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Defining Dysbiosis in Disorders of Movement and Motivation.
The gut microbiota has emerged as a critical player in shaping and modulating brain function and has been shown to influence numerous behaviors, including anxiety and depression-like behaviors, sociability, and cognition. However, the effects of the gut microbiota on specific disorders associated with thalamo-cortico-basal ganglia circuits, ranging from compulsive behavior and addiction to altered sensation and motor output, are only recently being explored. Wholesale depletion and alteration of gut microbial communities in rodent models of disorders, such as Parkinson's disease, autism, and addiction, robustly affect movement and motivated behavior. A new frontier therefore lies in identifying specific microbial alterations that affect these behaviors and understanding the underlying mechanisms of action. Comparing alterations in gut microbiota across multiple basal-ganglia associated disease states allows for identification of common mechanistic pathways that may interact with distinct environmental and genetic risk factors to produce disease-specific outcomes.
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Review of mechanisms of deoxynivalenol-induced anorexia: The role of gut microbiota.
Deoxynivalenol (DON) is one of the most important mycotoxins in cereal-based foods or other food productions, produced by Fusarium species. Because of the high occurrence of DON in food combined with vast consumption of cereals and grain worldwide, the DON-contaminated food is a very harmful factor for human and animal health. DON has been reported to induce anorexia at lower or chronic doses in animal models. However, further researches for DON-induced anorexia are limited. Previous publications demonstrated a close link between Bacteroidetes and Firmicutes, two kinds of gut microbiota, with weight loss and the effect of low administration of DON on neurotransmitters in the frontal cortex, cerebellum, hypothalamus, hippocampus and pons/medulla. These data are similar to other studies, which show selective 5HTα receptor agonists apparently causing hyperphagia whereas 5HT1β agonists appear to induce anorexia. Thus, the neurochemical effects of lower DON exposure can be as a result of peripheral toxicological events such as emesis, which overwhelmed its more subtle feed refusal activity. Besides, changes in the microbiota have an impact on stress-related behaviors like anxiety and depression, which can lead to weight loss through decreased feed intake. Gut dysbiosis is also associated with brain dysfunction and with behavioral changes. These conclusions illustrate as well a potential explanation for DON-induced anorexia.In this review, we summarize information about DON-induced anorexia from previous studies and provide our opinion for future investigations that could establish a link between gut microbiota, neurotransmitters, anorexia and weight loss under the DON exposure. Copyright © 2017 John Wiley & Sons, Ltd.
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Impact of long-term medication on estrobolome-associated β-glucuronidase and sulfatase activities: Implications for estrogen homeostasis in postmenopausal women.
Menopause leads to a decline in circulating estrogen levels, increasing cardiometabolic risk, contributing to bone loss, and decreasing quality of life. The estrobolome, a subset of microbes with β-glucuronidase (GUS) and sulfatase activities, regulates estrogen homeostasis through deconjugation and enterohepatic recycling, thereby influencing systemic estrogen availability. Common long-term pharmacological treatments in postmenopausal women may alter gut microbial composition and function, potentially affecting estrobolome activity and systemic estrogen levels. This narrative review examines current evidence on how long-term pharmacological treatments may affect estrobolome-associated GUS and sulfatase activities, with implications for estrogen metabolism and health outcomes in postmenopausal women. A targeted literature search was performed to identify clinical studies on commonly prescribed drugs for hypertension, diabetes, dyslipidemia, osteoporosis, and depression in postmenopausal women, focusing on microbial taxa with reported GUS or sulfatase activity. Among the evaluated pharmacological classes, antidiabetic drugs, particularly metformin, are the most extensively studied, followed by antidepressants. These treatments can modulate key gut bacterial genera with GUS and sulfatase activities, including Bifidobacterium, Roseburia, Faecalibacterium, and Clostridium, which are relevant to metabolic and estrogen homeostasis. However, no studies have directly assessed the impact of pharmacological treatments on GUS and sulfatase activity in postmenopausal women. Understanding how chronic medication influences estrobolome dynamics may help identify strategies to support estrogen balance and improve systemic metabolic, hormonal, vascular, and inflammatory profiles. This review highlights the interplay between long-term medication, gut microbiota, and estrogen homeostasis as a promising avenue for personalized microbiota-targeted therapies in postmenopausal health.
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Biodegradation of expanded polystyrene and low-density polyethylene foams in larvae of Tenebrio molitor Linnaeus (Coleoptera: Tenebrionidae): Broad versus limited extent depolymerization and microbe-dependence versus independence.
