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Endocannabinoids and the Gut-Brain Control of Food Intake and Obesity

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Endocannabinoids and the Gut-Brain Control of Food Intake and Obesity nutrients Review Endocannabinoids and the Gut-Brain Control of Food Intake and Obesity Nicholas V. DiPatrizio Division of Biomedical Sciences, School of Medicine, University of California Riverside, Riverside, CA 92521, USA; [email protected]; Tel.: +1-951-827-7252 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. Keywords: endocannabinoid; CB1 receptor; gut-brain; intestine; food intake; reward Citation: DiPatrizio, N.V. 1. Introduction Endocannabinoids and the Gut-Brain Gut-brain signaling plays an integral role in food intake, energy homeostasis, and Control of Food Intake and Obesity. possibly reward [1–3]. Our understanding of the biochemical and molecular pathways in- Nutrients 2021, 13, 1214. https://doi. volved in these processes and their dysregulation in obesity, however, remains incomplete. org/10.3390/nu13041214 Several signals, including gut-derived peptides, have been identified that control neuro- transmission from peripheral organs to the brain (see for comprehensive review [4]). These Academic Editors: Armin Alaedini, include cholecystokinin (CCK), which is released from subpopulations of enteroendocrine Christine Feinle-Bisset and Michael cells in the upper small-intestinal epithelium in response to the presence of nutrients in the Horowitz lumen and controls food intake and meal size by activating the afferent vagus nerve [1,5–9]. Recent studies in mice suggest that specialized enteroendocrine cells in the intestinal ep- Received: 1 March 2021 ithelium, termed “neuropods”, form functional synapses with gastric afferent vagal fibers Accepted: 2 April 2021 Published: 7 April 2021 and participate in the transduction of signals from food to neural signals carried by vagal afferent neurons to the brain [10]. Neuropods sense nutrients on their luminal side and, in Publisher’s Note: MDPI stays neutral turn, release glutamate and CCK in a coordinated manner that induces rapid or prolonged with regard to jurisdictional claims in firing of vagal afferent neurons, respectively [9]. These results highlight neuropods as a key published maps and institutional affil- cellular mechanism in nutrient sensing and associated gut-brain signaling. Other studies iations. suggest that vagal afferent neurotransmission recruits brain reward circuits and may par- ticipate in food reward [11–14]. For example, optogenetic activation of right gastric vagal afferent neurons increased (i) dopamine release in central reward pathways, (ii) operant responses associated with self-stimulation of brain reward neurons, and (iii) conditioned flavor and place preferences [11]. Specific biochemical and molecular signaling pathways Copyright: © 2021 by the author. Licensee MDPI, Basel, Switzerland. that control these functions, however, remain unclear. This article is an open access article The endocannabinoid (eCB) system is a lipid-derived signaling pathway that controls distributed under the terms and food intake, energy homeostasis, and reward, and is hijacked by chemicals in the cannabis conditions of the Creative Commons plant [15–19] (see Figure1). In general, activating the eCB system increases food intake [ 20] Attribution (CC BY) license (https:// and inhibiting its activity reduces food intake [21]. The eCB system is located throughout creativecommons.org/licenses/by/ the brain and plays an important role in these functions; however, mounting evidence 4.0/). also suggests that the eCB system in peripheral organs, including the small-intestinal Nutrients 2021, 13, 1214. https://doi.org/10.3390/nu13041214 https://www.mdpi.com/journal/nutrients Nutrients 2021, 13, x FOR PEER REVIEW 2 of 15 evidence also suggests that the eCB system in peripheral organs, including the small‐in‐ testinal epithelium, serves an integral role [22–36]. Indeed, pharmacological blockade of Nutrientsperipheral2021, 13, 1214 cannabinoid subtype‐1 receptors (CB1Rs) reduces food intake and improves2 of 15 metabolic dysfunction associated with obesity in rodents similarly to brain‐penetrant CB1R antagonists [21,23,24,27–30,37]. These studies highlight the peripheral eCB system as a possible target forepithelium, safe anti serves‐obesity an integral agents role [that22–36 are]. Indeed, devoid pharmacological of psychiatric