HEME-OXYGENASE-1 UPREGULATED BY S-ADENOSYLMETHIONINE.
POTENTIAL PROTECTION AGAINST NON-ALCOHOLIC FATTY
LIVER INDUCED BY HIGH FRUCTOSE DIET
GANKA BEKYAROVA1*, MARIA TZANEVA2, KAMELIA BRATOEVA1, ISCREN KOTZEV3, MARIA RADANOVA4
1Department of Physiology and Pathophysiology, Medical University – Varna, Bulgaria
2Department of General and Clinical Pathology, Medical University – Varna, Bulgaria
3Clinic of Gastroenterology MHAT “ST Marina“, Medical University – Varna, Bulgaria
4Department of Biochemistry, Molecular Medicine and Nutrigenomics, Medical University – Varna, Bulgaria
*corresponding author: gabekyarova2001@yahoo.com
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Abstract:
Excessive dietary fructose intake may have an important role in the current epidemics of fatty liver disease, obesity and
diabetes- features of metabolic syndrome. We evaluated the relationship between lipid peroxidation and other oxidative stress
biomarkers with changes in expression of heme oxygenase-1 (HO-1) in rat fatty liver, induced by high fructose diet (HFD)
and the effect of S-adenosylmethionine (SAMe). Twenty-one male rats were randomly assigned to three groups of seven
animals each: HFD (35% fructose in drinking water for 16 weeks) group, HFD + SAMe (20 mg/kg b.w. in drinking water for
16 weeks) group and control group. HO-1 expression, malonyl dialdehyde (MDA) (a marker of lipid peroxidation),
triglycerides (TG), SH group levels and histological studies were performed on hepatic tissue. HFD group showed
microvesicular steatosis without inflammation and fibrosis. In HFD+SAM group microvesicular steatosis was not
established. The HO-1 expression was significantly increased in HFD rats. SEMe augmented the increase in expression of
HO-1. The levels of MDA and TG were elevated in HFD group. In HFD rats with lower levels of SH exhibited higher
expression of HO-1. SAMe inhibited the increase in lipid peroxidation and TG levels and prevented the decrease in SH
levels. In conclusion, SAMe has an important hepatoprotective effect and its protection is most probably exerted by
increasing the expression of the antioxidant enzyme HO-1, in order to prevent the development of fatty liver.






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