Yellow mealworms (Tenebrio molitor larvae) are capable of biodegrading polystyrene (PS) and low-density polyethylene (LDPE). This study tested biodegradation of one expanded PS (EPS) with a weight-average molecular weight (Mw) 256.4 kDa and two LDPE foams with respective Mw of 130.6 kDa (PE-1) and 288.7 kDa (PE-2) in T. monitor larvae obtained in Beijing, China. The larvae consumed EPS and both LDPEs over a 60 day. Fourier transform infrared spectroscopy and thermogravimetric analyses of frass confirmed the formation of new oxygen-containing functional groups, as well as a change in physical property and chemical modification, indicating that biodegradation of EPS and LDPE occurred. Gel permeation chromatography analysis confirmed broad depolymerization of EPS and PE-1 (i.e., a decrease in both Mw and a number-average molecular weight (Mn)) but revealed limited extent depolymerization of PE-2 (i.e., increase in Mn and decrease in Mw). For all materials, the size-average molecular weight (Mz) was decreased. Biodegradation and oxidation of EPS and LDPE were confirmed using FTIR and TGA analysis. Depression of gut microbes by the antibiotic gentamicin resulted in significant inhibition of EPS depolymerization but did not stop LDPE depolymerization, resulting in the increase in Mn and revealing that PS biodegradation was gut microbe-dependent but LDPE biodegradation was less dependent or independent of gut microbes. Gut microbial community analysis indicated that, as expected, under different dietary conditions, the intestinal flora significantly shifted to communities associated with biodegradation of EPS and LDPE. The results indicated the complexity and limitation of biodegradation of plastics in plastics-eating T. molitor larvae.
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The Microbiota, the Gut and the Brain in Eating and Alcohol Use Disorders: A 'Ménage à Trois'?
AIMS: Accumulating evidence for the influence of the gut microbiota on the bidirectional communication along the gut-brain axis suggests a role of the gut microbiota in eating disorders (EDs) and alcohol and substance use disorders. The potential influence of altered gut microbiota (dysbiosis) on behaviors associated with such disorders may have implications for developing therapeutic interventions. METHODS: A systematic review of preclinical and clinical studies evaluating the gut microbiota, EDs and alcohol and substance use disorders was conducted using MEDLINE, Embase and Web of Science databases with the objective being to examine the role of the gut microbiota in behavioral correlates of these disorders. Original papers focused on the gut microbiota and potential behavioral implications were deemed eligible for consideration. RESULTS: The resulting 12 publications were limited to gut microbiota studies related to EDs and alcohol and substance use disorders. Some studies suggest that dysbiosis and gut microbial byproducts may influence the pathophysiology of EDs via direct and indirect interference with peptide hormone signaling. Additionally, dysbiosis was shown to be correlated with alcohol use disorder-related symptoms, i.e. craving, depression and anxiety. Finally, a mouse study suggests that manipulations in the gut microbiota may affect cocaine-related behaviors. CONCLUSIONS: Promising, albeit preliminary, findings suggest a potential role of the gut microbiota in behavioral correlates of EDs and alcohol and substance use disorders. SHORT SUMMARY: Preliminary evidence exists supporting the role of the gut microbiota in eating disorders and alcohol and substance use disorders, although additional investigation is needed to determine what is causative versus epiphenomenological.
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Chronic Social Stress and Immune Dysregulation: Integrating Neuroendocrine Signaling, Microbiota, and Tissue-Specific Responses.
Psychological stress arises when individuals perceive demands as exceeding their capacity to cope. Social stress can be acute, such as giving a presentation, producing transient increases in heart rate, blood pressure, and neuroendocrine activation, or chronic, in which stressors persist over extended periods. Chronic psychosocial stress disrupts immune homeostasis and contributes to anxiety, depression, and post-traumatic stress, while also increasing risk for infections, inflammatory and autoimmune diseases, cardiovascular disease, metabolic dysfunction, and cancer. Persistent stress engages interconnected neuroendocrine-immune networks, including the hypothalamic-pituitary-adrenal axis, the sympathetic-adrenomedullary system, and the gut microbiota-brain-immune axis, leading to sustained glucocorticoid and catecholamine signaling, gut dysbiosis, impaired barrier integrity, and altered microbial metabolite profiles. In this review, we summarize the molecular and cellular mechanisms by which these axes remodel innate and adaptive immunity and shape disease susceptibility. Using social defeat and social isolation in mice as model systems, we highlight how chronic social stress reprograms immune responses in key tissues, including the lung, brain, and gut.
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The role of microbiota-gut-brain axis in neuropsychiatric and neurological disorders.
