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. 2019 Nov 21;69(8):1423–1431. doi: 10.1136/gutjnl-2019-319372

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© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article 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, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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Schematic illustration of the proposed ketone body mechanism on GLP-1 producing enteroendocrine cells (EECs). Chronic free fatty acid (FFA) exposure induces increased mHMGCS expression and βHB production in jejunal epithelial cells in the villi tips. βHB reaches the EECs via the venous microcirculation of the villi, and acts via FFAR3/GPR41 to inhibit the production/release of GLP-1. RYGB surgery may interfere with this mechanism by decreasing FFA availability and mHMGCS expression. GAPDH, glyceraldehyde-3-phosphate dehydrogenase; GLP-1, glucagon-like peptide-1; mHMGCS, mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase; RYGB, Roux-en-Y gastric bypass.