Do Obese Bacteria Make us “Want them”? Intestinal Microbiota, Mesocorticolimbic Circuit and Non-Homeostatic Feeding

• Published in: Current behavioral neuroscience reports 2018-12, Vol.5 (4), p.211-217
• Main Authors: Urrutia-Piñones, Jocelyn, Illanes-González, Javiera, López-Aguilera, Alejandra, Julio-Pieper, Marcela, Bravo, Javier A.
• Format: Article
• Language: English
• Subjects: Adipocytes; Alzheimer's disease; Bacteria; Behavior; Behavioral Therapy; Brain and Microbiome (S O‘Mahony; Carbohydrates; Diet; Dopamine; Fatty acids; Food; Gene expression; Hypothalamus; Kinases; Ligands; Lipids; Medicine; Medicine & Public Health; Metabolism; Metabolites; Microbiota; Nervous system; Neurology; Pediatrics; Psychiatry; Section Editor; Topical Collection on Brain and Microbiome
• ISSN: 2196-2979; 2196-2979
• DOI: 10.1007/s40473-018-0161-x

Purpose of Review Highly palatable foods (HPF) have rewarding effects, and their consumption induces gut dysbiosis. Because intestinal microbes communicate bidirectionally with the brain, we reviewed the literature in order to link the effects of HPF on the brain reward system and on gut microbiota. Additionally, we propose these alterations contribute to the pathophysiology of obesity. Recent Findings Non-homeostatic consumption of HPF programs the brain to seek these foods from early-life. Fatty food induces gut dysbiosis, which might alter communications to the brain. Additionally, prebiotic fibre and short-chain fatty acids affect the neurochemistry of the rodent mesocorticolimbic circuit. Summary Consumption of HPF might start a vicious cycle by (1) activating the mesocorticolimbic circuit, leading to (2) non-homeostatic feeding, affecting the host’s metabolism and (3) altering gut microbes. The latter might impact the brain’s reward system, which becomes reinforced by signals from gut symbionts, thus contributing to the pathophysiology of obesity.