Abstract
Introduction. Evolution of nonalcoholic fatty liver disease (NAFLD) is often accompanied by increased levels of homocysteine, on the other hand hyperhomocysteinemia (HHC) is considered as an independent factor for steatosis and fibrosis of the liver. An important role in regulating of liver functional state has IGF-1 and gas mediator – hydrogen sulfide (H2S), but their role in the pathogenesis NAFLD associated with HHC, is not certain.The aim of the study – to investigate level of insulin-like growth factor-1 (IGF-1) in blood and concentration of H2S in the liver of rats with NAFLD induced by high fat diet (HFD) and its combination with HHC.Methods of the research. The experiment was performed on 56 white male rats. Animals were divided into 4 groups. Group 1 and group 2 received standard diet, group 3 and group 4 received HFD for 60 days. Rats from groups 2 and 4 were injected іntragastrically daily by thiolakton homocysteine in the dose of 100 mg/kg. After experiment the levels of homocysteine and IGF-1 in serum and H2S content in the liver of rats were determined.Results and Discussion. Homocysteine thiolactone or HFD and especially their combination causes a reduction of IGF-1 in serum and H2S content in the liver of rats. Rats with NAFLD associated with HHC had levels of H2S and IGF-1 significantly lower (respectively 22.6 % and 32.2 %) than that of rats with purely NAFLD. The level of homocysteine is inversely correlated with the level of IGF-1 in blood and the level of H2S in the liver (r= -0.68, -0.73, р<0.01). Formation of deficit аntifibrotic mediators (IGF-1 and H2S) may be a factor in the progression NAFLD associated with HHC.Conclusions. 60-day use of HFD or homocysteine thiolactone causes reduction of IGF-1 in serum and H2S content in the liver, but the most significant shortage of mediators is as result of the combination HFD with HHC.
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