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. 2017 May 25;7:2397. doi: 10.1038/s41598-017-02581-8

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© The Author(s) 2017

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/.

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Pharmacological inhibition of the GH signaling reverses most of the TgC6hp55 phenotypic characteristics. 4 groups of mice: 8 wt received saline, 8 wt received pegvisomant (PegV), 8 TgC6hp55 received saline and 8 TgC6hp55 received PegV. (A) Serum levels of Igf-1 in all 4 groups. (B) Body weight curve. *Represent comparison between TgC6hp55+saline versus TgC6hp55+PegV. (C) Body length comparison. (D) Comparison of liver, abdominal white adipose tissue (WAT), lung (both lungs), kidney (both kidneys) and spleen weight among 4 groups. (E) Comparison of the normalized organ weights from (7D) expressed as % of the mouse body weight. (F) Histopathological assessment of the lipid accumulation in the livers of all 4 groups (H/E staining). (G) Histopathological comparison of the adipocyte size from the abdominal white adipose tissue of all 4 groups (H/E staining). (H) Quantification of the adipocyte size shown in Fig. 7F. (F) and (G) are in 200x magnification/scale = 60 μm. Data represent mean ± SEM.