INDUCTION OF HEME OXYGENASE REVERTS ENDOPLASMIC RETICULUM STRESS GENERATED IN A RAT MODEL OF NON-ALCOHOLIC FATTY LIVER DISEASE

MORENA WISZNIEWSKI; CAROLINA VECINO; JUAN SALVADOR CALANNI; SILVIA I SANCHEZ PUCH; CORA CYMERYNG; ESTEBAN MARTÍN REPETTO

Congreso; REUNIÓN CONJUNTA DE SOCIEDADES DE BIOCIENCIAS; 2017

Non-alcoholic fatty liver disease is a common chronic liverdisease that has been associated with metabolic syndrome.Under certain stressful conditions, such as those describedin the liver of animals fed a sucrose-rich diet (SRD), normalfunctions of the endoplasmic reticulum become compromisedleading to the accumulation of misfolded proteins andinducing the unfolded protein response (UPR). Taking intoaccount that oxidative stress (OS) could trigger an UPR theaim of this study was to evaluate the effects of heme oxygenase-1 (HO-1) induction on the liver of SRD treated rats. MaleWistar rats were randomly distributed into control (C) or SRDgroups (30% sucrose in the drinking water over 12 weeks).Hemin treatment (15 mg/kg/48h, ip) was administered duringthe last two weeks of the dietary modification (H and SRD+Hgroups). Our results indicate that rats fed a SRD showedan increased liver content of TAG and cholesterol. We alsoobserved higher catalase and SOD activities, and TBARSlevels which were attenuated by hemin treatment. Hemintreatment did not modify triglyceride/HDL-c index (insulin resistanceparameter), glycaemia or the histological features(analyzed by H&E or Sudan IV) of the livers of C or SRDtreated rats, although HO-1 induction was confirmed in thesetissues. Nonetheless, hemin was effective in reverting theincrease in serum levels of transaminases (ALT), a marker ofliver damage, observed in SRD-treated rats (SRD+H p