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Background: Disorders of gut-brain interaction (DGBIs) have a complex pathophysiology that is often characterized by a relationship between food ingestion and triggering of symptoms. Understanding of the underlying mechanisms and the role of nutrients as a therapeutic target are rapidly evolving.
Aims And Methods: We performed a narrative review of the literature using the following keywords, their acronyms, and their associations: nutrients, disorders of gut-brain interaction; functional dyspepsia; malabsorption; irritable bowel syndrome; diarrhea; constipation.
Results: Functional dyspepsia displayed a significant correlation between volume, fat and/or wheat abundance, chemical composition of ingested food and symptoms of early satiety, fullness and weight loss. Carbohydrate malabsorption is related to enzyme deficiency throughout the GI tract. Food composition and richness in soluble vs. non-soluble fibers is related to constipation and diarrhea. The elimination of fermentable oligo-, di-, monosaccharides and polyols (FODMAPs) has a significant and non-unidirectional impact on irritable bowel syndrome (IBS) symptoms.
Conclusions: Food volume, nutritive and chemical composition, and its malabsorption are associated with symptom generation in DGBIs. Further multicenter, randomized-controlled clinical trials are needed to clarify the underlying pathophysiology.
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http://dx.doi.org/10.3390/nu16010176 | DOI Listing |
Front Microbiol
August 2025
Department of Neurology, The Affiliated Brain Hospital of Nanjing Medical University, Nanjing, China.
Background: Increasing evidence suggests a potential role of the gut microbiota in Parkinson's disease (PD). However, the relationship between the gut microbiome (GM) and PD dementia (PDD) remains debated, with their causal effects and underlying mechanisms not yet fully understood.
Methods: Utilizing data from large-scale genome-wide association studies (GWASs), this study applied bidirectional and mediating Mendelian randomization (MR) to investigate the causal relationship and underlying mechanisms between the GM and PDD.
Neuropsychiatr Dis Treat
September 2025
Department of Radiology, No. 926 Hospital, Joint Logistics Support Force of PLA, Kaiyuan, Yunnan, 661699, People's Republic of China.
Parkinson's disease (PD) represents a progressive neurodegenerative disorder with escalating global burden, with mechanistic studies revealing α-synuclein propagation through gut-brain axis, mitochondrial defects, and neuroinflammatory cascades driven by genetic-environmental interplay. Recent advancements in diagnostic paradigms have successfully combined α-synuclein seed amplification assays with multimodal neuroimaging techniques, achieving an impressive diagnostic accuracy of 92% during the prodromal stages of disease. Phase II trials highlight disease-modifying potential of α-synuclein-targeting immunotherapies (40% reduction in motor decline) and LRRK2 kinase inhibitors showing blood-brain barrier penetration.
View Article and Find Full Text PDFNeuropsychiatr Dis Treat
September 2025
Medical College, Tibet University, Lhasa, Tibet, People's Republic of China.
Background: Tripterygium glycoside (TG) has been reported to have the effect of ameliorating Alzheimer's disease (AD)-like symptoms in mice model. However, the underlying mechanism is largely unknown. This study aimed to investigate the potential mechanism of TG against AD by integrating metabolomics, 16s rRNA sequencing, network pharmacology, molecular docking, and molecular dynamics simulation.
View Article and Find Full Text PDFSci Signal
September 2025
Department of Surgery, University of Alabama Birmingham, Birmingham, AL 35233, USA.
Amphetamines are psychostimulants that are commonly used to treat neuropsychiatric disorders and are prone to misuse. The pathogenesis of amphetamine use disorder (AUD) is associated with dysbiosis (an imbalance in the body's microbiome) and bacterially produced short-chain fatty acids (SCFAs), which are implicated in the gut-brain axis. Amphetamine exposure in both rats and humans increases the amount of intestinal , which releases SFCAs.
View Article and Find Full Text PDFElife
September 2025
Department of Biology, University of Copenhagen, Copenhagen, Denmark.
Sickness-induced sleep is a behavior conserved across species that promotes recovery from illness, yet the underlying mechanisms are poorly understood. Here, we show that interleukin-6-like cytokine signaling from the gut to brain glial cells regulates sleep. Under healthy conditions, this pathway promotes wakefulness.
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