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Bound Phenolics Enhance the Antidepressant-Like Effect of Triticale Bran Insoluble Dietary Fiber in Obese Mice: Evidence for the Involvement of Immune Regulation and Microbiota Modulation.
The high comorbidity of obesity and depression causes serious public health events when systemic inflammation induced by disturbed immunity and gut microbiota is supposed to be involved. Previously, the promoting effect of triticale bran insoluble dietary fiber (TIDF) on anti-inflammatory bacteria besides inhibiting proinflammatory bacteria was uncovered with bound phenolics (BPs) in it of great importance, while the potential effects of TIDF on obesity-concomitant depression have not been reported yet. This study found that TIDF treatment could relieve depression-like behavior, systemic inflammation, and Th17/Treg imbalance in obese mice. The regulation of microbiota-derived SCFAs was closely involved. Besides down-regulating harmful bacteria while boosting Alistipes and Candidatus_Saccharimonas by both TIDF and its BPs-removed counterpart (T-D), BPs enhanced the microbiota-modulating effects of TIDF on specific SCFAs-producing genera, including Lachnospiraceae_NK4A136_group and Eubacterium_xylanophilum_group. Our study was deemed to promote the application of food nutritional factors in relieving obesity-concomitant emotional disturbance.
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The gut microbiota alleviates depression by remodeling gut-brain energy metabolism.
Although peripheral-brain crosstalk regulates energy metabolism, its role in depression remains unclear. Here, we used metabolic profiling to reveal elevated fecal creatine alongside reduced plasma and cerebrospinal fluid creatine in both patients with depression and mouse depression models. Exogenous creatine produced antidepressant-like effects mediated by gut microbiota. Bifidobacterium pseudolongum was identified as a significantly reduced gut bacterial species in depression, correlating with impaired creatine absorption. Subsequent supplementation with Bifidobacterium enhanced the antidepressant effects of creatine. Mechanistically, B. pseudolongum-derived acetate promoted the creatine transporter (Slc6a8) expression in intestinal epithelial cells via histone acetylation. The Slc6a8 mediated the antidepressant-like effects of creatine. Neuronal creatine deficiency influenced energetic metabolism and neurophysiological function. In patients with depression taking antidepressants, co-administration of creatine and Bifidobacterium increased plasma creatine levels and reduced depression scores. These findings identify the Bifidobacterium-creatine combination as a promising antidepressant strategy and highlight the critical role of gut-brain energy metabolism in depression.
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Fecal microbiota transplantation from chronic unpredictable mild stress mice donors affects anxiety-like and depression-like behavior in recipient mice via the gut microbiota-inflammation-brain axis.
Recent studies have demonstrated that there are significant changes in the gut microbiota (GM) of humans with depression and animal models of depression and chronic stress. In our present study, we determined whether an alteration in GM is a decisive factor in anxiety-like and depression-like behavior and its impact on brain neurochemistry. An antibiotic cocktail was used to deplete the GM of mice before they were colonized, via fecal microbiota transplantation (FMT), by the GM of control mice or mice that had been exposed to chronic unpredictable mild stress (CUMS donors). The CUMS-donor group of mice and the mice that were colonized by their microbiota (the CUMS-recipient group) both showed higher levels of anxiety- and depression-like behavior compared to the controls. The GM community of the CUMS-donor and CUMS-recipient was distinctively different from the controls, with the CUMS group characterized by a lower relative abundance of Lactobacillus and a higher relative abundance of Akkermansia. Interestingly, FMT affected both behavior and neuroinflammation. Mice given the CUMS microbiota had significant elevations of interferon-γ (IFN-γ) and the tumor necrosis factor-alpha (TNF-α) in the hippocampus, which were accompanied by upregulated indoleamine 2,3-dioxygenase 1 (IDO1) in the hippocampus. These results suggest that GM modulates pro-inflammatory cytokines in the hippocampus through dysfunctional microbiota-gut-brain axis, exacerbating anxiety- and depression-like phenotypes. Key Points Chronic unpredictable mild stress increased anxiety- and depression-like behavior in mice. Mice colonized with gut microbiota (GM) from stressed mice showed similar behaviors. The GM composition of the donor and recipient mice was also comparable. Their relative pattern of two bacteria has been tied to neuroinflammatory activity. The results suggest a link between GM, brain function, and anxiety and depression.
