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Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Diabetes. Dec 15, 2017; 8(12): 484-488
Published online Dec 15, 2017. doi: 10.4239/wjd.v8.i12.484
Gut-brain crosstalk regulates craving for fatty food
Rajendra Raghow
Rajendra Raghow, Department of Veterans Affairs Medical Center, Memphis, TN 38104, United States
Rajendra Raghow, Department of Pharmacology, University of Tennessee Health Science Center, Memphis, TN 38163, United States
Author contributions: Raghow R solely wrote this paper.
Conflict-of-interest statement: Raghow R declares that there is neither a conflict of interest with regard to the publication discussed in this FOV communication nor with respect to a commercial entity.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Rajendra Raghow, PhD, Professor, Department of Veterans Affairs Medical Center, 1030 Jefferson Avenue, Memphis, TN 38104, United States. rraghow@uthsc.edu
Telephone: +1-901-5238990 Fax: +1-901-5237274
Received: April 6, 2017
Peer-review started: April 10, 2017
First decision: July 10, 2017
Revised: July 20, 2017
Accepted: September 3, 2017
Article in press: September 4, 2017
Published online: December 15, 2017
Processing time: 245 Days and 8.7 Hours
Core Tip

Core tip: The mechanisms underlying a massive and sustained body weight loss after gastric bypass surgery remain poorly understood. Hankir et al describe how a fat-satiety signaling pathway that was greatly blunted in obese rats could be restored by Roux-en-Y gastric bypass (RYGB) surgery. The authors have demonstrated that RYGB rats on high fat diet (HFD) elicited an increased production of oleoylethanolamide (OEA) and activation of PPARα that led to a surge in dopamine release and activation of D1 in the dorsal striatum. The enhanced dopamine neurotransmission evoked by OEA was obligatorily dependent on intact vagus nerve that had no effect on the production of OEA in the small intestine. The heightened dopamine neurotransmission in the midbrain of RYGB rats was linked to their decreased preference for HFD. These elegant studies have provided a compelling mechanism by which RYGB surgery led to altered gut-brain communication to modify the reward circuitry involved in food preference and obesity. These observations have important clinical implications for the amelioration obesity and its pathological consequences.