Table 1.
Baseline characteristics and hemodynamics of rats fed for 1 month a control (CD) or a cafeteria (CafD) diet.
Figure 1.
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).
(original magnification, x100 or x200 as displayed in the figures).
Figure 2.
Liver inflammation and hepatic stellate cells phenotype.
A) 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) Cafeteria diet did not induce activation of HSC as assessed by immunohistochemistry for α-SMA.
Figure 3.
Ex-vivo assessment of liver circulation.
Portal Perfusion Pressure (PPP) in CafD (n = 12) and CD rats (n = 12) in the absence (A) or the presence (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).
Figure 4.
CafD rats show liver endothelial dysfunction.
A) Response to ACh in livers from control diet rats (CD; black squares; n = 6) and high fat diet rats (CafD; white circles; n = 6). B) NOS activity in liver homogenates from control rats (CD; n = 4) and cafeteria fed-rats (CafD; n = 4). C) Representative blots and densitometry readings of liver P-Akt (at Ser473) to Akt ratio and D) P-eNOS (at Ser1176) to eNOS ratio (western blotting). AU: Arbitrary Units.
Figure 5.
Representative blots and densitometry readings of liver P-eNOS (at Ser1176) to eNOS ratio (western blotting), five minutes after a portal injection of vehicle (white bars and -) or insulin (black bars and +).
Insulin increased eNOS phosphorylation in CD rats (A) but not in CafD rats (B).
Figure 6.
Cafeteria diet did not induce changes in A) SE-1 expression nor B) CD31, which are closely correlated with fenestrations and capillarization at the sinusoidal endothelial cells. C) Cafeteria diet did not induce de novo expression of CD34, a marker of loss of LSEC phenotype.