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

Alice de Wouters d’Oplinter, Sabrina J. P. Huwart, Patrice D. Cani +1 more2022Frontiers in NeuroscienceReview
10.3389/fnins.2022.947240PubMedFree full text
Endocrine (ADH/ACTH/MSH)GastrointestinalHypothalamic-PituitaryNeurological

Abstract

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.

References (1)

  • Regulation of hypothalamic proopiomelanocortin mRNA by leptin in ob/ob miceEndocrinology · 1997

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