Steatosis recovery after treatment with a balanced sunflower or olive oil-based diet: involvement of perisinusoidal stellate cells - PubMed (original) (raw)

Steatosis recovery after treatment with a balanced sunflower or olive oil-based diet: involvement of perisinusoidal stellate cells

Raquel Hernández et al. World J Gastroenterol. 2005.

Abstract

Aim: To analyze the relationship between perisinusoidal stellate cell (PSC) activation and the dietary fat quantity and composition in the treatment of hepatic steatosis.

Methods: Using an experimental rat model of steatosis based on the intake of a hyperlipidic diet (14% fat as olive oil or sunflower oil, HL-O and HL-S, respectively), we analyzed the liver's capability of recovery after the treatment with a normal-lipidic diet (5% fat as olive oil or sunflower oil, NL-O and NL-S, respectively) by immunocytochemical and Western blot analysis of glial fibrillary acidic protein (GFAP) expression in PSCs, collagen quantification and serum aminotransferase determination.

Results: The fatty infiltration in the steatotic livers decreased after the treatment with both NL diets, indicating liver recovery. This decrease was accompanied with a lower collagen deposition and aminotransferase level as well as changes in the PSC population that increased the GFAP expression. The above-mentioned effects were more pronounced in animals fed on NL-O based diet.

Conclusion: Treatment with a balanced diet enriched in olive oil contributes to the liver recovery from a steatotic process. The PSC phenotype is a marker of this hepatic-recovery model.

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Figures

Figure 1

Figure 1

Light micrographs of representative liver sections from rats of each dietary group stained for fat with OsO4. A: High-lipidic olive oil; B: normal-lipidic olive oil; C: high-lipidic sunflower oil; D: normal-lipidic sunflower oil. PT: portal triad; CV: central vein. Scale bar, 100 μm.

Figure 2

Figure 2

Collagen quantification in the high fat-induced steatotic liver (HL-O, HL-S) after its treatment with a normal-lipidic diet (NL-O, NL-S). Data are mean±SD of four determinations. HL-O, high-lipidic olive oil; NL-O normal-lipidic olive oil; HL-S, high-lipidic sunflower oil; NL-S normal-lipidic sunflower oil. Significantly greater than in corresponding HL group: a_P_<0.05 vs HL-S, 1_P_<0.02 vs NL-O.

Figure 3

Figure 3

Distribution and location of GFAP immunoreactivity. A: GFAP-positive cells were distributed evenly in the lobule; B: GFAP-IR cells with processes circumscribing a hepatic sinusoid; C: GFAP-IR cell showing lipid droplets in its cytoplasm; D: GFAP-IR cell sending processes towards the vascular vessel. HS, hepatic sinusoid. CV, central vein; black arrow, lipid droplets; scale bar A: 100 mm; scale bars B-D: 10 μm.

Figure 4

Figure 4

Light micrographs of representative liver sections from rats of each dietary group immunostained with GFAP antiserum. A: High-lipidic olive oil; B: normal-lipidic olive oil; C: high-lipidic sunflower oil; D: normal-lipidic sunflower oil. Scale bar, 10 μm.

Figure 5

Figure 5

Western blot analysis of GFAP expression. Top panel: densitometric quantification of GFAP in the high-fat-induced steatotic liver (HL-O and HL-S), and after its treatment with a normal-lipidic diet (NL-O, NL-S). Results were average values of four experimental animals in each group. HL-O, high-lipidic olive oil; NL-O, normal-lipidic olive oil; HL-S, high-lipidic sunflower oil; NL-S, normal-lipidic sunflower oil. Bottom panel: representative autoradiography of the corresponding GFAP band. α-Tubulin immunodetection was also included as a protein-loading control. Protein expression is significantly greater than in HL-O group (b_P_<0.001).

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