Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 May 11;12:2662. doi: 10.1038/s41467-021-22940-4

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 7 — a Representative immunostaining images from n = 3–4 mice as shown in b for p-AMPK in hypothalamic sections were shown from control (a, Non-diabetic), T1D with saline treatment (a, T1D + saline), T1D with leptin treatment (a, T1D + leptin), and T1D with both leptin and 2-DG treatments (T1D + leptin+2-DG) at fed conditions. b Comparison in the percentage of LepR^Arc neurons with p-AMPK expression among the four groups (one-way ANOVA, n = 4 for nondiabetic controls and T1D-saline and n = 3 for T1D-leptin and T1D-leptin-2-DG, F(3, 10) = 42.27, ***P < 0.0001, nondiabetes vs T1D-saline; **P = 0.0051, T1D-saline vs T1D-leptin; ***P = 0.004, T1D-leptin vs T1D-leptin-2_DG). c Representative pictures from n = 1 mouse showing colocalization between p-AMPK (green) and c-Fos (red) in the Arc of T1D LepR-Cre mice. d, e Wild-type mice (8–9 weeks of age, males) were made T1D and then i.c.v. treated with leptin to restore euglycemia. These mice were then treated with i.c.v. injections of either saline or AICAR, an agonist of AMPK. Comparisons in blood glucose were shown following i.c.v. AICAR (d, two-way ANOVA, n = 3/each, F(1, 20) = 35.91, *P = 0.0374, saline vs AICAR at the 90-min time point) and in blood glucagon at 90 min after AICAR injection (e, two-tailed unpaired Student’s t tests, n = 8/each, t = 3.862, df = 14; n = 9/each, **P = 0.0017). f Diagram depicting hyperglycemia in T1D caused by heightened Arc GABAergic neuron activity due to energy deprivation and low leptin levels (top) and euglycemia restoration by leptin inhibition of neuron activity through reversing energy deprivation (bottom). 3: the third ventricle and Arc: arcuate nucleus. Data presented as mean ± SEM. 3V the third ventricle, Arc arcuate nucleus; Scale bar: 100 µM.