMed, Scopus, and Cochrane Library databases were screened through January 19, 2016. Randomized controlled trials (RCTs) that compared LFD to other diets were included if they assessed symptoms of IBS or abdominal pain in patients with IBS. Safety, quality of life, anxiety, depression, and effect on gut microbiota were defined as secondary outcomes. Standardized mean difference (SMD) and 95% confidence interval (CI) were calculated. RESULTS: Nine RCTs with a total of 596 subjects were included. Three RCTs compared LFD with a habitual diet, two RCTs provided all meals and compared LFD with a western diet, one RCT each compared LFD with a diet high in FODMAPs or a sham diet, and two RCTs compared with other diet recommendations for IBS. A meta-analysis revealed significant group differences for LFD compared with other diets with regard to gastrointestinal symptoms (SMD = -0.62; 95% CI = -0.93 to -0.31; P = 0.0001), abdominal pain (SMD = -0.50; 95% CI = -0.77 to -0.22; P = 0.008), and health-related quality of life (SMD = 0.36; 95% CI = 0.10-0.62; P = 0.007). Three studies reported a significant reduction in luminal bifidobacteria after LFD. Adverse events were assessed in three RCTs only and no intervention-related adverse events were reported. CONCLUSIONS: This meta-analysis found evidence of the short-term efficacy and safety of LFD in patients with IBS. However, only a preliminary recommendation for LFD can be made until long-term effects are investigated.