Hematoxylin/eosin (H/E), oil-red, Mason’s Thricrome images and steatosis area from livers from rats fed a control diet (CD) or a high fat diet (CafD).

<p>(original magnification, x100 or x200 as displayed in the figures).</p

Liver inflammation and hepatic stellate cells phenotype.

<p><b>A</b>) Immunohistochemistry showing CD43 (a pan-leukocyte marker) immunostaining in livers from high fat feeding (CafD) and control rats (CD). The administration for 1 month of a high fat diet did not induce liver inflammation (original magnification: x200). <b>B</b>) Cafeteria diet did not induce activation of HSC as assessed by immunohistochemistry for α-SMA.</p

Ex-vivo assessment of liver circulation.

<p>Portal Perfusion Pressure (PPP) in CafD (n = 12) and CD rats (n = 12) in the absence (<b>A</b>) or the presence (<b>B</b>) of the NO donor sodium nitroprusside (SNP). Livers from rats fed cafeteria diet showed an increased PPP. No differences were observed in the presence of SNP (CD: control diet; CafD: cafeteria diet).</p

Baseline characteristics and hemodynamics of rats fed for 1 month a control (CD) or a cafeteria (CafD) diet.

<p>Data is presented as mean ± SD. (FFA: free fatty acids).</p

Endothelial cells phenotype.

<p>Cafeteria diet did not induce changes in <b>A</b>) SE-1 expression nor <b>B</b>) CD31, which are closely correlated with fenestrations and capillarization at the sinusoidal endothelial cells. <b>C</b>) Cafeteria diet did not induce <i>de novo</i> expression of CD34, a marker of loss of LSEC phenotype.</p