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

. 2014 Feb 20;15(2):3040–3063. doi: 10.3390/ijms15023040

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

© 2014 by the authors; licensee MDPI, Basel, Switzerland

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).

PMC Copyright notice

Figure 2. — (a) Adipocyte diameter: The mean diameter of the L adipocytes was significantly higher compared with that of the F group. The mean adipocyte diameters of both the L and the F rats were significantly higher than that of the N group. The data represent the means ± SE (100 cells/animal, 8 animals/group). * p < 0.05 vs. N rats; and ^# p < 0.05 vs. L rats; (b) Representative Western blot analysis of TGFβ1 and corresponding densitometric analysis on the relative protein levels. The data represent the means ± SE. * p < 0.05 vs. N rats; (c) Histological sections of rats fed a control diet (N), high-lard diet (L) or high-fish oil diet (F) that indicate the presence and relative abundance of crown-like structures (CLSs) around hypertrophic adipocytes. No CLSs were observed in the N rats; (d) Immunostaining of histological sections of the N, L and F rats. MCP1: No immunostaining for MCP1 was observed in the N rats. Immunoreactivity was present in CLSs (dashed arrow) and in the rim of the cytoplasm of adipocytes in the L and F rats (arrow). TGFβ1: The immunostaining was weak in the N section, whereas the L section demonstrated the strongest immunostaining among the groups. InsR (insulin receptor): Following insulin administration (15 min after an i.p. injection of insulin (homologue rapid-acting, 10 units/kg body wt; Novartis)), the N and F eWAT sections exhibited strong immunoreactivity in some areas (arrows), whereas weak immunoreactivity was localised in the L adipocytes (arrows). Glut4: After the insulin injection, the immunostaining for the glucose transporter Glut4 demonstrated an identical distribution as that of InsR and was evident in N and F (arrows) sections, whereas the L section demonstrated weak Glut4 immunostaining that occurred in areas with apparent stromal-vascular cell localization (arrows). PPARγ: Immunoreactivity was observed in the adipocyte cytoplasm and in the vascular stromal cells in all groups of rats. In the F rats, we found the highest immunolabelling of both adipocyte cytoplasm and nuclei, which was consistent with the translocation of PPAR into the nuclei (arrows).

Figure 2. — (a) Adipocyte diameter: The mean diameter of the L adipocytes was significantly higher compared with that of the F group. The mean adipocyte diameters of both the L and the F rats were significantly higher than that of the N group. The data represent the means ± SE (100 cells/animal, 8 animals/group). * p < 0.05 vs. N rats; and ^# p < 0.05 vs. L rats; (b) Representative Western blot analysis of TGFβ1 and corresponding densitometric analysis on the relative protein levels. The data represent the means ± SE. * p < 0.05 vs. N rats; (c) Histological sections of rats fed a control diet (N), high-lard diet (L) or high-fish oil diet (F) that indicate the presence and relative abundance of crown-like structures (CLSs) around hypertrophic adipocytes. No CLSs were observed in the N rats; (d) Immunostaining of histological sections of the N, L and F rats. MCP1: No immunostaining for MCP1 was observed in the N rats. Immunoreactivity was present in CLSs (dashed arrow) and in the rim of the cytoplasm of adipocytes in the L and F rats (arrow). TGFβ1: The immunostaining was weak in the N section, whereas the L section demonstrated the strongest immunostaining among the groups. InsR (insulin receptor): Following insulin administration (15 min after an i.p. injection of insulin (homologue rapid-acting, 10 units/kg body wt; Novartis)), the N and F eWAT sections exhibited strong immunoreactivity in some areas (arrows), whereas weak immunoreactivity was localised in the L adipocytes (arrows). Glut4: After the insulin injection, the immunostaining for the glucose transporter Glut4 demonstrated an identical distribution as that of InsR and was evident in N and F (arrows) sections, whereas the L section demonstrated weak Glut4 immunostaining that occurred in areas with apparent stromal-vascular cell localization (arrows). PPARγ: Immunoreactivity was observed in the adipocyte cytoplasm and in the vascular stromal cells in all groups of rats. In the F rats, we found the highest immunolabelling of both adipocyte cytoplasm and nuclei, which was consistent with the translocation of PPAR into the nuclei (arrows).