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Targeting the Gut-Brain Axis Through Insulin-like Growth Factors: Therapeutic Implications and Future Directions.
The gut-brain axis represents a sophisticated bidirectional communication network connecting the gastrointestinal tract and central nervous system through neural, endocrine, and immune pathways. Insulin-like growth factors (IGFs), particularly IGF-1 and IGF-2, function as pivotal mediators within this communication framework. These polypeptide growth factors regulate intestinal barrier integrity, microbiota homeostasis, neurogenesis, and synaptic plasticity mechanisms. Clinical evidence from 1989 to 2024 demonstrates that gut microbiota-derived short-chain fatty acids enhance IGF-1 production through novel molecular mechanisms. This narrative review examines IGF roles in gut-brain communication and evaluates therapeutic potential for neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, and depression, as well as inflammatory bowel disorders. Current clinical trials investigating IGF-based interventions show preliminary promising results, though studies remain limited in scope and patient numbers. Key therapeutic challenges include delivery mechanisms across biological barriers, oncogenic safety concerns related to cell proliferation, and substantial individual variability in treatment responses. Future directions emphasize development of tissue-specific IGF modulators, microbiome-targeted interventions, and precision medicine approaches utilizing advanced biomarkers. Understanding IGF-mediated gut-brain communication presents therapeutic opportunities for complex pathological conditions simultaneously affecting gastrointestinal and neurological systems.
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Lactobacillus intestinalis YT2 restores the gut microbiota and improves menopausal symptoms in ovariectomized rats.
There are many studies focusing on the alleviation of menopausal symptoms; however, little is known about the role of gut microorganisms in menopausal symptoms. Ovariectomized (OVX) rats were administered a novel strain (YT2) of Lactobacillus intestinalis (a species with significantly reduced abundance in OVX rats) and the potential probiotic effect on the improvement of menopausal symptoms was evaluated. Of note, the gut microbial composition completely shifted after ovariectomy in rats. Treatment with L. intestinalis YT2 significantly alleviated menopausal symptoms, such as increased fat mass, decreased bone mineral density, increased pain sensitivity, depression-like behaviour, and cognitive impairment. Additionally, the administration of L. intestinalis YT2 restored the intestinal microbial composition, including an increased Firmicutes/Bacteroides ratio. L. intestinalis YT2 also promoted gut barrier integrity by increasing the mRNA levels of tight junction-related markers. In conclusion, L. intestinalis YT2 treatment alleviated menopausal symptoms via the modulation of the gut microbiota. Importantly, these results suggest that L. intestinalis YT2 should be considered as a therapeutic probiotic agent for menopausal women.
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A Narrative Review on the Advance of Probiotics to Metabiotics.
Recently, the term metabiotics has emerged as a new concept of probiotics. This concept entails combining existing probiotic components with metabolic by-products improve specific physiological functionalities. Representative ingredients of these metabiotics include short-chain fatty acids (SCFAs), bacteriocins, polysaccharides, and peptides. The new concept is highly regarded as it complements the side effects of existing probiotics and is safe and easy to administer. Known health functions of metabiotics are mainly immune regulation, anti-inflammatory, anticancer, and brain-neurological health. Research has been actively conducted on the health benefits related to the composition of intestinal microorganisms. Among them, the focus has been on brain neurological health, which requires extensive research. This study showed that neurological disorders, such as depression, anxiety, autism spectrum disorder, Alzheimer's disease, and Parkinson's disease, can be treated and prevented according to the gut-brain axis theory by changing the intestinal microflora. In addition, various studies are being conducted on the immunomodulatory and anticancer effects of substances related to metabiotics of the microbiome. In particular, its efficacy is expected to be confirmed through human studies on various cancers. Therefore, developing various health functional effects of the next-generation probiotics such as metabiotics to prevent or treatment of various diseases is anticipated.
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Clinical insights into the mechanisms of infectious microbes and microbiota in chronic neurologic and psychiatric diseases.
Chronic neurologic and psychiatric diseases such as schizophrenia, depression, Parkinson's, and Alzheimer's are increasingly linked to infectious microorganisms and gut microbiota. This review explores how pathogenic microorganisms and microbial communities impact neuropsychiatric, neurodegenerative, and neuroinflammatory processes, highlighting the gut-brain axis' crucial communication network in influencing behavior and brain function. Infectious agents like bacteria, viruses, and fungi cause disease by causing neurotoxic reactions, disrupting the blood-brain barrier, and activating neuroinflammatory cascades. Gut dysbiosis impacts immunological homeostasis and neural transmission by altering the synthesis of metabolites from microorganisms, such as short-chain fatty acids and neurotransmitter precursors. Neurodegeneration and psychiatric diseases are influenced by molecular mechanisms such as toll-like receptor signaling, microglial activation, and mitochondrial dysfunction. This review highlights the potential of microbiota-targeted treatments such as probiotics, prebiotics, and microbiome transplantation as novel treatments for chronic diseases. Understanding the intricate interactions between infectious microorganisms, microbiota, and the central nervous system enables the formation of precision medicine strategies to challenge the rising incidence of neurologic and psychiatric diseases. Future research should explore causal relationships and identify specific microbial biomarkers to enhance early diagnosis, prevention, and personalized treatment plans.
