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Rosiglitazone and bezafibrate modulate gene expression in a rat model of non-alcoholic fatty liver disease--a historical prospective.

Schmilovitz-Weiss H, Hochhauser E, Cohen M, Chepurko Y, Yitzhaki S, Grossman E, Leibowitz A, Ackerman Z, Ben-Ari Z - Lipids Health Dis (2013)

Bottom Line: The proteins of MnSOD2, PPAR-α and PPAR-γ in the FED rats decreased (2.5, 2, and 2.2, respectively) (p<0.05).A consistent reduction in hepatic expression of MnSOD2, PPAR-α and PPAR-γ in the FED rats compared with controls was observed.Administration of either rosiglitazone or bezafibrate to the FED rats restored these genes to a pre-morbid state.

View Article: PubMed Central - HTML - PubMed

Affiliation: Division of Gastroenterology, Rabin Medical Center, Hasharon Hospital, Petach Tikva, Israel. hemdaw1@netvision.net.il

ABSTRACT

Background: Genetic factors implicated in the pathogenesis of non-alcoholic fatty liver disease are poorly understood. Our aim was to characterize three genes involved in a rat model of non-alcoholic fatty liver disease and investigate the effect of rosiglitazone and bezafibrate.

Method: Five rats were fed a chow diet (controls) and 18 a fructose-enriched diet (FED) for 5 weeks: 6 were administered rosiglitazone and 6 bezafibrate during the last 2 weeks and 6 were not treated at all. Livers were examined by reverse transcription-PCR for the genes encoding peroxisome proliferator-activated receptors (PPAR), PPAR-α, PPAR-γ, and Mn superoxide dismutase2 (Mn SOD2). Western blot was used for proteins levels.

Result: The FED rats showed a decrease in mRNA of MnSOD2, PPAR-α, and PPAR-γ (3, 3.5 fold, and 27%, respectively) (p<0.05). The 3 genes normalized in response to rosiglitazone and bezafibrate. The proteins of MnSOD2, PPAR-α and PPAR-γ in the FED rats decreased (2.5, 2, and 2.2, respectively) (p<0.05). Following administration of rosiglitazone, proteins of MnSOD2, PPAR-α and PPAR-γ in the FED rats increased (reaching 1.5-fold, a 20% increase and normalization, respectively), (p<0.05). Administration of bezafibrate to the FED rats restored the proteins of 3 genes to baseline.

Conclusion: A consistent reduction in hepatic expression of MnSOD2, PPAR-α and PPAR-γ in the FED rats compared with controls was observed. Administration of either rosiglitazone or bezafibrate to the FED rats restored these genes to a pre-morbid state.

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Effect of rosiglitazone and bezafibrate on PPAR- γ gene expression (A) and protein level (B). * = p<0.05.
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Figure 3: Effect of rosiglitazone and bezafibrate on PPAR- γ gene expression (A) and protein level (B). * = p<0.05.

Mentions: Hepatic PPAR-γ mRNA expression decreased by 27% in the FED rats compared with the controls levels (p<0.05). Hepatic protein level decreased 2.2-fold. Rosiglitazone and bezafibrate administration restored gene expression to baseline. Protein levels reached 20% above the control levels (p<0.05) in the rosiglitazone treated group and reached control levels in the bezafibrate-treated rats (Figure 3A and 3B).


Rosiglitazone and bezafibrate modulate gene expression in a rat model of non-alcoholic fatty liver disease--a historical prospective.

Schmilovitz-Weiss H, Hochhauser E, Cohen M, Chepurko Y, Yitzhaki S, Grossman E, Leibowitz A, Ackerman Z, Ben-Ari Z - Lipids Health Dis (2013)

Effect of rosiglitazone and bezafibrate on PPAR- γ gene expression (A) and protein level (B). * = p<0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3643834&req=5

Figure 3: Effect of rosiglitazone and bezafibrate on PPAR- γ gene expression (A) and protein level (B). * = p<0.05.
Mentions: Hepatic PPAR-γ mRNA expression decreased by 27% in the FED rats compared with the controls levels (p<0.05). Hepatic protein level decreased 2.2-fold. Rosiglitazone and bezafibrate administration restored gene expression to baseline. Protein levels reached 20% above the control levels (p<0.05) in the rosiglitazone treated group and reached control levels in the bezafibrate-treated rats (Figure 3A and 3B).

Bottom Line: The proteins of MnSOD2, PPAR-α and PPAR-γ in the FED rats decreased (2.5, 2, and 2.2, respectively) (p<0.05).A consistent reduction in hepatic expression of MnSOD2, PPAR-α and PPAR-γ in the FED rats compared with controls was observed.Administration of either rosiglitazone or bezafibrate to the FED rats restored these genes to a pre-morbid state.

View Article: PubMed Central - HTML - PubMed

Affiliation: Division of Gastroenterology, Rabin Medical Center, Hasharon Hospital, Petach Tikva, Israel. hemdaw1@netvision.net.il

ABSTRACT

Background: Genetic factors implicated in the pathogenesis of non-alcoholic fatty liver disease are poorly understood. Our aim was to characterize three genes involved in a rat model of non-alcoholic fatty liver disease and investigate the effect of rosiglitazone and bezafibrate.

Method: Five rats were fed a chow diet (controls) and 18 a fructose-enriched diet (FED) for 5 weeks: 6 were administered rosiglitazone and 6 bezafibrate during the last 2 weeks and 6 were not treated at all. Livers were examined by reverse transcription-PCR for the genes encoding peroxisome proliferator-activated receptors (PPAR), PPAR-α, PPAR-γ, and Mn superoxide dismutase2 (Mn SOD2). Western blot was used for proteins levels.

Result: The FED rats showed a decrease in mRNA of MnSOD2, PPAR-α, and PPAR-γ (3, 3.5 fold, and 27%, respectively) (p<0.05). The 3 genes normalized in response to rosiglitazone and bezafibrate. The proteins of MnSOD2, PPAR-α and PPAR-γ in the FED rats decreased (2.5, 2, and 2.2, respectively) (p<0.05). Following administration of rosiglitazone, proteins of MnSOD2, PPAR-α and PPAR-γ in the FED rats increased (reaching 1.5-fold, a 20% increase and normalization, respectively), (p<0.05). Administration of bezafibrate to the FED rats restored the proteins of 3 genes to baseline.

Conclusion: A consistent reduction in hepatic expression of MnSOD2, PPAR-α and PPAR-γ in the FED rats compared with controls was observed. Administration of either rosiglitazone or bezafibrate to the FED rats restored these genes to a pre-morbid state.

Show MeSH
Related in: MedlinePlus