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Gut microbiota is involved in the antidepressant-like effect of (S)-norketamine in an inflammation model of depression.
The non-competitive glutamatergic N-methyl-d-aspartate receptor (NMDAR) antagonist, (R, S)-ketamine (ketamine), is known to exert rapid and long-lasting antidepressant-like effects. However, the widely use of ketamine is restricted owing to severe psychotomimetic side-effects and abuse liability. Very recently, we demonstrated that a major metabolite of ketamine, norketamine, in particular the (S)-enantiomer, had a potent antidepressant-like effect. We here examined the effects of a low-dose of norketamine enantiomers on depression symptoms and detected the changes in the composition of gut microbiota. In the behavioral tests, (S)-norketamine, but not (R)-norketamine, showed antidepressant-like effects in the lipopolysaccharide (LPS)-induced mice. At the genus level, (S)-norketamine, but not (R)-norketamine, significantly attenuated the increase in the levels of Escherichia-Shigella and Adlercreutzia, as well as the reduction in the levels of Harryflintia. At the species level, both (S)-norketamine and (R)-norketamine significantly attenuated the increase in the levels of bacterium ic1379 and Bacteroides sp. Marseille-P3166. Notably, (S)-norketamine was more potent than (R)-norketamine at reducing the levels of bacterium ic1379 and Bacteroides sp. Marseille-P3166. Furthermore, (S)-norketamine, but not (R)-norketamine, significantly attenuated the increased levels of Bacteroides caecigallinarum. In conclusion, this study suggests that the antidepressant-like effects of (S)-norketamine might be associated with the changes in the composition of gut microbiota. Therapeutic strategies improving the gut microbiota might facilitate the benefits for depression treatment.
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The impact of depression-mediated gut microbiota composition on Irritable Bowel Syndrome: A Mendelian study.
OBJECTIVE: This study uses a two-sample Mendelian randomization (MR) analysis to delineate the causal influence of gut microbiota on the occurrence of irritable bowel syndrome (IBS), concurrently assessing the potential mediating function of depression within this framework. METHODS: Several two-sample MR methods were used to assess the causal repercussions of gut microbiota on the onset of both IBS and depression. Following this, gut microbiota and depression, which demonstrated notable causal associations, were integrated as exposure variables in a multivariable Mendelian randomization (MVMR) framework to construct a model encompassing gut microbiota, depression, and IBS. Mediation effects were assessed by examining the indirect pathway of gut microbiota → depression → IBS. RESULTS: Two-sample MR analysis unveiled a statistically significant causal association (P < 0.05) between specific bacterial group within the gut microbiota, notably p_Actinobacteria(OR = 0.829225), c_Clostridia(OR = 0.798897), s_Desulfovibrio_piger(OR = 1.163912), g_Streptococcus(OR = 1.132735), c_Actinobacteria(OR = 0.829224), and the onset of IBS. In the MVMR analysis, the relationship between depression and IBS was significant across Model 3, Model 7, Model 8, and Model 13 (P < 0.05). Assessment of mediation effects revealed that c_Clostridia and o_Clostridiales indirectly impacted IBS through depression, with masking effect ratios of 168.46 % and 168.44 %, respectively. CONCLUSION: These findings underscore a resilient causal association between the composition of gut microbiota and the initiation of IBS. Furthermore, depression serves as a mediator for particular groups of gut bacteria, thereby contributing to the development of IBS. These observations imply that interventions targeting mental health may potentially alleviate the risk of IBS onset attributable to adverse configurations of gut microbiota.
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Intermittent fasting protects against stress-induced depression and demyelination via the gut microbiota-brain axis.
