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. 2014 Sep 9;124(10):4473–4488. doi: 10.1172/JCI75276

Figure 2. Liraglutide treatment regulates ARC gene expression and ARC neuronal activity.

Figure 2

(A) 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. (B) 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 Fishers post-hoc test. (C) Voltage-clamp recording of ARC-NPY neurons showed an increased outward current in the presence of GLP-1(7-36)amide (blue line) and an inward current with NMDA (red line). (D) Simultaneous GABA receptor inhibition by bicuculline (black line) showed a lack of change in the current with the addition of GLP-1(7-36)amide; however, NMDA retained the ability to cause an inward current. (E) The action of GLP-1(7-36) amide was not directly through GLP-1Rs on NPY/AgRP neurons, as no colocalization was observed between GLP-1R– (red, yellow arrows) and NPY/AgRP-positive (green, white arrows) neurons. Scale bars: 100 μm. (F) The effects of GLP-1(7-36)amide in the presence of bicuculline or NMDA on ARC-NPY neurons are summarized (mean ± SEM).