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 Jun 23;58(9):4666–4681. doi: 10.1007/s12035-021-02441-7

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 5 — Effects of AdipoRon treatment on expression levels of adiponectin, BDNF, and activation of AMPK and PGC-1α signalling. A STZ-diabetes reduced serum adiponectin levels (Tukey’s post hoc test: ^##P < 0.005 vs. Control-Vehicle). AdipoRon treatment restored serum adiponectin levels in diabetic mice, as voluntary running did (Tukey’s post hoc test: *P < 0.05 vs. STZ-Vehicle). AdipoRon treatment increased serum adiponectin levels in control mice (Tukey’s post hoc test: **P < 0.005 vs. Control-Vehicle) while exercise could not (Tukey’s post hoc test: P > 0.05 vs. Control-Vehicle). n = 7 per group. Previously reported Control-Vehicle and Control-AdipoRon data were used to support this study (44). B Diabetes significantly reduced adiponectin level in DG (Tukey’s post hoc test: ^##P < 0.005 vs. Control-Vehicle), whereas AdipoRon treatment reduced adiponectin levels in control (Tukey’s post hoc test: **P < 0.005 vs. Control-Vehicle). AdipoRon treatment did not restore adiponectin levels in DG from diabetic mice. n = 5 replicates. C Diabetes reduced serum BDNF levels (Tukey’s post hoc test: ^##P < 0.005 vs. Control-Vehicle). AdipoRon and exercise treatment increased serum BDNF levels in control animals (Tukey’s post hoc test: **P < 0.005 vs. Control-Vehicle), while both treatments restored serum BNDF levels in diabetic mice (Tukey’s post hoc test: **P < 0.005 vs. STZ-Vehicle). n = 7 per group. Previously reported Control-Vehicle and Control-AdipoRon data were used to support this study (44). D Diabetes did not alter BDNF level in DG, whereas AdipoRon treatment increased BDNF levels in control (Tukey’s post hoc test: **P < 0.005 vs. Control-Vehicle) and diabetic mice (Tukey’s post hoc test: *P < 0.05 vs. STZ-Vehicle). n = 5 replicates. E Representative images of western blot analysis. (n = 4 technical replicates from 7 pairs of DG pooled-sample/group). F AdipoRon treatment also increased p-AMPKα^Thr172 expression in the hippocampal DG (LSD post hoc test: *P < 0.05 vs. Control-Vehicle). G AdipoRon treatment significantly suppressed the expressions of p-PGC-1α^Ser571, a phosphorylated inhibitory form of PGC-1α, in the DG of control (LSD post hoc test: *P < 0.05 vs. Control-Vehicle) and diabetic mice (LSD post hoc test: ** P < 0.05 vs. STZ-Vehicle)