Advances in Brain–Gut–Microbiome Interactions: A Comprehensive Update on Signaling Mechanisms, Disorders, and Therapeutic Implications

Dong, Tien S.; Mayer, Emeran

doi:10.1016/j.jcmgh.2024.01.024

Cited by 8 publications

(1 citation statement)

References 126 publications

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“…The gut houses a robust immune system, and communication with the CNS involves signaling molecules like cytokines and chemokines. Additionally, products derived from the gut microbiome can modulate immune cell functions, potentially triggering local or systemic inflammation [97][98][99].…”

Section: Brain-gut-liver Axismentioning

confidence: 99%

Underlying Mechanisms behind the Brain–Gut–Liver Axis and Metabolic-Associated Fatty Liver Disease (MAFLD): An Update

De Cól,

de Lima,

Pompeu

et al. 2024

IJMS

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Metabolic-associated fatty liver disease (MAFLD) includes several metabolic dysfunctions caused by dysregulation in the brain–gut–liver axis and, consequently, increases cardiovascular risks and fatty liver dysfunction. In MAFLD, type 2 diabetes mellitus, obesity, and metabolic syndrome are frequently present; these conditions are related to liver lipogenesis and systemic inflammation. This study aimed to review the connection between the brain–gut–liver axis and MAFLD. The inflammatory process, cellular alterations in hepatocytes and stellate cells, hypercaloric diet, and sedentarism aggravate the prognosis of patients with MAFLD. Thus, to understand the modulation of the physiopathology of MAFLD, it is necessary to include the organokines involved in this process (adipokines, myokines, osteokines, and hepatokines) and their clinical relevance to project future perspectives of this condition and bring to light new possibilities in therapeutic approaches. Adipokines are responsible for the activation of distinct cellular signaling in different tissues, such as insulin and pro-inflammatory cytokines, which is important for balancing substances to avoid MAFLD and its progression. Myokines improve the quantity and quality of adipose tissues, contributing to avoiding the development of MAFLD. Finally, hepatokines are decisive in improving or not improving the progression of this disease through the regulation of pro-inflammatory and anti-inflammatory organokines.

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Section: Brain-gut-liver Axismentioning

confidence: 99%