Emerging evidence indicates that the gut microbiota play a crucial role in the bidirectional communication between the gut and the brain suggesting that the gut microbes may shape neural development, modulate neurotransmission and affect behavior, and thereby contribute to the pathogenesis and/or progression of many neurodevelopmental, neuropsychiatric, and neurological conditions. This review summarizes recent data on the role of microbiota-gut-brain axis in the pathophysiology of neuropsychiatric and neurological disorders including depression, anxiety, schizophrenia, autism spectrum disorders, Parkinson's disease, migraine, and epilepsy. Also, the involvement of microbiota in gut disorders co-existing with neuropsychiatric conditions is highlighted. We discuss data from both in vivo preclinical experiments and clinical reports including: (1) studies in germ-free animals, (2) studies exploring the gut microbiota composition in animal models of diseases or in humans, (3) studies evaluating the effects of probiotic, prebiotic or antibiotic treatment as well as (4) the effects of fecal microbiota transplantation.
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Probiotics for Inflammatory Bowel Disease; A Deep Dive into their Impact on Disease Course and Associated Health Risks.
To date, the underlying pathology of inflammatory bowel disease (IBD) is undetermined. Disturbance of intestinal gut microbiota was implicated in many health diseases, including IBD. Increasing evidence suggests that probiotics play a beneficial role in restoring the balance of the gut ecosystem. This review searched multiple databases for relevant works that examined probiotics' possible benefits in adults with IBD. Probiotic mode of action in ulcerative colitis patients and Crohn's disease were examined with respect to probiotic strain, their benefits, and their advantages in adult cases. Eligible studies for inclusion were assessed and analyzed. They were effective in reducing IBD disease course, inducing and maintaining remission, particularly for ulcerative colitis patients, with good efficacy and safety profile. However, the evidence for Crohn's disease was lacking. Probiotics positively affect IBD-related risks, reducing the risk of gastrointestinal malignancy and optimizing treating them. Additionally, they improved reduced fertility odds for both genders. The osteoporosis risk among IBD patients was also reduced, although the duration of use and dose were still not established. There was an encouraging role for them in reducing IBD -cardiovascular risks among cases with acute myocardial infarction and those with chronic heart failure. Finally, they had novel use in reducing IBD-related depression and improved overall mental health. In conclusion, we recommend probiotics as an adjuvant therapeutic option for IBD therapy for ulcerative colitis; however, their role in Crohn's disease needs further research.
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Multistage oral astaxanthin targeted delivery system: Increasing serotonin levels with a dual therapeutic effect for alleviating inflammatory bowel disease and psychiatric disorders.
Inflammatory bowel disease (IBD) is associated with a notably high prevalence of psychiatric disorders. Since oxidative stress is an important feature of intestinal inflammation, astaxanthin (AXT), an effective and highly safe antioxidant, shows high therapeutic potential. Nonetheless, the utilization of AXT is hampered by its limited solubility and susceptibility. In this study, a multistage system (ALM@AG) was developed for enhancing the bioavailability and the targeted delivery of AXT. Moreover, ALM@AG was capable of targeting to the location of colon lesions by administering drugs, which was beneficial for effective treatments of colitis. The results showed that ALM@AG demonstrated high effectiveness in reducing inflammation, modulating gut microbiota, repairing intestinal barrier, and restoring metabolic homeostasis. Remarkably, ALM@AG exhibited a significant effect on treating depression-like behaviors suffering from colitis by regulating neurotransmitters and relieving brain inflammation. Notably, this study deeply explored interactions among genes, microbiota, and metabolites in the progression of IBD accompanied by psychiatric disorders, which may propose novel perspectives for investigating the gut-brain axis.
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The ketogenic diet influences taxonomic and functional composition of the gut microbiota in children with severe epilepsy.
The gut microbiota has been linked to various neurological disorders via the gut-brain axis. Diet influences the composition of the gut microbiota. The ketogenic diet (KD) is a high-fat, adequate-protein, low-carbohydrate diet established for treatment of therapy-resistant epilepsy in children. Its efficacy in reducing seizures has been confirmed, but the mechanisms remain elusive. The diet has also shown positive effects in a wide range of other diseases, including Alzheimer's, depression, autism, cancer, and type 2 diabetes. We collected fecal samples from 12 children with therapy-resistant epilepsy before starting KD and after 3 months on the diet. Parents did not start KD and served as diet controls. Applying shotgun metagenomic DNA sequencing, both taxonomic and functional profiles were established. Here we report that alpha diversity is not changed significantly during the diet, but differences in both taxonomic and functional composition are detected. Relative abundance of bifidobacteria as well as E. rectale and Dialister is significantly diminished during the intervention. An increase in relative abundance of E. coli is observed on KD. Functional analysis revealed changes in 29 SEED subsystems including the reduction of seven pathways involved in carbohydrate metabolism. Decomposition of these shifts indicates that bifidobacteria and Escherichia are important contributors to the observed functional shifts. As relative abundance of health-promoting, fiber-consuming bacteria becomes less abundant during KD, we raise concern about the effects of the diet on the gut microbiota and overall health. Further studies need to investigate whether these changes are necessary for the therapeutic effect of KD.