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Heat-killed Enterococcus fecalis (EC-12) supplement alters the expression of neurotransmitter receptor genes in the prefrontal cortex and alleviates anxiety-like behavior in mice.
Gut microbiota plays a crucial role in the maintenance of mental health and influences mental disorders such as depression and anxiety. Several studies have reported the beneficial affects of probiotics in mental health. Heat-killed Enterococcus faecalis strain EC-12 (EC-12), a lactic acid bacterium induces activation of the immune system. However, little is known about the effect of EC-12 on mental health. In the present study, the anti-anxiety effect of EC-12 was elucidated in vivo. Male mice fed on diet supplemented with EC-12 showed decreased anxiety-like behavior in open-field and elevated plus-mazetest. In addition, EC-12 supplementation exhibited an anti-depressive trend in mice subjected to forced swim test. The expression of neurotransmitter receptor genes: Adrb3 and Avpr1a were significantly enhanced in EC-12 supplemented mice compared to that of the control mice. In mice, analyses of gut microbiota composition by next generation sequencing revealed significant increase in Butyricicoccus and Enterococcus with EC-12 supplementation. Significant difference was not detected in the expression of neurotransmitter receptor genes in the prefrontal cortex with the administration of sodium butyrate compared to that of the control group. The mechanism associated with EC-12 mediated reduced anxiety-like behavior and altered gene expression in the brain needs to be further elucidated. Taken together, the present study is the first to report the possibility of exploiting the anti-anxiety effect of heat-killed EC-12 as a novel probiotic to promote mental health.
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The Mechanism of Secretion and Metabolism of Gut-Derived 5-Hydroxytryptamine.
Serotonin, also known as 5-hydroxytryptamine (5-HT), is a metabolite of tryptophan and is reported to modulate the development and neurogenesis of the enteric nervous system, gut motility, secretion, inflammation, sensation, and epithelial development. Approximately 95% of 5-HT in the body is synthesized and secreted by enterochromaffin (EC) cells, the most common type of neuroendocrine cells in the gastrointestinal (GI) tract, through sensing signals from the intestinal lumen and the circulatory system. Gut microbiota, nutrients, and hormones are the main factors that play a vital role in regulating 5-HT secretion by EC cells. Apart from being an important neurotransmitter and a paracrine signaling molecule in the gut, gut-derived 5-HT was also shown to exert other biological functions (in autism and depression) far beyond the gut. Moreover, studies conducted on the regulation of 5-HT in the immune system demonstrated that 5-HT exerts anti-inflammatory and proinflammatory effects on the gut by binding to different receptors under intestinal inflammatory conditions. Understanding the regulatory mechanisms through which 5-HT participates in cell metabolism and physiology can provide potential therapeutic strategies for treating intestinal diseases. Herein, we review recent evidence to recapitulate the mechanisms of synthesis, secretion, regulation, and biofunction of 5-HT to improve the nutrition and health of humans.
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The chemo-gut study: investigating the long-term effects of chemotherapy on gut microbiota, metabolic, immune, psychological and cognitive parameters in young adult Cancer survivors; study protocol.
BACKGROUND: The gut microbiota is an important modulator of immune, metabolic, psychological and cognitive mechanisms. Chemotherapy adversely affects the gut microbiota, inducing acute dysbiosis, and alters physiological and psychological function. Cancer among young adults has risen 38% in recent decades. Understanding chemotherapy's long-term effects on gut microbiota and psycho-physiological function is critical to improve survivors' physical and mental health, but remains unexamined. Restoration of the gut microbiota via targeted therapies (e.g. probiotics) could potentially prevent or reverse the psycho-physiological deficits often found in young survivors following chemotherapy, ultimately leading to reduced symptom burden and improved health. METHODS: This longitudinal study investigates chemotherapy induced long-term gut dysbiosis, and associations between gut microbiota, and immune, metabolic, cognitive and psychological parameters using data collected at < 2 month (T1), 3-4 months (T2), and 5-6 months (T3) post-chemotherapy. Participants will be 18-39 year old blood or solid tumor cancer survivors (n = 50), and a healthy sibling, partner or friend as a control (n = 50). Gut microbiota composition will be measured from fecal samples using 16 s RNA sequencing. Psychological and cognitive patient reported outcome measures will include depression, anxiety, post-traumatic stress disorder symptoms, pain, fatigue, and social and cognitive function. Dual-energy X-ray Absorptiometry (DXA) will be used to measure fat and lean mass, and bone mineral concentration. Pro-inflammatory cytokines, C-reactive protein (CRP), lipopolysaccharide (LPS), serotonin, and brain derived neurotrophic factor (BDNF) will be measured in serum, and long-term cortisol will be assayed from hair. Regression and linear mixed model (LMM) analyses will examine associations across time points (T1 - T3), between groups, and covariates with gut microbiota, cognitive, psychological, and physiological parameters. CONCLUSION: Knowing what bacterial species are depleted after chemotherapy, how long these effects last, and the physiological mechanisms that may drive psychological and cognitive issues among survivors will allow for targeted, integrative interventions to be developed, helping to prevent or reverse some of the late-effects of treatment that many young cancer survivors face. This protocol has been approved by the Health Research Ethics Board of Alberta Cancer Committee (ID: HREBA.CC-19-0018).
