Gut microbiota and mTOR signaling: Insight on a new pathophysiological interaction

The gut microbiota plays a substantial role in regulating the host metabolic and immune functions. Dysbiosis, resulting from disruption of gut microbiota, predisposes many morbid pathologies like obesity and its associated comorbidities, diabetes and inflammatory conditions including some types of c...

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Bibliographic Details
Published inMicrobial pathogenesis Vol. 118; pp. 98 - 104
Main Authors Noureldein, Mohamed H., Eid, Assaad A.
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.05.2018
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Summary:The gut microbiota plays a substantial role in regulating the host metabolic and immune functions. Dysbiosis, resulting from disruption of gut microbiota, predisposes many morbid pathologies like obesity and its associated comorbidities, diabetes and inflammatory conditions including some types of cancer. There are numerous proposed signaling pathways through which alterations in gut microbiota and its metabolites can disturb the host's normal physiological functions. Interestingly, many of these processes happen to be controlled by the mammalian target of rapamycin (mTOR). The mTOR pathway responds to environmental changes and regulates accordingly many intracellular processes such as transcription, translation, cell growth, cytoskeletal organization and autophagy. In this review, we aim to highlight the cross-talk between the gut microbiota and the mTOR pathway and discuss how this emerging field of research gives a beautiful insight into how the mentioned cross-talk impacts the body's homeostasis thus leading to undesirable complications including obesity, diabetes, colon and pancreatic cancer, immune system malfunctioning and ageing. Although there are a limited number of studies investigating the crosstalk between the gut microbiota and the mTOR pathway, the results obtained so far are enough to elucidate the key role of the mTOR signaling in microbiota-associated metabolic and immune regulations.
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ISSN:0882-4010
1096-1208
DOI:10.1016/j.micpath.2018.03.021