Abstract
Gut-brain signaling controls food intake and energy homeostasis, and its activity is thought to be dysregulated in obesity. We will explore new studies that suggest the endocannabinoid (eCB) system in the upper gastrointestinal tract plays an important role in controlling gut-brain neurotransmission carried by the vagus nerve and the intake of palatable food and other reinforcers. A focus will be on studies that reveal both indirect and direct interactions between eCB signaling and vagal afferent neurons. These investigations identify (i) an indirect mechanism that controls nutrient-induced release of peptides from the gut epithelium that directly interact with corresponding receptors on vagal afferent neurons, and (ii) a direct mechanism via interactions between eCBs and cannabinoid receptors expressed on vagal afferent neurons. Moreover, the impact of diet-induced obesity on these pathways will be considered.
Highlights
Gut-brain signaling plays an integral role in food intake, energy homeostasis, and possibly reward [1,2,3]
To test the necessity for cannabinoid subtype-1 receptors (CB1 Rs) in the intestinal epithelium in the intake of palatable foods, we developed transgenic mice (Cnr1tm1 .1 mrl /Vil-CRE ERT2) that are conditionally deficient in CB1 Rs in the intestinal epithelium [63]
Preferences for western diet were reduced for up to 12 h in IntCB1 -/mice. These results provide direct evidence that CB1 Rs in the murine intestinal epithelium are required for acute preferences for palatable foods
Summary
Gut-brain signaling plays an integral role in food intake, energy homeostasis, and possibly reward [1,2,3]. Several signals, including gut-derived peptides, have been identified that control neurotransmission from peripheral organs to the brain (see for comprehensive review [4]) These include cholecystokinin (CCK), which is released from subpopulations of enteroendocrine cells in the upper small-intestinal epithelium in response to the presence of nutrients in the lumen and controls food intake and meal size by activating the afferent vagus nerve [1,5,6,7,8,9]. After a fast in rats [40], (iii) hyperphagia associated with western diet-induced obesity in ern diet‐induced obese mice These studies suggest a critical role for eCB signaling in the mice [25,41], and (iv) restored nutrient-induced secretion of satiation peptides in western gut in the intake of diet-induced palatable foods. Glycerol (2-AG) and arachidonoyl ethanolamide (anandamide), their metabolic enzymes, and cannabinoid receptor sub-type 1 (CB1 R), cannabinoid receptor sub-type-2 (CB2 Rs), and
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