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Polyphenols in the management of brain disorders: Modulation of the microbiota-gut-brain axis.
The modulation of the microbiota-gut-brain axis with a view to preventing and treating brain disorders became recently a hot topic for the scientific community. Dietary polyphenols are multifaceted compounds that have demonstrated to be highly advantageous to counteract inflammation, oxidative stress, and neurodegeneration, among other pathological conditions, being useful in the prevention and treatment of several chronic disorders. The potential of these compounds to prevent and treat brain disorders has not been only related to their capacity to reach the brain, depending on their chemical structure, and interact directly with brain cells, but also to their ability to modulate the communication between the brain and the gut, interfering with multiple branches of this axis. Preclinical studies have demonstrated the potential of these food bioactive compounds in brain diseases, namely, neurodevelopmental, such as Down's syndrome and Autism spectrum disorder, neurodegenerative, such as Parkinson's disease and Alzheimer's disease, and psychiatric disorders, such as depression and anxiety. Until now, dietary polyphenols have been recognized as promising nutraceuticals to combat brain disorders. However, the impact of these compounds on the gut-brain interconnection remains poorly elucidated. Also, clinical assays are crucial to further support the beneficial effects of these compounds as demonstrated in preclinical research.
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ACTH(6-9)-Pro-Gly-Pro ameliorates anxiety-like and depressive-like behaviour and gut mucosal microbiota composition in rats under conditions of chronic restraint stress.
The effects of the peptide ACTH(6-9)-Pro-Gly-Pro at doses of 5; 50; 500 μg/kg on the Wistar rats' behaviour and gut mucosal microbiota composition under conditions of chronic immobilization stress (CRS) were studied. CRS increased anxiety-like and depressive-like behaviour, disturbances in locomotor activity and gut dysbiosis. Administration of ACTH(6-9)-Pro-Gly-Pro showed many phenotypic results. Peptide demonstrated anti-depressant activity at doses of 5 and 500 μg/kg by a decrease in the total immobile time in the FST. ACTH(6-9)-Pro-Gly-Pro administered at a dose of 50 μg/kg resulted in an anxiolytic effect which is shown by an increase in the time in the open arms of EPM (p < 0.05) and a decrease in the time in the closed arms (p < 0.05). Moreover, the peptide led to a decrease in alpha- and beta-diversity of the gut microbiota (p < 0.01). Correlation and linear regression analysis demonstrated central mechanisms of ACTH(6-9)-Pro-Gly-Pro anxiolytic activity and both central and peripheral ones in an anti-depressant effect. In this way, peptide ACTH(6-9)-Pro-Gly-Pro could prevent the development of behavioural disturbances and gut dysbiosis caused by chronic restraint stress.
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Sex Differences in Immune and Gut Microbiota Responses to Military Training.
PURPOSE: Military training includes multiple stressors that together may increase risk for illness by degrading immune function and altering gut microbiota. However, whether sex differences exist in those responses is undetermined. This study aimed to determine immune and gut microbiota responses during military training and identify sex differences in those responses. METHODS: Seventy-two military cadets (33% female) participated in an arduous 17-d training event. Blood, saliva, and stool were collected upon beginning (PRE) and completing (POST) training. Immune function was assessed by salivary secretory IgA (SIgA), latent virus reactivation, peripheral leukocyte distribution, circulating cytokines, and mitogen-stimulated cytokine profiles. Gut microbiota composition was assessed by 16S rRNA amplicon sequencing. RESULTS: Participants experienced a ~4% body weight loss and sex-independent increases in concentrations of cortisol, myoglobin, catecholamines, and multiple cytokines. The granulocyte-to-lymphocyte ratio increased and SIgA decreased PRE to POST in males but not females ( Pinteraction ≤ 0.02). Mitogen-stimulated cytokine profiles were generally reduced at POST versus PRE independent of sex. No differences in virus reactivation were observed. Sex differences in gut microbiota responses were limited to Bifidobacterium and Ruminococcus , which increased in males relative to females (log 2 fold change (FC) = 2.0-2.4; qinteraction = 0.19). Independent of sex, 24 genera differed at POST versus PRE with Lactobacillus demonstrating the largest decrease (log 2 FC = -0.90; qtime = 0.02) and Veillonella the largest increase (log 2 FC = 1.09; qtime = 0.03). Multiple correlations between markers of stress, immune function, and gut microbiota composition were observed ( q ≤ 0.15). CONCLUSIONS: Immune redistribution, leukocyte compromise, and interrelated changes in gut microbiota composition were evident within this training environment. Those responses demonstrated associations with markers of stress severity but also sex differences, suggesting a more pronounced depression of immune function in males.