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. 2019 Apr 12;10:155. doi: 10.3389/fendo.2019.00155

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Copyright © 2019 Knudsen and Lau.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Liraglutide and the mouse brain. Distribution of liraglutide⁵⁹⁴ or exendin(9-39)⁵⁹⁴ in brain. (A,B) liraglutide⁵⁹⁴ had access to ARC, in which it bound the GLP-1R and internalized. (B) High-magnification image showed that liraglutide⁵⁹⁴ was internalized and the fluorescent signal was located in the cytoplasm. Staining, Hoechst nuclear stain (blue) and liraglutide⁵⁹⁴/exendin(9-39)⁵⁹⁴(red). Scale bars: 100 μm. Liraglutide treatment regulates ARC gene expression and ARC neuronal activity. (C) Liraglutide treatment for 28 days in DIO rats significantly increased mean Cart mRNA levels in the ARC (^*p < 0.001 liraglutide vs. vehicle and vs. weight matched), whereas Pomc expression was unaffected. (D) Npy and Agrp mRNA levels were significantly increased in weight-matched rats–but not following treatment with liraglutide (†p < 0.05 weight matched vs. vehicle and vs. liraglutide). Data are mean ± SEM, and statistical analyses were performed using 1-way ANOVA, with Fisher's post hoc test. Images (E,F) show neuronal accumulation and activity following GLP-1R simulation. Specifically, panel (E) shows CART- and liraglutide⁵⁹⁴-positive cells shown as mean ± SEM. Staining, Hoechst nuclear strain (blue), liraglutide594 (red) and CART (green). Scale bar: 25 μm. Panel (F) shows the effects of GLP-1(7-36)amide on firing rate of spontaneous action potentials in POMC/CART neurons. (G) Proposed regulation of neuronal activation by liraglutide. Summary diagram demonstrating the suggested regulatory pathway of GLP-1 on ARC NPY and POMC neurons. GLP-1 stimulates POMC neurons directly through the GLP-1R and is suggested to indirectly inhibit ARC-NPY neurons through a local inhibitory GABA neuron. ANOVA, analysis of variance; ARC, arcuate nucleus; CART, cocaine- and amphetamine-regulated transcript; DIO, diabetes induced obesity; GABA, gamma-amino butyric acid; GLP-1, glucagon-like peptide-1; GLP-1R, glucagon-like peptide-1 receptor; NYP, neuropeptide Y; POMC, proopiomelanocortin; SEM, standard error of the mean; veh, vehicle. Republished with permission of American Society For Clinical Investigation, from Secher et al. (117), Copyright 2018; permission conveyed through Copyright Clearance Center, Inc.