The gutbrain axis mediates sugar preference

Tan, Hwei-Ee; Sisti, Alexander C.; Jin, Hao; Vignovich, Martin; Villavicencio, Miguel; Tsang, Katherine; Goffer, Yossef; Zuker, Charles S.

doi:10.1530/ey.18.15.6

Cited by 17 publications

(59 citation statements)

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“…As mentioned earlier, food intake is also influenced by nonhomeostatic signals, inducing food intake for pleasure. The hedonic intake of food depends mainly on taste, odor, texture, and appearance (Rosenstein and Oster, 1988;Sorokowska et al, 2017;Tan et al, 2020). The reward system was essential for our hunter-gatherer ancestors to favor a good energy storage in order to increase the survival rate.…”

Section: Non-homeostatic Control Of Food Intake In Physiologymentioning

confidence: 99%

Gut microbes and food reward: From the gut to the brain

et al. 2022

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Inappropriate food intake behavior is one of the main drivers for fat mass development leading to obesity. Importantly the gut microbiota-mediated signals have emerged as key actors regulating food intake acting mainly on the hypothalamus, and thereby controlling hunger or satiety/satiation feelings. However, food intake is also controlled by the hedonic and reward systems leading to food intake based on pleasure (i.e., non-homeostatic control of food intake). This review focus on both the homeostatic and the non-homeostatic controls of food intake and the implication of the gut microbiota on the control of these systems. The gut-brain axis is involved in the communications between the gut microbes and the brain to modulate host food intake behaviors through systemic and nervous pathways. Therefore, here we describe several mediators of the gut-brain axis including gastrointestinal hormones, neurotransmitters, bioactive lipids as well as bacterial metabolites and compounds. The modulation of gut-brain axis by gut microbes is deeply addressed in the context of host food intake with a specific focus on hedonic feeding. Finally, we also discuss possible gut microbiota-based therapeutic approaches that could lead to potential clinical applications to restore food reward alterations. Therapeutic applications to tackle these dysregulations is of utmost importance since most of the available solutions to treat obesity present low success rate.

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Section: Non-homeostatic Control Of Food Intake In Physiologymentioning

confidence: 99%

Gut microbes and food reward: From the gut to the brain

et al. 2022

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“…Following food ingestion, information about nutrient composition and quantity from vagal inputs is relayed to the nucleus tractus solitarius (NTS) in the hindbrain. From there, NTS neurons project to the parabrachial nucleus (PBN) and to the forebrain to promote satiety and reward responses to foods with positive valence (Campos et al, 2016;Han et al, 2018;Tan et al, 2020). A major neuronal circuit that influences appetite and controls food intake involves agoutirelated peptide (AgRP)-and proopiomelanocortin (POMC)-expressing neurons in the arcuate nucleus of the hypothalamus (Waterson and Horvath, 2015).…”

Section: Sensing and Responding To Food Componentsmentioning

confidence: 99%

Food allergy as a biological food quality control system

Florsheim

Sullivan

Khoury-Hanold

et al. 2021

Cell

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“…Indirect evidence implicates this catecholaminergic neuron population as a potential target, as these neurons are directly innervated by vagal sensory neurons (Appleyard et al, 2007) and express cFos in proportion to the volume of ingested meals (Kreisler et al, 2014) and following intravenous injection of a peripherally restricted GLP‐1 agonist (Yamamoto et al, 2003). Additional candidate populations include NTS proenkephalin neurons, recently identified as targets of a vagal‐dependent gut sugar‐sensing circuit (Tan et al, 2020) and calcitonin (CT) receptor‐expressing neurons, which suppress eating, receive vagal input and are activated by peripheral cholecystokinin and exendin‐4 (Cheng et al, 2020). Cre‐dependent circuit mapping approaches have provided valuable insights into the gut‐brain circuitry mediating GLP‐1 signalling (Bai et al, 2019; Brierley et al, 2021).…”

Section: Open Questions Regarding Vagal‐dependent Regulation Of Eatin...mentioning

confidence: 99%

Reappraising the role of the vagus nerve in GLP‐1‐mediated regulation of eating

Brierley

Lartigue

2021

British J Pharmacology

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Here, we provide a focused review of the evidence for the roles of the vagus nerve in mediating the regulatory effects of peripherally and centrally produced GLP-1 on eating behaviour and energy balance. We particularly focus on recent studies which have used selective genetic, viral, and transcriptomic approaches to provide important insights into the anatomical and functional organisation of GLP-1-mediated gut-brain signalling pathways. A number of these studies have challenged canonical ideas of how GLP-1 acts in the periphery and the brain to regulate eating behaviour, with important implications for the development of pharmacological treatments for obesity.LINKED ARTICLES: This article is part of a themed issue on GLP1 receptor ligands

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The gutbrain axis mediates sugar preference

Cited by 17 publications

References 0 publications

Gut microbes and food reward: From the gut to the brain

Gut microbes and food reward: From the gut to the brain

Food allergy as a biological food quality control system

Reappraising the role of the vagus nerve in GLP‐1‐mediated regulation of eating

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The gutbrain axis mediates sugar preference

Cited by 17 publications

References 0 publications

Gut microbes and food reward: From the gut to the brain

Gut microbes and food reward: From the gut to the brain

Food allergy as a biological food quality control system

Reappraising the role of the vagus nerve in GLP‐1‐mediated regulation of eating

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The gutbrain axis mediates sugar preference