Chronic stress is a major risk factor for depression and disrupts myelin integrity in brain regions involved in emotional regulation. Although intermittent fasting (IF) improves metabolic and inflammatory states, its effects on stress-induced depression and demyelination remain unclear. Here, we investigated whether IF alleviates depression-like behaviors and myelin deficits in mice exposed to chronic restraint stress (CRS) and whether these effects involve modulation of the gut microbiota. Adult male C57BL/6 J mice underwent 14 days of CRS while maintained on either an ad libitum (AL) diet or an IF regimen. CRS induced robust depression-like phenotypes-characterized by increased immobility in the forced swimming test and reduced sucrose preference-without affecting locomotor activity, whereas IF significantly attenuated these behavioral abnormalities. Black-Gold II staining and myelin basic protein (MBP) immunofluorescence revealed marked demyelination in the corpus callosum, medial prefrontal cortex, and hippocampus of CRS mice, which was substantially reversed by IF. 16S rRNA sequencing demonstrated that IF reshaped gut microbial diversity and community composition under stress. Species-level analyses identified Prevotellamassilia timonensis and Muricoprocola aceti as positively associated with myelin integrity and behavioral improvement, whereas Anaeroplasma abactoclasticum showed negative associations. Functional pathway prediction further indicated that IF partially normalized stress-induced alterations in microbial metabolic functions. Collectively, these findings demonstrate that IF mitigates depression-like behaviors and preserves myelin integrity in CRS-exposed mice, potentially through gut microbiota-mediated mechanisms. IF may therefore represent a promising non-pharmacological strategy for alleviating stress-related neurobiological dysfunction.
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Combination of vitamin D3 and fructooligosaccharides upregulates colonic vitamin D receptor in C57BL/6J mice and affects anxiety-related behavior in a sex-specific manner.
Depression and anxiety disorders are among the most common mental health disorders that affect US adults today, frequently related to vitamin D (VD) insufficiency. Along with VD, growing evidence suggests gut microbiota likely play a role in neuropsychiatric disorders. Here, we investigated if modulation of gut microbiota would disrupt host VD status and promote behaviors related to depression and anxiety in adult mice. Six-week-old male and female C57BL/6J mice (n = 10/mice/group) were randomly assigned to receive (1) control diet (CTR), control diet treated with antibiotics (AB), control diet with total 5000 IU of VD (VD), VD treated with antibiotics (VD + AB), VD supplemented with 5% w/w fructooligosaccharides (FOS; VF), and VF diet treated with antibiotics (VF + AB), respectively, for 8 weeks. Our study demonstrated that VD status was not affected by antibiotic regimen. VD alone ameliorates anxiety-related behavior in female mice, and that combination with FOS (i.e., VF) did not further improve the outcome. Male mice, in contrast, exhibit greater anxiety with VF, but not VD, when compared with CTR mice. Colonic VD receptor was elevated in VF-treated mice in both sexes, compared with CTR, which was positively correlated to colonic TPH1, a rate-limiting enzyme for serotonin synthesis. Taken together, our data indicate that the effect of VF on anxiety-related behavior is sex-specific, which may partially be attributed to the activation of colonic VD signaling and subsequent serotonin synthesis. The synergistic or additive effect of VD and FOS on mood disorders remained to be investigated.
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Association between Depression, Anxiety Symptoms and Gut Microbiota in Chinese Elderly with Functional Constipation.
UNLABELLED: This study aimed to investigate the relationship between anxiety, depression, and gut microbiota in elderly patients with FC. METHODS: in this cross-sectional study, a total of 198 elderly participants (85 male and 113 female) aged over 60 years were recruited. The study was conducted in Changsha city, China. The participants completed an online questionnaire, including The Patient Health Questionnaire-9 (PHQ-9), Generalized Anxiety Disorder-7 (GAD-7), The Patient Assessment of Symptoms (PAC-SYM), and The Patient Assessment of Quality of Life (PAC-QoL). We selected the 16S rDNA V3 + V4 region as the amplification region and sequenced the gut microbiota using the Illumina Novaseq PE250 high-throughput sequencing platform. RESULTS: in total, 30.3% of patients with constipation had depression, while 21.3% had anxiety. The relative abundance of intestinal microbiota in the normal group was higher than that in the anxiety and depression group. According to LEfSe analysis, the relative abundance of g_Peptoniphilus and g_Geobacter in the people without depression and anxiety was higher. The relative abundance of g_Pseudoramibacter-Eubacterium and g_Candidatus-Solibacter in the depression group was lower, and the relative abundance of g_Bacteroides and g_Paraprevotella, g_Cc_115 in the anxiety group was higher. In addition, according to the correlation analysis, g_Aquicella and g_Limnohabitans were negatively correlated with constipation symptoms, anxiety, and depression. CONCLUSIONS: this study found that gut microbiota composition may be associated with a higher incidence of anxiety and depression in patients with FC, thus providing insight into the mechanisms that ameliorate mood disorders in patients with FC.
