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. 2021 Sep 13;11:18114. doi: 10.1038/s41598-021-97624-6

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© 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/.

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Mice treated with TUDCA display ameliorated hypothalamic leptin signaling. Serum leptin levels (A) and gene expression of Lep-R (B) normalized by GAPDH in the hypothalamus. Acute food intake after leptin (5 mg/kg, i.p.) load (C). Representative western blot images of p-JAK2, total JAK2, p-STAT3, total STAT3 and GAPDH in the hypothalamus (D). Protein content of p-JAK2 (Tyr1007/8) normalized by total JAK2 (E) and p-STAT3 (Tyr705) normalized by total STAT3 (F) in the hypothalamus, 45 min after leptin (5 mg/kg, i.p.) load. GAPDH was employed as a housekeeping protein for total JAK2 and STAT3 normalization. Data are expressed as means ± SEM (n = 4–8). Different letters indicate significant differences between groups (P ≤ 0.05), based on one-way ANOVA test followed by Tukey post-hoc-test. AU arbitrary units.