blockade side of‐effects peripheral cannabinoid subtype-1 receptors (CB1Rs) reduces food intake and improves metabolic associated with drugs that access CB1Rs in the brain (e.g., rimonabant [38]). dysfunction associated with obesity in rodents similarly to brain-penetrant CB1R antago- The eCB systemnists in the[21,23 rodent,24,27–30 small,37]. These‐intestinal studies epithelium highlight the peripheralbecomes eCB activated system as (i a) possibledur‐ ing oral exposure totarget dietary for safe fats anti-obesity [23,39], ( agentsii) during that are a devoidfast [22,24,40], of psychiatric and side-effects (iii) after associated chronic with exposure to obesogenicdrugs diets that access [25,40,41]. CB1Rs inMoreover, the brain (e.g., pharmacological rimonabant [38]). inhibition of periph‐ The eCB system in the rodent small-intestinal epithelium becomes activated (i) during eral CB1Rs blocked (ioral) cephalic exposure‐phase to dietary consumption fats [23,39], of (ii) dietary during a fats fast in [22 rats,24,40 [23,39],], and (iii (ii)) after refeed chronic‐ ing after a fast in ratsexposure [40], (iii to) obesogenic hyperphagia diets [ 25associated,40,41]. Moreover, with pharmacologicalwestern diet‐ inhibitioninduced of obesity peripheral in mice [25,41], and (CBiv1)Rs restored blocked (nutrienti) cephalic-phase‐induced consumption secretion of dietaryof satiation fats in ratspeptides [23,39], (ii)in westrefeeding‐ ern diet‐induced obeseafter mice. a fast inThese rats [40 studies], (iii) hyperphagia suggest a associated critical role with for western eCB diet-induced signaling obesityin the in mice [25,41], and (iv) restored nutrient-induced secretion of satiation peptides in western gut in the intake of diet-inducedpalatable foods. obese mice.We will These review studies recent suggest experiments a critical role for that eCB expand signaling our in the understanding of rolesgut infor the the intake eCB of system palatable in foods. the Wegut will in reviewgut‐brain recent neurotransmission experiments that expand as‐ our sociated with food intake,understanding energy of homeostasis, roles for the eCB and system reward. in the An gut emphasis in gut-brain will neurotransmission be on stud‐ associated with food intake, energy homeostasis, and reward. An emphasis will be on ies that reveal both indirect and direct mechanisms of control for CB1Rs over gut‐brain studies that reveal both indirect and direct mechanisms of control for CB1Rs over gut-brain signaling and dysregulationsignaling and of these dysregulation pathways of these in pathwaysrodent models in rodent of models diet‐ ofinduced diet-induced obesity. obesity. Figure 1. 1.Endocannabinoid Endocannabinoid metabolic metabolic pathways. pathways. Biosynthesis ofBiosynthesis the endocannabinoid, of the 2-arachidonoyl-endocannabinoid,sn-glycerol 2‐arachi (2-AG),‐ is donoylfacilitated‐sn by‐ diacylglycerolglycerol (2‐AG), lipase- is (DGL) facilitated dependent by hydrolysis diacylglycerol of the 2-AG lipase precursor,‐ (DGL) 1,stearoyl,2-arachidonoyl- dependent hydrolysissn-glycerol of (SAG). 2-AG is degraded by monoacylglycerol lipase (MGL), and to a lesser degree by alpha-beta-hydrolase domain 6 the 2‐AG precursor, 1,stearoyl,2‐arachidonoyl‐sn‐glycerol (SAG). 2‐AG is degraded by monoacyl‐ (ABHD6), into arachidonic acid and glycerol. Biosynthesis of the fatty acid ethanolamide, arachidonoyl ethanolamide (AEA, glycerolanandamide), lipase is controlled (MGL), by andN-acylphosphatidylethanolamide to a lesser degree by alpha phospholipase‐beta‐hydrolase D- (NAPE-PLD) domain dependent 6 (ABHD6), hydrolysis into of the arachidonicAEA precursor, acidN-arachidonoylphosphatidylethanolamide and glycerol. Biosynthesis of the (NArPE). fatty AEA acid is degradedethanolamide, by fatty acid arachidonoyl amide hydrolase ethanola (FAAH)‐ mideinto arachidonic (AEA, anandamide), acid and ethanolamine. is controlled 2-AG and by AEA N‐ activateacylphosphatidylethanolamide cannabinoid subtype-1 receptors phospholipase (CB1R) and cannabinoid D‐ (NAPEsubtype-2‐PLD) receptors dependent (CB2R) in cellshydrolysis throughout of the body AEA (see precursor, for review N [42‐arachidonoylphosphatidylethanola,43]). Alternate endocannabinoid metabolic‐ midepathways (NArPE). have also AEA been suggested.is degraded The by primary fatty intoxicating acid amide chemical hydrolase in the (FAAH) cannabis plant, into Darachidonic9 tetrahydrocannabinol acid and
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