Key Points
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Animals feed their gut bacteria, which are fully dependent on their host for providing the nutrients necessary for growth and maintenance of the bacterial population
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Food intake is followed by cephalic reflex-mediated secretions of nutrients into the gut, which activate the gut–brain satiety pathways via release of intestinal hormones
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Regular nutrient provision to cultured bacteria or nutrient infusion into the colon stimulates immediate bacterial growth that lasts 20 min
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The dynamics of the regular nutrient-induced growth of bacteria are similar to the dynamics of meal-induced intestinal satiety hormone (for example, PYY) release
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Bacterial molecules and metabolites, whose production depends on bacterial growth phases, regulate intestinal release of satiety hormones
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Systemic bacterial molecules directly activate central appetite pathways that might integrate the energy status of both the host and its gut microbiota
Abstract
The life of all animals is dominated by alternating feelings of hunger and satiety — the main involuntary motivations for feeding-related behaviour. Gut bacteria depend fully on their host for providing the nutrients necessary for their growth. The intrinsic ability of bacteria to regulate their growth and to maintain their population within the gut suggests that gut bacteria can interfere with molecular pathways controlling energy balance in the host. The current model of appetite control is based mainly on gut–brain signalling and the animal's own needs to maintain energy homeostasis; an alternative model might also involve bacteria–host communications. Several bacterial components and metabolites have been shown to stimulate intestinal satiety pathways; at the same time, their production depends on bacterial growth cycles. This short-term bacterial growth-linked modulation of intestinal satiety can be coupled with long-term regulation of appetite, controlled by the neuropeptidergic circuitry in the hypothalamus. Indeed, several bacterial products are detected in the systemic circulation, which might act directly on hypothalamic neurons. This Review analyses the data relevant to possible involvement of the gut bacteria in the regulation of host appetite and proposes an integrative homeostatic model of appetite control that includes energy needs of both the host and its gut bacteria.
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Change history
18 November 2016
In Figure 4 of the above article published online 12 September 2016, hunger signalling to the host was incorrectly labelled as decreased, when it should have been labelled as increased. This has been corrected in the online versions of the article. We apologize for this error.
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The author is grateful to all colleagues who participated in and inspired the reviewed research and to his wife being a fervent and pertinent critic.
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Fetissov, S. Role of the gut microbiota in host appetite control: bacterial growth to animal feeding behaviour. Nat Rev Endocrinol 13, 11–25 (2017). https://doi.org/10.1038/nrendo.2016.150
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DOI: https://doi.org/10.1038/nrendo.2016.150
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