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Pre-injury hypercholesterolemia is associated with microbiota-associated neurobehavioral vulnerability following traumatic brain injury.
Traumatic brain injury (TBI) is increasingly recognized as a systemic disorder associated with long-term neuropsychiatric sequelae. However, substantial inter-individual variability suggests that pre-injury metabolic status may influence neurobehavioral vulnerability following TBI. We investigated whether pre-injury hypercholesterolemia is associated with altered microbiota-associated neurobehavioral interactions after TBI. Male Sprague-Dawley rats were fed a high-fat diet prior to moderate fluid percussion injury, followed by behavioral, biochemical, histological, and microbiota analyses on day 15 post-injury. Pre-injury hypercholesterolemia was associated with increased depression-like behavior, reduced peripheral serotonin levels, greater TTC-negative injury burden, and increased TUNEL positivity. These changes co-occurred with reduced microbial diversity, depletion of Prevotella spp., and enrichment of Akkermansia muciniphila. Predicted microbial functional annotations suggested alterations in amino acid and tryptophan-related pathways associated with behavioral and biochemical measures. Correlation analyses demonstrated inverse associations between peripheral serotonin levels and depression-like behavior, while Akkermansia muciniphila abundance was negatively correlated with peripheral serotonin levels. Network analyses further revealed coordinated associations among microbial taxa, peripheral serotonergic-related markers, and behavioral outcomes. Together, these findings support coordinated microbiota-associated neurobehavioral interactions following traumatic brain injury.
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[Mechanism of total flavone of Abelmoschus manihot in treating ulcerative colitis and depression via intestinal flora-glycerophospholipid metabolism- macrophage polarization pathway].
This study delves into the mechanism of total flavone of Abelmoschus manihot(TFA) in treating ulcerative colitis(UC) and depression via inhibiting M1 polarization of macrophages and reshaping intestinal flora and glycerolphospholipid metabolism. The study established a mouse model of UC and depression induced by chronic restraint stress(CRS) and dextran sulfate sodium(DSS). The fecal microbiota transplantation(FMT) experiment after TFA intervention was conducted. Mice in the FMT donor group were modeled and treated, and fecal samples were taken to prepare the bacterial solution. Mice in the FMT receptor group were treated with antibiotic intervention, and then administered bacterial solution by gavage from mice in the donor group, followed by UC depression modeling. After the experiment, behavioral tests were conducted to evaluate depressive-like behaviors by measuring the levels of 5-hydroxytryptamine(5-HT) and brain-derived neurotrophic factor(BDNF) in the hippocampus of mice. The levels of tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),and interleukin-1β(IL-1β)in the brain and colon tissue of mice were also measured, and the polarization status of macrophages was evaluated by measuring the mRNA levels of CD86 and CD206. 16S ribosomal RNA(16S rRNA) sequencing technology was used to analyze changes in the intestinal flora of mice. Wide target lipidomics was used to detect serum lipid metabolite levels in mice after FMT,and correlation analysis was conducted between lipids and differential intestinal flora significantly regulated by TFA. In vitro experiments, representative glycerophospholipid metabolites and glycerophospholipid inhibitors were used to intervene in Raw264.7 macrophages, and the mRNA levels of TNF-α,IL-6,IL-1β,CD86,and CD206 were detected. The results showed that TFA and FMT after intervention could significantly improve depressive-like behavior and intestinal inflammation in mice with UC and depression, significantly downregulate pro-inflammatory cytokines and CD86 mRNA expression in brain and colon tissue, inhibiting M1 polarization of macrophages, and significantly upregulate CD206 mRNA expression, promoting M2 polarization of macrophages. In addition, the high-dose group had a more significant effect. After TFA intervention, FMT significantly corrected the metabolic disorder of glycerophospholipids in mice with UC and depression, and there was a significant correlation between differential intestinal flora and glycerophospholipids. In vitro experiments showed that glycerophospholipid metabolites, especially lysophosphatidylcholine(LPC),significantly upregulated pro-inflammatory cytokines and CD86 mRNA expression, promote M1 polarization of macrophages, while glycerophospholipid inhibitors had the opposite effect. The results indicate that TFA effectively treats depression and UC by correcting intestinal flora dysbiosis and reshaping glycerophospholipid metabolism, thereby inhibiting M1 polarization of macrophages.